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Chronic consumption of ethanol in adult rats and humans leads to reduced AVP-producing neurons, and prenatal ethanol (PE) exposure has been reported to cause changes in the morphology of AVP-producing cells in the suprachiasmatic nucleus of young rats. The present studies further characterize the effects of PE exposure on AVP in the young adult rat, its hypothalamic synthesis, pituitary storage, and osmotically stimulated release. Pregnant rats were fed a liquid diet with 35% of the calories from ethanol or a control liquid diet for days 7–22 of pregnancy. Water consumption and urine excretion rate were measured in the offspring at 60–68 days of age. Subsequently, the offspring were infused with 5% NaCl at 0.05 ml·kg−1·min−1 with plasma samples taken before and at three 40-min intervals during infusion for measurement of AVP and osmolality. Urine output and water intake were ∼20% greater in PE-exposed rats than in rats with no PE exposure, and female rats had a greater water intake than males. The relationship between plasma osmolality and AVP in PE-exposed rats was parallel to, but shifted to the right of, the control rats, indicating an increase in osmotic threshold for AVP release. Pituitary AVP was reduced by 13% and hypothalamic AVP mRNA content was reduced by 35% in PE-exposed rats. Our data suggest that PE exposure can cause a permanent condition of a mild partial central diabetes insipidus.

Demands of medical residency training would be expected to result in physical deconditioning. This study determined the effects of residency on physical fitness.A prospective cohort study of the change in physical conditioning during residency using the Army Physical Fitness Test as a standardized measure of fitness was conducted. Ninety-four active duty U.S. Army physicians were followed during their medical residency training from July 1999 to June 2002. Army Physical Fitness Test results from interval tests performed throughout residency were compared to baseline results at matriculation. Changes in total score, number of push-ups and sit-ups completed in 2 minutes, 2-mile run time, and weight were recorded. Correlations between initial and final scores were evaluated.All measured parameters worsened with statistical significance noted in the weight (p0.01), push-ups (p0.05), and 2-mile run (p0.01). Statistically significant negative correlations between initial and subsequent tests were noted in push-ups (p = 0.004), sit-ups (p = 0.0003), and total score (p = 0.0192).Physical fitness declines during medical residency training. This effect is most notable in residents with higher levels of fitness at the start of medical education. Further studies are necessary to evaluate for a similar decline among civilian residents.

OBJECTIVE The goal of this study was to determine attitudes toward oral contraceptive pill (OCP)-induced amenorrhea among U.S. Army women. METHODS A volunteer sample (N = 154) of Army Active Duty, Reserve, and National Guard women completed an anonymous survey. RESULTS Desire for temporary amenorrhea was high with 86% (+/- 6%, 95% confidence interval [CI]) and 83% (+/-6%, 95% CI) desiring amenorrhea during field training and deployments, respectively. Fifty-four percent were unaware that OCPs can induce amenorrhea; only 7% (+/-4%, 95% CI) have used this practice during deployment. If made available with education, 49% (+/-8%, 95% CI) would use this practice. Logistic burdens of menstruation were associated with higher rates of desirability for OCP use with soldiers desiring OCPs rating their inconveniences significantly higher than those who did not desire OCPs (p < 0.05). CONCLUSION Although a significant number of soldiers desire OCP-induced amenorrhea, a large deficit in knowledge exists. Routine education as an Army-wide standard is warranted.

This study was conducted to determine whether 100% FiO2 during hemorrhage would improve maintenance of mean arterial blood pressure and to assess the cardiovascular, arginine vasopressin, and renin-angiotensin system roles in the response. This also allowed evaluation of FiO2 effects on the baroreceptor control of these hormone systems. Six conscious female goats were hemorrhaged (0.5 mL x kg(-1) x min(-1)) for 30 minutes, while breathing 11%, 21%, or 100% O2. Mean arterial blood pressure was maintained only when the goats breathed 100% O2. FiO2 did not affect O2 consumption or delivery during hemorrhage. Increases in renin and arginine vasopressin were equal or reduced with 100% FiO2 and therefore did not contribute to the improved mean arterial blood pressure maintenance. Inspiration of 100% FiO2 during hemorrhage, therefore, may improve perfusion pressure with no changes in O2 consumption or delivery. Also, 100% FiO2 eliminated the negative correlation between both hormones and right atrial pressure, suggesting altered baroreceptor control of the hormones.

During mixed gas saturation diving (to 3-49.5 ATA) daily urine flow increases by about 500 ml/day, with no changes in fluid intake and glomerular filtration rate. The diuresis is accompanied by a significant decrease in urine osmolality and increase in excretion of such solutes as urea, K+, Na+, Ca2+ and inorganic phosphate (Pi). The fall in urine osmolality is mainly due to a reduction of free water reabsorption which is associated with a suppression of insensible water loss and the attendant inhibition of antidiuretic hormone (ADH) system. The increase in urea excretion may be associated with a reduction of urea reabsorption at the collecting duct as a consequence of ADH suppression. The rise in K+ excretion is due to a facilitated K+ secretion at the distal tubule as a result of increased aldosterone, urine flow and excretion of impermeable anions such as Pi. The activation of aldosterone system is partly attributed to a transient dehydration induced by early hyperbaric diuresis. The increase in Na+ excretion in the face of enhanced aldosterone secretion indicates that the Na+ transport in the proximal tubule is markedly inhibited (by unknown mechanism). The Pi excretion increases with no changes in plasma level of parathyroid hormone (PTH), thus it may be due to an inhibition of Na(+)-Pi cotransport in the proximal tubule. The increase in Ca2+ excretion may be secondary to the inhibition of Na+ transport at the proximal tubule. Precise information on the proximal tubular Na+ transport is important to understand the mechanisms of impaired solute transport under hyperbaric conditions.

The sections in this article are: 1 Rationale 2 High Pressure Nervous Syndrome 2.1 Signs and Symptoms 2.2 Prevention of HPNS 2.3 Mechanisms of HPNS 3 Thermoregulatory Function 3.1 Physical Characteristics of Helium Environment 3.2 Comfortable Temperature 3.3 Convective Heat Loss 3.4 Radiation 3.5 Evaporation 3.6 Respiratory Heat Loss 3.7 Possible Metabolic Effects 3.8 Physical Activity 3.9 Specific Technical Problems 4 Work Capacity 5 Cardiopulmonary Functions 5.1 Respiratory Functions 5.2 Cardiovascular Functions 6 Body Fluid Balance 6.1 Physical Characteristics of the Environment Which Affect Body Fluid Balance 6.2 Characteristics of Hyperbaric Diuresis 6.3 Mechanisms of Hyperbaric Diuresis 6.4 Effects of Immersion 7 Conclusions

Over the past decade several new routes of neurohypophysial hormone metabolism have been identified. These include nonhepatic splanchnic clearance and renal clearance in addition to filtration that appears to be receptor mediated. The intraluminal degradation of VP in the proximal tubule, and distal tubular secretion, at least in one species, has been identified. The brain has been identified as a site for VP and OT metabolism, and the amniotic sac may be a major site for VP clearance in the guinea pig fetus. There have been generalized findings regarding VP and OT metabolism. First, VP metabolism in the whole body and in the amniotic sac appears to increase with increasing concentrations of hormone; this does not appear to be the case with OT. Also, evidence has been presented that suggests a potential for the formation of biologically active metabolites. There have been several associations of pathophysiological states with altered VP or OT metabolism, sometimes with plasma levels remaining unchanged. Lastly, caution is emphasized when measuring these hormones by RIA, and differences in specificities of antisera toward hormone metabolites must be considered.

Previous work indicates that the magnitude and direction of renal responses to exercise depend on the exercise intensity. To examine mechanisms responsible for these findings, renal and hormonal responses were studied in eight healthy male subjects (29.6 +/- 1.9 yr) before and immediately after four 20-min bouts of submaximal exercise (cycle ergometry) at work loads representing 25, 40, 60, and 80% of maximal oxygen consumption. Urine flow, osmotic clearance, glomerular filtration rate, and sodium excretion (UNa+V) all tended to rise at the 25% work load but were markedly reduced at the higher work intensities. Changes in urine flow paralleled changes in glomerular filtration rate (r = 0.91). Plasma vasopressin (ADH), aldosterone, and plasma renin activity tended to increase progressively with increases in work load, with the increases for all hormones reaching statistical significance when the level of exercise reached greater than or equal to 60% of maximal oxygen consumption. However, atrial natriuretic peptide was elevated (P less than 0.05) at all work loads from greater than 1.6-fold of control levels at the 25% work load to greater than 7-fold at the 80% work load. The increase in urine flow (6 of 8 subjects) and UNa+V (7 of 8 subjects) may be due to the increase in atrial natriuretic peptide and/or a 10% suppression (P less than 0.05) of ADH at the 25% work load.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of 7 successive days of prolonged jogging on aerobic performance and biochemical markers of muscle and red blood cell damage were examined in 10 moderately fit men, ages 27 +/- 2 yr (mean +/- SE). The subjects jogged for 2 h per day at 78 +/- 4% of maximal heart rates and covered a total of 129 +/- 2 km, nearly eight times their regular weekly training distance. At baseline, maximal oxygen uptake (VO2max) during treadmill tests averaged 3.45 +/- 0.24 L/min, or 44.7 +/- 1.4 ml/kg/min. On follow-up tests 2d after the week of increased training, VO2max (3.56 +/- 0.17 L/min) and treadmill performance were not significantly improved. Body weight declined from 79.5 +/- 4.6 kg to 77.8 +/- 4.4 kg (p less than 0.05) because of reduced body fatness (16.8 +/- 2.3% to 13.6 +/- 1.7%, p less than 0.05). Weight-adjusted VO2max increased to 46.4 +/- 2.0 ml/kg/min (p less than 0.05). However, heart rate and systolic blood pressure were not significantly changed at rest, or during submaximal and maximal treadmill exercise. Mean hemoglobin concentration at treadmill testing declined from 14.9 +/- 0.3 g/dl to 13.3 +/- 0.3 g/dl (p less than 0.05). Leg muscle soreness, especially in the thigh region, persisted in all subjects after 3 d. Soreness was accompanied by chronic elevations (p less than 0.05) in serum levels of myoglobin, creatine kinase (CK), lactic dehydrogenase (LD), aminoaspartate, and the isoenzymes CK-MB and LD1,2. Serum haptoglobin levels after jogging fell from 86 +/- 9 mg/dl to 60 +/- 8 mg/dl (p less than 0.05), suggestive of footstrike hemolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Hormonal, electrolyte, and renal responses were measured before, during, and after a marathon (42.2 km) in 14 runners: 8 young (Y) (mean age 27.8 yr) and 6 middle aged (MA) (mean aged 46.7 yr). No differences between groups in prerun values for heart rate (HR), plasma osmolality (OSM), antidiuretic hormone (ADH), aldosterone (ALDO), atrial natriuretic factor (ANF), or plasma renin activity (PRA) were found. Renal and urinary measurements were also similar between groups before the marathon. After 10 km of running, both groups had significant increases in HR, ALDO, ANF, and PRA, while OSM, Na+, and ADH remained unchanged from prerun values. The increase in plasma ANF concentrations at this point was significantly greater in the MA subjects compared with the Y (mean increase 104.1 vs. 42.8 pg/ml, respectively; P less than 0.01). Immediate postmarathon values for OSM, ADH, and Na+ were significantly higher than initial values in both groups, while HR, PRA, and ALDO continued to increase above the elevated levels found at 10 km. ANF values immediately postmarathon remained higher than prerun concentrations but were significantly reduced from those obtained at 10 km. In contrast, HR continued to rise until the completion of the run. These data are consistent with recent reports of an exaggerated ANF response in older subjects in response to central blood volume expansion.

Introduction: Hyperbaria-induced diuresis is accompanied by decreased basal and stimulated release of arginine vasopressin (AVP) and decreased blood volume possibly contributing to the reported orthostatic intolerance. Since hyperosmolality is not a consistent finding, the explanation of blood volume reduction at hyperbaria must involve an osmotic component to the diuresis. Investigations of a possible involvement of atrial natriuretic peptide (ANP) to the hyperbaric diuresis have revealed mixed results. Methods: Urinary excretion of electrolytes, AVP, and aldosterone were measured in four male subjects studied at 1 atmosphere absolute (ATA) and at 46 and 37 ATA (0.5 atmospheres pressure O 2 : 5% N 2 : remainder He) during a 35-d saturation dive. Also, the supine and 90° tilt-stimulated plasma levels of AVP, plasma renin activity (PRA), and aldosterone, and the suppressed responses of ANP and the cardiovascular responses to tilt were determined at these pressures. Results: Tilt-stimulated levels of PRA were increased two- to threefold and the AVP response was eliminated throughout hyperbaria, except in two episodes of tilt-induced syncope where AVP was elevated 10- to 20-fold. This pattern supports most previous reports. Contrary to some reports, both supine and tilt-suppressed levels of ANP were reduced by about 50% at all three tilt experiments conducted at hyperbaria compared to predive control values. Discussion: These results suggest an altered ANP response at pressures of 37 ATA or greater, which is consistent with an appropriate ANP response to blood volume reduction and further suggest that the hyperbaric diuresis is not dependent on increased ANP.

Reference values of blood volume (BV) and plasma volume (PV) of animal species are given as functions of body weight and gender specification generally is not given. Considering the common observation of a decreased hematocrit (Hct) in the females of many species, the BV, the PV, or both must differ between genders. The present study was performed to determine the magnitude of those differences. We measured Hct and PV in 24 female and 23 male Sprague-Dawley rats in their 12th week of life. The rats were surgically prepared with indwelling femoral arterial catheters 4 d prior to the determination of BV. Evan's Blue dye dilution was used to determine PV in conscious, quietly resting animals. BV was calculated as PV/(1-Hct). Mean Hct was 2% lower in female rats than males, and PV (mean +/- 1 standard deviation) was 4.86 +/- 0.54 ml/100 g in females compared with 4.12 +/- 0.32 ml/100 g in males. Calculated BV in female rats was 7.84 +/- 0.70 ml/100 g compared with 6.86 +/- 0.53 ml/100 g in males. When precise estimates of BV or PV are needed for research or dosing purposes, gender differences of 18% for PV and 14% for BV must be considered. In addition, species other than the rat may have similar discrepancies between sexes, and the prudent investigator must determine individual volume assessments of both sexes before assumptions of BV and PV for a species can be made.

Arginine vasopressin (AVP) synthesis, storage and osmotically stimulated release are reduced in young adult rats exposed prenatally to ethanol (PE). Whether the reduced release of AVP to the osmotic stimulus is due to impairment of the vasopressin system or specifically to an osmoreceptor mediated release is not known. The present experiments were done, therefore, to determine if a hemorrhage-induced AVP response would also be diminished in PE exposed rats. Pregnant rats were fed either a control liquid diet (no prenatal ethanol, NPE) or a liquid diet with 35% of the calories from ethanol from day 7–21 of pregnancy. Offspring were weaned at 3 weeks of life. At 11 weeks of age femoral arterial catheters were surgically placed, and blood volumes determined at 12 weeks. Three days later, two hemorrhages of 10% of the blood volume were performed with samples taken prior to and 10 minutes after the hemorrhages. Following a 20% blood loss, plasma AVP was 19% higher in NPE rats than in the PE rats despite no differences in mean arterial blood pressure. Also, hypothalamic AVP mRNA and pituitary AVP content were reduced in PE rats. Furthermore, confirming an earlier report of gender difference in AVP release, the hemorrhage-induced hormone response was two-fold greater in female rats than male rats regardless of previous ethanol exposure. These studies demonstrate that the AVP response to hemorrhage is reduced in PE rats independent of differences in MABP. The data are compatible with a theory of a reduced number of hemorrhage responsive vasopressinergic neurons capable of stimulated AVP release in PE rats.

The goal of this study was to determine attitudes toward oral contraceptive pill (OCP)-induced amenorrhea among U.S. Army women.A volunteer sample (N = 154) of Army Active Duty, Reserve, and National Guard women completed an anonymous survey.Desire for temporary amenorrhea was high with 86% (+/- 6%, 95% confidence interval [CI]) and 83% (+/-6%, 95% CI) desiring amenorrhea during field training and deployments, respectively. Fifty-four percent were unaware that OCPs can induce amenorrhea; only 7% (+/-4%, 95% CI) have used this practice during deployment. If made available with education, 49% (+/-8%, 95% CI) would use this practice. Logistic burdens of menstruation were associated with higher rates of desirability for OCP use with soldiers desiring OCPs rating their inconveniences significantly higher than those who did not desire OCPs (p0.05).Although a significant number of soldiers desire OCP-induced amenorrhea, a large deficit in knowledge exists. Routine education as an Army-wide standard is warranted.

This study was conducted to determine whether 100% FiO2 during hemorrhage would improve maintenance of mean arterial blood pressure and to assess the cardiovascular, arginine vasopressin, and renin-angiotensin system roles in the response. This also allowed evaluation of FiO2 effects on the baroreceptor control of these hormone systems. Six conscious female goats were hemorrhaged (0.5 mL x kg(-1) x min(-1)) for 30 minutes, while breathing 11%, 21%, or 100% O2. Mean arterial blood pressure was maintained only when the goats breathed 100% O2. FiO2 did not affect O2 consumption or delivery during hemorrhage. Increases in renin and arginine vasopressin were equal or reduced with 100% FiO2 and therefore did not contribute to the improved mean arterial blood pressure maintenance. Inspiration of 100% FiO2 during hemorrhage, therefore, may improve perfusion pressure with no changes in O2 consumption or delivery. Also, 100% FiO2 eliminated the negative correlation between both hormones and right atrial pressure, suggesting altered baroreceptor control of the hormones.

Estrogen and progesterone interference with renal actions of arginine vasopressin (AVP) has been shown. Thus we hypothesized that women will have a higher water turnover than men and that the greatest difference will be during the luteal phase of the menstrual cycle. Seven men (32 ± 3 yr) and six women (33 ± 2 yr) drank 12 ml water/kg lean body mass on different days at 0800 and at 2000 following 10 h of fast and a standardized meal at 0600 and 1800. Women participated on days 4–11 and 19–25 of the menstrual cycle. Initial urine and plasma osmolalities and urine flow rates were similar in all experiments. The cumulative urine voided over 3 h following the morning drink was less in men (73 ± 12% of the water load) compared with women in either the follicular (100 ± 3%) or luteal phases (102 ± 10%) of the menstrual cycle. Nighttime values (30–43% of the water load) were lower in all experiments and were not different between sexes or menstrual cycle phases. Plasma AVP was higher at night and may contribute to this diurnal response. The data are generally consistent with the stated hypothesis; however, possibly owing to the greatly reduced urine flow in both sexes at night, a difference between sexes was not observed at that time.

To determine the efficacy of azithromycin in the treatment of patients with typical cat-scratch disease.Prospective, randomized, double blind, placebo-controlled clinical trial.Large military medical center and its referring clinics.Active duty military members and their dependents with laboratory-confirmed, clinically typical cat-scratch disease.Study participants assigned by randomization to treatment with oral azithromycin or placebo for 5 days.Lymph node volume was calculated using three dimensional ultrasonography at entry and at weekly intervals. The ultrasonographer was blinded to the treatment groups. Endpoint evaluations were predetermined as time in days to 80% resolution of the initial total lymph node volume.Demographic and clinical data showed that the azithromycin and placebo treatment groups were comparable at entry although the placebo group tended to be older. Eighty percent decrease of initial lymph node volume was documented in 7 of 14 azithromycin-treated patients compared with 1 of 15 placebo-treated controls during the first 30 days of observation (P = 0.026). After 30 days there was no significant difference in rate or degree of resolution between the two groups.Treatment of patients with typical cat-scratch disease with oral azithromycin for five days affords significant clinical benefit as measured by total decrease in lymph node volume within the first month of treatment.

Seven adults, 2 women in the follicular phase or the menstrual cycle and 5 men, were studied. We intend to provide information relating to age, gender, and the phase of the menstrual cycle when the study is complete. The question addressed to date, regards the mechanism explaining the diurnal urinary response to a water load of 12 ml/kg lean body mass. We observed a 20% greater (P < 0.05) diuresis in response to a water load during the daytime compared to nighftime, despite a slightly lower resting plasma osmolality (Posm) during the nighttime. The plasma osmolality resulting after the drink was similar during the daytime and nighttime. Despite this, plasma vasopressin levels were lower after the drink during the daytime compared to the nighttime (P

The possibility that the decreased urinary flow during continuous positive-pressure breathing (CPPB) may be a consequence of a reflex mediated via the cardiopulmonary baroreceptors to increase neurohumoral secretion or to change the sympathetic outflow was assessed. Muscle sympathetic nerve activity (MSNA) on the right peroneal nerve, vasoactive hormones, and renal and cardiovascular responses were measured during CPPB (+12 mmHg) in 10 male subjects (22.0 +/- 0.6 yr, 66.8 +/- 1.5 kg body wt). The experiments consisted of a 1-h control, 1 h with CPPB (experimental) or without CPPB (a time control), and a 1-h recovery period. Two blood samples were taken during each period for measurements of arginine vasopressin (AVP), plasma aldosterone (PAldo), plasma renin activity (PRA), norepinephrine, and atrial natriuretic peptide (ANP), and urine was collected hourly for the measurement of urine volume and electrolytes and clearances. MSNA rapidly increased (P < 0.05) at the onset of CPPB, continued to increase during exposure, and rapidly returned to the normal level at recovery. The MSNA changes coincided with increased plasma NE and were concurrent with a reduced (P < 0.05) urine output associated with a reduction of both free water and osmolal clearances, Na+ and osmolal excretions, and creatinine clearance (glomerular filtration rate). AVP and PRA increased (P < 0.05), whereas PAldo and ANP were unchanged. The results are consistent with the concept that increased sympathetic outflow may play a role in the reduction of urinary output and Na+ excretion during unloading of the cardiopulmonary receptors.

We examined the ontogeny of relaxation responses to three categories of calcium channel antagonists, represented by verapamil, diltiazem, and nifedipine, for both potential-operated (KCl-mediated) and receptor-operated channels [norepinephrine (NE)-mediated] in rat thoracic aorta. Aortic rings from 2− to 3-d, 1-wk, and 12-wk-old Sprague Dawley rats were mounted in an organ bath, bathed in Krebs' solution, and connected to a force-displacement transducer to measure isometric tension. Endothelium intact vessels at optimal passive force were exposed to a single ED50 of isotonic KCl or NE, equilibrium contraction was measured, then vessels were washed and exposed for 30 min to 1 μM verapamil, 1 μM diltiazem, or 0.1 μM nifedipine, followed by another dose of KCl or NE. Verapamil and diltiazem demonstrated significant (p < 0.05) age-related increases in effectiveness for blocking KCl-mediated contraction [(% reduction of control contraction ± SEM) (Verapamil: 2–3 d, 67.7 ± 4.2; 1 wk, 72.5 ± 1.8; 12 wk, 89.5 ± 1.0. Diltiazem: 2–3 d, 64.6 ± 2.9; 1 wk, 73.5 ± 3.0; 12 wk, 83.1 ± 1.8]. Nifedipine was equally effective at all ages: 2–3 d, 85.6 ± 1 1.3; wk, 90.0 ± 1.6; and 12 wk, 91.3 ± 1.4. Verapamil and diltiazem also showed significant age-related increases in effectiveness for blocking NE-mediated contraction (Verapamil: 2–3 d, 6.2 ± 3.9; 1 wk, 28.0 ± 4.8; 12 wk, 44.1 ± 6.0. Diltiazem: 2–3 d, 8.0 ± 3.1; 1 wk, 20.5 ± 3.9; 12 wk, 46.5 ± 4.8). Again, nifedipine was equally effective at all ages: 2–3 d, 42.0 ± 6.8; 1 wk, 35.8 ± 3.9; and 12 wk, 37.5 ± 3.2. In summary, for the categories of calcium channel antagonists that interact at the phenylalkytomine (verapamil) and benzothiazepine (diltiazem) binding sites, there were age-related increases in effectiveness for blocking both potential-operated and receptor-operated channels. However, for nifedipine, which binds to the 1,4-dihydropyridine binding site, no maturational change was observed. These results suggest that the ontogeny of calcium channel antagonists' function may vary depending on the site of binding within the calcium channel.

The paper in this issue of The Journal of Physiology entitled ‘Aerobic exercise before diving reduces venous gas bubble formation in humans’, by Dujic et al. (2004) extends their findings in animals (Wisloff & Brubakk, 2001) to human subjects, and confirms that exercise performed prior to exposure to modest pressures, equivalent to 18 m of sea water depth, can ameliorate venous bubble formation upon decompression. Since bubble formation is associated with decompression sickness (DCS), this article impacts broadly on the field of diving physiology. If confirmed, it potentially affects a large population. First, in addition to pilots and diving professionals who are impacted by profession, there are an estimated 854 000 new certifications for SCUBA divers issued worldwide each year (Professional Association of Diving Instructors, web page). Second, the article provides clarification and changes the commonly accepted view of the effects of exercise on decompression-induced bubble formation. Third, the theoretical explanation for the response whereby a reduction in bubble nuclei may result from the heavy exercise, thereby accounting for the reduced bubble formation upon decompression, represents a plausible and potentially important avenue for more research. The previously held general concepts of exercise and bubble formation resulting from decompression involved the understanding that exercise at depth would increase blood flow and consequently nitrogen uptake. With more nitrogen in the body the time required to unload the additional nitrogen would then be greater. Indeed, studies have shown that if exercise occurred during one dive, and a similar dive was conducted with no exercise, more nitrogen was eliminated while resting at sea level following the dive when exercise was performed (Dick et al. 1984). This is in line with the finding that more bubbles were detected when subjects exercised during or immediately following completion of decompression, and the intravascular bubbles impede the elimination of inert gases. Summarization of prior reports generally led to the conclusion that exercise performed either prior to or during exposure to pressure would increase the risk of DCS (Vann & Thalmann, 1993). Such impressions suggested that otherwise unexplainable cases of DCS might have been due to strenuous exercise performed prior to an incident. This was the case even in a highly controlled US Navy dive (Hughes & Eckenhoff, 1986). On the other hand, more recent reports indicate that if exercise is performed at a modest intensity during decompression, Doppler-detected gas emboli are reduced (Jankowski et al. 1997). The beneficial effects of exercise during decompression are similarly thought to be a consequence of increased blood flow but in this case resulting in increased gas elimination. So the timing of exercise performed at depth and the intensity of the exercise become critical factors in whether or not the effects are harmful or beneficial. The controversy over the impact of exercise on the outcome of decompression is not new. In Haldane's time, both Royal and US Navies routinely imposed exercise on their divers during decompression, believing that the elevated circulatory state would accelerate the elimination of nitrogen. The practice ended when many experiments demonstrated that various exercise regimens before, during and following decompression either from depth or to altitude increased the incidence of DCS. A long period followed where exercise was prohibited during and following decompression. Later, sporadic reports appeared showing beneficial effects of exercise during decompression. So far no definitive conclusion can be drawn regarding the effect of exercise on DCS before, during or after decompression. However, it is apparent that a beneficial effect of exercise performed during decompression is dependent on type and intensity of exercise. The present study stresses the importance of the timing of the pre-dive exercise. In other studies by this group that were conducted in rats, a beneficial effect of pre-dive exercise did not occur if the exercise was done too close to, i.e. within 10 h, or too much in advance of, e.g. 48 h, the dive time (Wisloff et al. 2004). If the mechanism of exercise-induced suppression of bubble formation is related to nitric oxide (NO) production, then the timing of NO administration in relation to its prophylactic effects on bubble formation should be similar. In the same study, Wisloff et al. (2004) reported that administration of an NO-releasing agent reduced bubble formation even when given 30 min prior to hyperbaric exposure. Thus, the timing of the responses to exercise and NO administration were quite different. It is not clear why exercise performed only within a window of time near 24 h prior to the dive can produce the effect if the mechanism is linked to an NO-dependent reduction in bubble nuclei. Whether or not the effect of exercise on bubble formation operates through the formation of NO as the authors hypothesize, or through yet another mechanism, the present study significantly advances our understanding of the effects of pre-dive exercise, and provides another means of ameliorating the formation of bubbles upon decompression in humans. The contribution of this effect will need further standardization and study before pre-dive exercise can be widely adopted as a predictable safeguard against DCS. For instance, better knowledge is needed of how much exercise is necessary to provide a certain degree of protection, and how this can measured. Clarification of the mechanism may be helpful in this regard.

OBJECTIVE: To determine the efficacy of azithromycin in the treatment of patients with typical cat scratch disease (CSD).

Endurance exercise training alters the regulation of body fluids. To investigate specifics of these alterations, hormonal, electrolyte, and renal responses to water ingestion (1% of lean body wt) were studied in six moderately trained (T) and 6 untrained (UT) male subjects. No differences between groups for base-line hormonal, electrolyte, or renal measurements were found. After water ingestion, atrial natriuretic factor remained unaltered in both groups. Predrink plasma antidiuretic hormone (ADH) levels of 0.51 +/- (SE) 0.19 (UT) and 0.47 +/- 0.07 microU/ml (T) remained unchanged in the T group but were reduced from min 9 through 90 in the UT group. At 30 min postdrink, UT subjects had lower ADH values than T subjects (0.18 +/- 0.02 vs. 0.33 +/- 0.05 microU/ml), while plasma osmolality was similarly reduced by approximately 3 mosmol/kg in both groups. Urine flow rates increased in both groups from similar values of 0.85 +/- 0.24 (UT) and 0.67 +/- 0.11 ml/min (T) to peak flows of 4.6 +/- 1.6 for UT and 2.7 +/- 1.1 ml/min (T) to peak T, P less than or equal to 0.05) at 60 min postdrink. Urine osmolality was reduced from similar values of 809.1 +/- 62.1 and 867.0 +/- 56.1 mosmol/kg to values of 248.8 +/- 87.6 and 469 +/- 146.1 mosmol/kg for UT and T, respectively (UT vs. T, P less than 0.05), at 60 min. Reduced ADH before reductions in plasma osmolality in the UT but not the T subjects suggests that T subjects have a reduced oropharyngeal inhibition of ADH.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiorenal-endocrine responses to 3-h head-out immersion (HOI) (water temperature = 34.5 +/- 0.5 degrees C) were studied during day (0900–1400 h) and night (2300–0400 h) in six hydropenic male human subjects. Although HOI induced a reversible increase in urine flow in all subjects, the response was faster and greater in magnitude during the day compared with night (P less than 0.05). Na excretion and osmolal clearance (Cosm) also followed the identical response pattern as urine flow, and in fact, the HOI-induced diuresis was entirely accounted for by the increased Cosm. Endogenous creatinine clearance was not different between the day and the night and remained unchanged during HOI. Both plasma renin activity and aldosterone concentration and urinary aldosterone excretion were nearly twofold greater during the day compared with night before HOI but decreased to the same level during HOI in both daytime and the nighttime series (P less than 0.05). There was no correlation between the Na excretion rate and renin-aldosterone levels either before or during HOI. Plasma antidiuretic hormone (ADH) level was comparable between day and night before HOI and decreased to a similar level during HOI in both daytime and nighttime series (P less than 0.05 for nighttime HOI). Cardiac output increased from 3.3 1/min before HOI to 5–6 1/min during HOI without showing any significant circadian difference. Hematocrit, hemoglobin, and plasma concentrations remained unchanged under all conditions. It is concluded that the renal response to HOI is subject to nocturnal inhibition, which cannot be attributed to circadian differences in the degree of HOI-induced central blood pooling, renin-aldosterone, or ADH responses.

The circulatory, renal, and hormonal responses during 100 min of thermoneutral (37 degrees C) head-out water immersion (WI) were investigated in conscious intact (INT) and cardiac-denervated (CD) dogs. In the INT group, both left and right atrial and aortic transmural distending pressures and left ventricular contractile performance (LV dP/dtmax) increased, and total peripheral resistance remained unchanged. Cardiac output (QCO) increased in association with an increase in heart rate and LV dP/dtmax. Urine flow (V), sodium excretion (UNaV), and osmolal clearance (Cosmol) all increased, whereas glomerular filtration rate, as indicated by creatinine clearance (CCr), remained constant. The diuresis and natriuresis occurred in the absence of any significant changes in plasma levels of antidiuretic hormone (ADH), aldosterone, or plasma renin activity. The CD animals showed a similar hemodynamic response except that the increase in QCO was now associated with an increase in stroke volume and no change in heart rate or LV dP/dtmax. Although the increase in V was similar in both magnitude and time course of the INT animals, there was no significant change in UNaV. Thus there is a striking change in the character of the response of the denervated group in that the natriuresis is abolished and, instead, a water diuresis occurred. Free water clearance increased, but no significant changes in Cosmol or CCr were observed. In addition plasma ADH levels significantly declined during WI in the CD group. These data indicate that cardiac receptors are important in determining the nature of the renal response to WI.

A route for fetal 8-arginine vasopressin (AVP) clearance has not yet been established. The results of this study indicate that in the fetal guinea pig, the amniotic sac is a site for AVP metabolism. When fetal plasma, urine, and amniotic fluid were fractionated on HPLC, AVP was identified only in fetal plasma and urine. In addition, when AVP and inulin were injected into the amniotic sac in vivo during the last week of gestation, the AVP to inulin ratio decreased (P less than 0.05) over a 2-h period, indicating a swallowing-independent disappearance of AVP. Furthermore, when tritiated AVP was similarly injected, the radioactivity to inulin ratio remained constant, suggesting that AVP was not diffusing out of the amniotic sac. Two hours after the injection into the amniotic sac, amniotic fluid was collected and fractionated by HPLC, and only 42% of the total radioactivity was intact AVP. The remainder was identified in two other products (M1 and M2). Tritiated AVP incubated with amniotic fluid and amnionic membrane in vitro produced both M1 and M2. Tritiated AVP incubated with amnionic membrane in artificial amniotic solution produced only M1. Tritiated AVP incubated in only amniotic fluid produced M2, with only slight M1 production. Thus, neither metabolite was necessary for the production of the other; M1 was amnionic membrane dependent, and M2 was amniotic fluid dependent. In conclusion, the amniotic sac may play a role in the clearance of AVP from the fetal system.

Atrial natriuretic factor is reported to be elevated during and immediately following exercise and is thought to play a role in fluid homeostasis and cardiovascular regulation. The predominant stimuli for atrial natriuretic factor release during exercise appear to be increases in atrial pressures or atrial distension, both of which are reported to increase with exercise. The intensity and perhaps duration of exercise also influence the magnitude of the atrial natriuretic factor response. It is not clear if the rise in plasma atrial natriuretic factor during exercise plays any role in altering renal function since high intensity exercise is typically associated with an antidiuresis. However, elevations in plasma atrial natriuretic factor may in part be responsible for the increase in urine flow reported when exercise is performed at low or moderate intensities. Atrial natriuretic factor also has vascular effects which may be important in buffering or moderating the blood pressure response to exercise. The atrial natriuretic factor response to exercise and basal levels of the hormone are greatly elevated in patients who suffer from a variety of cardiovascular and pulmonary disease conditions. These elevated plasma atrial natriuretic factor values are associated with increases in atrial pressure and appear to be related to the severity of disease. Although much controversy exists regarding the renal and vascular effects of atrial natriuretic factor, the measurement of this hormone, particularly during exercise, may be of clinical value by providing an additional tool to evaluate patients and determine the effectiveness of various treatment regimens.

The trained condition is associated with alterations in fluid regulation. In attempt to elucidate mechanisms responsible for these differences, resting, postexercise (maximal treadmill exercise of 8–13 min duration), and recovery measurements were made in seven trained (mean peak O2 consumption was 60.5 +/- 1.6 ml.kg-1.min-1) and seven untrained (mean peak O2 consumption was 40.7 +/- 1.7 ml.kg-1.min-1) male subjects. Samples were obtained by venipuncture with subjects seated. No significant differences in resting plasma osmolality (Osm), sodium, potassium, antidiuretic hormone (ADH), aldosterone, renin activity, or atrial natriuretic factor were found between groups. Maximal exercise produced significant increases in all of the above variables. Values immediately postexercise were similar between groups except for plasma Osm and sodium, which were significantly higher in the untrained group. Despite a reduction in plasma volume of equal magnitude in both groups, trained subjects demonstrated an increase in vascular proteins and mean corpuscular volume during exercise. This increase in plasma protein may be an important initiating factor responsible for the elevated plasma volume after 1-h recovery from exercise in the trained group. Lastly, similar ADH responses despite lower Osm in trained subjects may indicate that training increases the sensitivity of ADH to osmotic stimulation.

Various renal functions were studied in the Baikal seal (Pusa sibirica), which inhabits freshwater, and in the ringed seal (P. hispida), its marine counterpart. The urine osmolality progressively increased during dehydration (and fasting), reaching a plateau after 35 h. The average maximum urine osmolality was 2,374±60 and 2,052 ± 100 mOsm/kg in the Baikal and ringed seals, respectively. Urea and electrolytes (Na, K, and Cl) accounted for 82.6% and 9.3%, respectively, of total urine osmolality in the Baikal seal, and for 72.6% and 16.1%, respectively, in the ringed seal. Administration of 500 ml 0.15 M NaCl solution (stomach tubing) during fasting had little effect on the level of urine osmolality; however, the contribution of urea to total urine osmolality decreased (to 60%) while that of electrolytes increased (to 23%). Using the endogenous creatinine clearance as a measure of glomerular filtration rate, it was estimated that about 0.2% of filtered water and 0.05% of filtered Na are excreted during dehy...

We determined the regional blood flow responses to head-out water immersion (WI) in intact (INT) and cardiac-denervated (CD) conscious dogs. Immersing dogs in thermoneutral water (37 degrees C) in the quadruped position for 100 min resulted in significant increases in cardiac output (Qco) above control values by 38.7% in the INT dogs and 39.2% in the CD dogs (P less than 0.01). Arterial pressure increased by 32 and 34.7% in the INT and CD groups, respectively, during WI, with no significant changes occurring in the calculated total peripheral resistance. Regional blood flow responses were measured with 15-microns radiolabeled microspheres. Flows in the INT and CD groups increased significantly to the heart (40, 38%), skin (93, 96%), fat (79, 83%), diaphragm (44, 48%), and intercostal muscles (58, 55%), whereas there were no changes in renal cortical blood flows during WI. Total brain blood flows did not change significantly on immersion; however, blood flows in both INT and CD animals were increased to the cerebellum (19, 22%), but a significant decrease in pituitary flow (52%) was observed only in the CD group during WI. Gastrointestinal tissue flows increased only during early WI in both INT (45%) and CD (47%) animals. However, blood flows to the skeletal muscles increased only during late WI in the INT (53%) and CD (47%) groups. There were no significant differences between the INT and CD groups. Rectal temperatures and systemic O2 consumption (VO2) were unchanged during WI in both groups of animals. These observations indicate that WI leads to a sustained elevation of Qco accompanied by selective increases in regional tissue perfusion that may be accounted for in some tissues by an increase in metabolic demand or by local heating responses and produces a time-dependent redistribution of blood flow away from the gastrointestinal tissues toward skeletal muscle tissues, which may be due to a partial uncoupling of the normal Q/VO2 relationship. This may be caused by thermal or central neurohumoral mechanisms. These regional circulatory responses are not dependent on the presence of the cardiac nerves.

The subject of the regulation of the body fluids is indeed complex, including elements of the endocri ne, renal, nervous and cardiovascular systems. Because of the difficulty of the experi mental methods, most of us have had tunnel vision in our research and reviews, although there have been some notable exceptions with respect to the latter (e.g., 58, 59, 121, 123). However, limitations of space and of our competence and a voluminous literature compel us to confine the scope of this review to a single topic: the control of the secretion of hormones involved in the regulation of extra­ cellular volume, osmolarity, and concentrations of sodium and potassiu m . In this context, we shall then review vasopressin, the renin-angiotensi

A study was conducted of the effects of posture and of sodium depletion on the plasma concentration of vasopressin (ADH) and the plasma renin activity (PRA) in normal human subjects. Measurements were made while the subjects were in bed after 8 hr of water deprivation, and then after a 4-hr period of ambulation. These studies were first performed while the subjects were on a normal sodium intake and again, when they were depleted of sodium. During the period of ambulation, the subjects performed their normal daily tasks, but continued to abstain from food and water. Ambulation, sodium depletion or a combination of these two procedures were without effect on the plasma ADH concentration. PRA, on the other hand, was increased by both ambulation and sodium depletion. It is suggested that under the conditions of these experiments, the renin-angiotensin system does not play a significant role in the control of the release of ADH.

The relationship between iv infusions of angiotensin II and vasopressin release has been investigated in the anesthetized dog. In dogs sedated with morphine and anesthetized with a mixture of chloralose and urethane, a 40-min iv infusion of angiotensin II ranging from 10-60 ng/ kg/min failed to stimulate the release of vasopressin. This was observed when the control plasma levels of vasopressin were moderately elevated due to anesthesia and surgical trauma, approximately 15 M*U/ml, or when suppressed by hydration to approximately 3 nU/ml. In hydrated dogs anesthetized with pentobarbital and subjected to less surgery, the starting levels of vasopressin were 1.2 H-U/ml. In these dogs a 75-min infusion of 10 ng/kg/min of angiotensin II into a common carotid artery also failed to stimulate the release of vasopressin. {Endocrinology 90: 1647, 1972) T T HAS BEEN reported that the administra•*• tion of angiotensin directly into the ventricles of the brain in the anesthetized dog (1), the hydrated conscious goat (2), and the conscious rat (3) results in an increased release of vasopressin from the posterior pituitary. It has also been claimed that the circulating levels of vasopressin are elevated following the infusion of angiotensin II via a peripheral vein in the conscious dog (4) and a common carotid artery in the dog anesthetized with pentobarbital (1). However, the changes in the plasma vasopressin concentration in these experiments in which the angiotensin was injected into the circulation were quite small, and the results of only three experiments were reported by Mouw et al. (1). In addition, one wonders to what extent the findings in the conscious dogs (4) were influenced by emotional reactions to the experimental procedure and to the increase in blood pressure induced by the angiotensin. In view of these considerations and reports of several situations in which plasma levels of renin and vasopressin fail to change in a parallel fashion (5,6), it seemed advisable to reinvestigate the effect of the systemic infusion of angiotensin Received October 28, 1971. This work has been supported by grants HL-12990 from the National Heart Institute, USPHS, and HL-14242 (Specialized Center of Research in Hypertension). Computer assistance was supported by grant HL-09495 from the National Heart Institute, USPHS. The authors express their gratitude for the able technical assistance of Miss J. T. Crofton and Mr. S. E. Pienaar. II on the plasma concentration of vasopressin. Because of the cardiovascular effects of angiotensin, some of these studies were accompanied by measurements of arterial mean and pulse pressures and left atrial pressure, factors which play an important role in the control of vasopressin release. The infusion of angiotensin II in hydrated dogs anesthetized with either pentobarbital, or sedated with morphine and anesthetized with urethane and chloralose produced no effect on the plasma levels of vasopressin in the present investigation. Similar observations are obtained in normally hydrated dogs under morphine-urethane-chloralose anesthesia. Materials and Methods All experiments were performed on male mongrel dogs weighing 14.5-26.0 kg. Some dogs were sedated with a sc injection of 0.1 ml/kg of 2.0% morphine and anesthetized with an iv infusion of a mixture of urethane (6.0%) and chlorolose (0.6%) in 0.9% saline, approximately 9.0 ml/kg. Others were anesthetized with iv infusions of approximately 1.0 ml/ kg of 3.0% sodium pentobarbital. Surgery. The trachea and right and left femoral arteries and veins were cannulated in all dogs. In the dogs receiving morphine, urethane and chloralose anesthesia, the chest was opened in the fourth intercostal space on the left side, so that the left atrium could be catheterized via the atrial appendage. During this procedure the dog's respiration was maintained by positive pressure ventilation. The intercostal incision was then closed and a catheter was left in the pleural cavity. The chest was evacuated, arti

Urinary excretion rates of antidiuretic hormone were determined by radioimmunoassay in children with bacterial (6) and viral (11) meningitis, and in children with other febrile illnesses (7). These values were compared to normal data obtained from 50 healthy, normally hydrated children ranging in age from 1 week to 9 years. Plasma sodium concentrations were measured in the sick children; urine osmolality and creatinine concentrations were measured in all children. Upon admission, all children with bacterial meningitis and 64% of those with viral meningitis had urinary antidiuretic hormone excretion rates greater than 2 S.D. above values obtained from age-matched controls. Fifty-seven percent of children with other febrile illnesses had similarly elevated antidiuretic hormone values; however, only in the bacterial and viral meningitis groups were antidiuretic hormone excretion rates inappropriate because they occurred when serum sodium concentrations were found to be normal or low normal (i.e., 136 +/- 2 mEq/L and 137 +/- 1 mEq/L, respectively). The average serum sodium in the group with other febrile illnesses was higher (146 +/- 5 mEq/L; p less than 0.05) and could represent an appropriate stimulus for antidiuretic hormone release. In spite of high levels of antidiuretic hormone, most viral meningitis patients did not concentrate their urine, probably because all except 2 were younger than 2 months of age. We conclude that viral meningitis, like bacterial meningitis, frequently is associated with inappropriate antidiuretic hormone secretion; however, most children with viral meningitis may be protected from developing hyponatremia because of their inability to concentrate their urine.

The effect of the hypoxic environment on body fluid regulating systems is influenced by both the direct and indirect effects of hypoxia. Regarding the direct physiological effects, for instance, hypoxemia can directly stimulate the carotid body chemoreceptors with subsequent stimulation of antidiuretic hormone (ADH) release (79), and by mechanisms still unclear, hypoxia reduces the secretion of aldosterone (15,16,39,57,62,81,84,85). In the natural setting, coincident environmental factors such as cold and exercise, discussed elsewhere in this text, and possibly hypobaria, may influence the responses to hypoxia. Additionally, the indirect effects of short-term hypoxia on respiration and cardiovascular reflexes also effect water and electrolyte regulating hormones, and the longer-term effects of decreased appetite impact on electrolyte balances which cause compensatory responses of these hormone systems. Finally, there are the poorly understood indirect consequences of “stress” on various hormonal systems, particularly those of ADH and glucocorticoids, that cannot be excluded from the mechanisms of hypoxia-induced effects on these systems.

Publisher Summary This chapter discusses the role of the renin–angiotensin system of renal renin origin and circulating angiotensin in the control of antidiuretic hormone (ADH) release. Earlier experiments indicate that the renin–angiotensin system and ADH respond differently to various stimuli and do not appear to be interdependent under most circumstances. Increases in plasma ADH concentration resulting from blood volume reduction occur without concurrent increases in plasma renin activity (PRA). It appears that under conditions of normal plasma osmolality, the mechanism of ADH stimulation by intravenous infusions is minimal because infusion of renin into normally hydrated dogs to produce high physiological levels of PRA failed to effect plasma ADH concentration in an experiment described in the chapter. Similar infusions of renin into the same dogs when they were dehydrated elevated plasma ADH concentration. The site of action of circulating angiotensin in the release of ADH is still not established.

To test the hypothesis that atrial natriuretic factor (ANF) has a centrally mediated action on body fluid homeostasis, the effects of intracerebroventricularly (ICV) infused ANF on plasma vasopressin (AVP) concentration and urinary water and electrolyte excretion were investigated in euhydrated and water-deprived conscious sheep. ICV ANF decreased plasma AVP concentration and increased urinary free water excretion in euhydrated sheep, with excretion of Na and K unaltered. However, ICV ANF did not affect urinary volume, free water clearance, or excretion of Na and K in dehydrated animals, although plasma AVP concentration was significantly decreased. The relationship between urine volume and plasma AVP concentration was fitted by a power curve: urine volume = 0.79 X [AVP]-0.71; urine volume changes very little as a function of AVP concentration at the higher ranges. Intravenous infusion of the same amount of ANF was without effect on plasma AVP concentration or urinary excretion in both euhydrated and dehydrated animals. Mean arterial pressure was unchanged throughout all experiments. These results are consistent with the hypothesis that central ANF inhibits AVP secretion.

Precise control of fluid and electrolyte homeostasis is essential for the survival of man. The performance of exercise results in a significant disturbance of water and electrolyte homeostasis. These alterations during exercise are due to the loss of fluids and electrolytes primarily in sweat and to voluntary dehydration associated with an inappropriate suppression of thirst. During the performance of exercise, as well as during recovery, compensatory measures occur to rectify these changes. A variety of hormones are important in the compensatory responses to correct water and electrolyte disturbances. The goal of this chapter is to describe the changes in water and electrolyte homeostasis resulting from exercise and the responses, regulation, and actions of the hormones important in correcting these imbalances.

In recent years, there has been a renewed interest in the study of the physiological responses elicited during head-out water immersion (WI) in both humans and animals. This interest is based on the observation that WI leads to stereotyped cardiovascular, renal, fluid shift, and endocrine responses which develop rapidly. The homeostatic basis or rationale for this response pattern which involves the integrated responses of multiple systems is unclear at the present time. Therefore one goal of this chapter is to attempt to identify certain critical physiologic variables which may be regulated during the course of this complex response pattern which is generally elicited during the simple act of returning to the aquatic environment from whence we came. The major focus of this analysis will be on the hypothesis originally proposed by Gauer and Henry (34) concerning a physiologic link between heart and kidney and the particular role this link may play in governing the hormonal responses elicited during WI. In this regard, a number of excellent reviews representing several points of view related to this issue have been published (25,34,35,74).

With the advent of a new diving technique “the saturation dive” about three decades ago, human divers are now able to engage in a multi-day dive to a considerable depth. In a dry simulation (chamber) dive carried out at Duke University in 1981, several divers exposed themselves to a depth of 686 m (nearly 70 atmospheres absolute or ATA) for 24 h and then safely returned to sea level. Apparently, human divers seem to be able to cope with such high pressures and can maintain normal activities albeit on a somewhat limited basis.

The dependence of vasopressin release in response to hemorrhage on the reninangiotensin system was investigated. A nonhypotensive hemorrhage of 12 ml/kg body weight (approximately 15% of the blood volume) was used as a stimulus for vasopressin release in anesthetized dogs. The right renal artery and vein were ligated, and a snare was placed around the left renal blood vessels. When the renal artery and vein were unobstructed by the snare, hemorrhage resulted in an increase in both the plasma vasopressin concentration and the plasma renin activity. When the renal vessels were occluded, hemorrhage resulted in a greater increase in the plasma vasopressin concentration, although the plasma renin activity remained unchanged. It would appear that the renin-angiotensin system does not play an important role in stimulating vasopressin release in response to a reduction in blood volume in the anesthetized dog. (Endocrinology 90: 453, 1972)

An investigation was made of the effect of angiotensin II on the release of ADH in response to an osmotic stimulus. Dogs anesthetized with pentobarbital were hydrated initially by the infusion of 4% glucose iv, in order to bring the plasma concentrations of ADH and renin to low levels. Subsequent infusion of 2.5M NaCl iv, 1.38 ml/kg per min, resulted in a progressive increase in the plasma ADH concentration in response to the increasing plasma osmolality. The relationship between the plasma ADH concentration and plasma osmolality appeared to be rectilinear over the range studied. When the hypertonic saline infusion was accompanied by an infusion of angiotensin II, 10 ng/kg per min, into a common carotid artery, the increase in the plasma ADH concentration was significantly greater. Infusion of angiotensin II alone in the dose tested and under the reported experimental conditions was without a significant effect on the plasma ADH level. It is concluded that angiotensin II can potentiate the release of ADH ...