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Short-chain fatty acid production and assimilation is unlikely to occur at significant levels in the newborn because the colon at birth is sterile, and only gradually acquires an anaerobic flora. This study profiled short-chain fatty acid levels in the colon lumen over the initial 21 days of life. Fecal samples were removed surgically from the cecum, right, and left colon from 36 York piglets, 0-21 days of life. Samples were subjected to in vitro dialysis and centrifugation methods to quantitate fecal water short-chain fatty acids, electrolytes, osmolality, and pH. A three-way analysis of variance examined piglet age, colon site of fecal samples, and method of fecal water analysis, for each variable. No differences were found between techniques of fecal water collection. Newborns showed production of short-chain fatty acids as early as the 1st day of life in limited amounts. Levels were stable between days 5 and 14, and then abruptly accumulated in the lumen. Acetate was predominant early, with propionate and butyrate responsible for late peaks. The production and assimilation of short-chain fatty acids was nearly complete proximal to the left colon. Age and colon site showed significant interactions for each fatty acid (p less than 0.001). The combined osmolar contributions of short-chain fatty acids and electrolytes accounted completely for the luminal osmolality after the 2nd wk of life. Previously there was an "osmolar gap" suggesting that lactose or its breakdown products were present in the lumen and were being removed by pathways other than through short-chain fatty acid production.

It is known that atrial extracts (AE) and synthetic atrial natriuretic factor (ANF) can increase glomerular filtration rate (GFR) and electrolyte and water excretion both in vivo and in vitro. It is not clear, however, if ANF-induced increases in filtered load (increased GFR) are required to produce natriuresis and diuresis. We perfused isolated rat kidneys with AE or synthetic ANF at constant pressure in a single-pass system. Extracts of atrial tissue (1 mg/ml) and high concentrations of ANF (31 and 61 ng/ml) significantly increased both GFR and electrolyte and water excretion. During continued infusion of ANF, GFR stabilized at increased levels, but sodium and water excretion continued to increase. After the termination of infusions, GFR and potassium excretion returned to control levels, but sodium and water excretion remained significantly elevated. Infusion of a low concentration of ANF (3 ng/ml) significantly increased sodium and water excretion without changing either GFR or potassium excretion. We conclude that increases in GFR are not a prerequisite for natriuresis and diuresis in response to ANF, but that increases in GFR can potentiate the response. Furthermore, our data suggest that ANF increases potassium excretion only if it increases GFR.

Before or during labor in humans, changes in peripheral levels of estrogen and progesterone are not evident. Local alterations of estrogen, progesterone, and prolactin concentrations may be present and be accompanied by prostaglandin changes. The purpose of this study was to investigate the differences in concentrations of these hormones across the uterus and to evaluate their interrelationships in patients at term gestation with and without labor. Blood samples were obtained from a radial artery and a uterine vein in 22 women without and in 10 with labor. The difference between levels in the two blood vessels was designated as the gradient. Neither levels nor gradients were different between the two groups for estrone, estradiol, estriol, progesterone, or prolactin. The plasma levels of prostaglandin F2 alpha, 13,14-dihydro-15-keto-prostaglandin F2 alpha, and prostaglandin E2 were significantly increased in labor. Prostacyclin levels, as indicated by the 6-keto-prostaglandin F1 alpha metabolite, were not altered. The gradients for prostaglandin F2 alpha and E2 were significantly increased in labor. The results of the study also suggested that, in gestation at term, serum prolactin is produced mainly by the pituitary and that estrone may originate from peripheral conversion of estradiol. We conclude that in humans prostaglandin gradients of the E and F groups are increased in labor. These increases are not associated with changes in sex steroids or prolactin. Prostacyclin metabolite gradients also appear not to be altered in labor, suggesting that some prostaglandins are selectively increased in early labor either by enhanced production or decreased metabolism or both.

Two subclasses of adenosine receptors, A1 and A2, have been described. The purpose of these experiments was to determine and compare the renal effects of several adenosine receptor agonists: adenosine (Ado), 2-chloroadenosine (2CA, nonselective), N6-cyclohexyladenosine (CHA, A1 selective), and N6-ethylcarboxamide adenosine (NECA, A2 selective). Rat kidneys were perfused at constant pressure (105 +/- 5 mmHg) using a Krebs-Henseleit buffer containing 3.5 g/100 ml Ficoll and 1.0 g/100 ml bovine serum albumin. Three clearance periods were obtained in each kidney, i.e., control, experimental [drug at 1 microM or vehicle (NaCl)], and recovery. Perfusate flow was increased by Ado, 2CA, and NECA but not affected by CHA. Glomerular filtration was increased by NECA, decreased by CHA, and not affected by Ado and 2CA. Afferent arteriolar resistance was decreased by NECA, increased by CHA, and unaffected by Ado and 2CA. Efferent arteriolar resistance was decreased by all agonists. CHA tended to decrease renin secretion whereas NECA significantly increased it. The results suggest that the renal vasculature possesses both A1 and A2 adenosine receptors and that activation of A2 receptors mediates arteriolar dilation and stimulation of renin secretion whereas activation of A1 receptors mediates arteriolar constriction and possibly inhibition of renin secretion.

Plasma progesterone, oestradiol, 13,14-dihydro, 15-keto, prostaglandin F2 alpha (PGFM) and luteinising hormone were measured in daily samples from eight dairy cows for 15 days before and after spontaneous calving, and compared to patterns obtained from 15 cows during and after induction of parturition with dexamethasone +/- prostaglandin. The average (+/- sd) length of pregnancy in the control cows was 285 +/- 3.04 days compared to 264 +/- 7.4 days in the induced group. Only nine cows required prostaglandin on day 11 after dexamethasone, which resulted in all nine calving 1.7 +/- 0.3 days later. Eight of the 15 treated cows retained the fetal membranes; however, the calving to first heat interval for all treated cows was 46.7 +/- 10 days (range 30 to 66 days) and calving to conception 52.4 +/- 17 days (range 30 to 85 days) compared to 42.1 +/- 15 days (range 28 to 64 days) and 76.5 +/- 24 days (range 54 to 115 days) respectively for the eight cows which calved without induction. The pre-partum hormone profiles were similar in all cows. Hormone profiles in the post partum period were also similar in all cows, irrespective of previous history. Baseline values for progesterone and oestradiol were not reached until 4.6 +/- 1.7 days and 2.75 +/- 0.7 days post partum respectively, whereas PGFM values increased for two or three days, reaching baseline levels 8.87 +/- 2.10 days later. Five cows had secondary peaks of PGFM on days 5,6 and 7. Luteinising hormone values increased steadily after calving in all cows.(ABSTRACT TRUNCATED AT 250 WORDS)

The difficulty of devising a standard treatment regime for cattle which would predictably terminate pregnancies in the 200 to 250 day range is described. Eight 15-month-old heifers which had been accidentally mated when approximately eight months old were examined by rectal palpation and condition scored. To induce abortion an intramuscular injection of 20 mg dexamethasone phenylpropionate was given followed 11 days later by an intramuscular injection of 500 microgram cloprostenol. A record was made of the time of calving along with calving and post calving details. Two of the heifers aborted before the injection of cloprostenol. The other six aborted within 48 hours of receiving this injection. The practical problems associated with aborting immature cattle are discussed as well as the financial aspects.

The in vivo and in vitro rates of renin secretion were measured in kidneys from five groups of dogs in which renal perfusion pressure, salt diet, and neural input were varied to cause large changes in renin secretion rates and renal renin content. It was found that both the in vivo and in vitro secretory rates were proportional to the renal renin content. However, in vitro secretion rates were dependent on content up to 100 ng angiotensin I/mg tissue per h. At higher renin contents no increment in in vitro secretion rate was seen. In vivo secretion rate did not appear to reach a maximum until renal renin content was above 250 ng AI/mg tissue per h. The data are interpreted to support the hypothesis that there exist at least two pools of renin. One releases renin at a fractional rate of about 1.5% of the total content per hour. The other releases renin at a rate dependent on the magnitude of the stimuli acting on the kidneys. It is also suggested that the rate of renin synthesis may be a determinant of the basla rate of renin secretion.

The importance of kininase I (carboxypeptidase N) in the catabolism of circulating kinins is not known. DL-2-Mercaptomethyl-3-guanidinoethylthiopropanoic acid (MGTA) has been reported to be an inhibitor of kininase I both in vitro and in vivo. In order to evaluate the possible role of kininase I in the in vivo inactivation of bradykinin, the authors studied the blood pressure responses of pentobarbital-anesthetized rats to bradykinin before and after the i.v. administration of MGTA (a 10-mg/kg bolus followed by 1 mg/kg/min continuous infusion). MGTA potentiated bradykinin-induced hypotension. The specificity of MGTA for kininase I was tested using other peptide and nonpeptide vasoactive substances. MGTA potentiated the hypertension due to angiotensin I, angiotensin II and vasopressin, but it did not affect the response to phenylephrine. On the other hand, MGTA did not potentiate the hypotensive action of acetylcholine, but it did potentiate that of sodium nitroprusside. The potentiation of bradykinin-induced hypotension is compatible with inhibition of kininase I by MGTA. The data suggest, however, that MGTA is not selective for any enzyme that inactivates kinins, inasmuch as other peptides and nonpeptide vasoactive substances are also potentiated.

Exogenous adenosine inhibits renin secretion and can either vasoconstrict or vasodilate the renal vasculature in vivo. In previous experiments, we found that micromolar concentrations of N6-cyclohexyl adenosine and 5'-N-ethylcarboxamide adenosine, analogs which are relatively selective for A1 and A2 adenosine receptors, respectively, tended to have opposite effects on both afferent arteriolar resistance and renin secretory rate in isolated rat kidneys perfused at constant pressure. Because the affinities of A1 and A2 receptors differ considerably, the purpose of the present experiments was to determine the concentration dependencies of the renal hemodynamic (perfusion pressure or perfusate flow, glomerular filtration rate, filtration fraction) and the renin secretory effects of adenosine, N6-cyclohexyl adenosine and 5'-N-ethylcarboxamide adenosine. Both the renovascular and the renin secretory effects of CHA were biphasic; at submicromolar concentrations, total and afferent arteriolar resistances were increased and renin secretion was inhibited. At higher concentrations, these effects were reversed or abolished. 5'-N-Ethylcarboxamide adenosine and adenosine decreased total and segmental (afferent and efferent) resistances and stimulated renin secretion. Taken together, the results are consistent with the suggestions that A1 and A2 receptors mediate inhibition and stimulation of renin secretion, that afferent arteriolar A1 and A2 receptors mediate constriction and dilation and that efferent arteriolar A2 receptors mediate dilation.

The acute (0.5-3.0 h) response of the contralateral kidney to unilateral renal artery constriction was studied in 7 pentobarbital-anesthetized dogs. Within 30 min after unilateral renal artery constriction to a pressure of about 60 mm Hg, contralateral vascular resistance, sodium excretion and filtration fraction increased significantly while glomerular filtration rate, blood flow and plasma flow did not change. Renin secretion decreased dramatically within 30 min, demonstrating a negative venous minus arterial plasma renin activity in some dogs. Unilateral renal artery constriction did not change the rate of angiotensin II extraction across the contralateral kidney or the urinary renin activity (measured in 4 dogs). These results indicate that the acute response of the contralateral kidney to unilateral renal artery constriction is somewhat different from that seen in the chronic state.

Two subjects each were exposed to pressure equivalents of 50 (SHAD I) and 60 (SHAD II) feet of sea water gauge (FSWG) for 30 and 28 d, respectively. Red blood cell (RBC) count, hemoglobin (Hb) content, and reticulocyte count of venous blood from divers were measured before, during, and after these exposures. RBC count of the divers decreased a maximum of 7.1% in the 50-ft dive and 10.7% in the 60-ft dive compared to surface control values. Hb content fell 7.7% and 11.1% in the 50- and 60-ft dives, respectively, when compared to nondiving subjects. Reticulocyte counts tended to increase late in the pressurization phase and during the recovery. The total month-long responses of Hgb in SHAD I, and RBC, Hgb, and reticulocyte count in SHAD II were significantly altered when compared to those of the surface control subjects. The changes in these factors were directly attributable to the month-long exposure to the total hyperbaric environment. The threshold for hematological effects of chronic exposure to compressed air would seem to lie between 50 and 60 FSWG.

Commercial ELISA kits for the determination of steroid hormones in milk and blood of domestic animals have been used by veterinary surgeons in practice as a method of pregnancy diagnosis in cattle, horses and pigs. In goats, the complex metabolism of steroid hormones in the mammary gland has made the test unsatisfactory. In five non-pregnant Saanen does, milk and blood samples were taken daily through a complete oestrous cycle, and the concentrations of progesterone measured by ELISA. A wide variation in the pattern of progesterone concentration was recorded. In seven non-pregnant and early pregnant does (less than 35 days) the mean concentration of oestrogens in milk was 0.5 ng/ml. Pregnancy in 88 does was subsequently predicted, based upon a concentration of oestrone sulphate in milk over 0.5 mg/ml, and was approximately 80 per cent accurate for determination of both pregnancy and non-pregnancy when compared with actual kidding data. Reasons are given for these errors.

Seventeen pregnant rabbits were studied under conscious, unstressed conditions after catheterization of the right ventricle (RV), a femoral artery (A), and a uterine vein (UV). Respiratory gas tensions, pH, and oxygen saturations and contents were determined serially throughout the latter half of gestation. The uterine coefficient of oxygen extraction increased with gestational age (R = 0.86) and became 60.6% +/- 0.3% during the last 4 days of pregnancy. To compare uterine perfusion with whole body perfusion in relationship to oxygen demands, the (Ao2 - UVo2/Ao2 - RVo2) ratio was computed. The ratio was greater than or equal to 1 after 20 days of gestation, which demonstrated that in regard to oxygen demands the rabbit uterus is relatively underperfused compared to the rest of the maternal organism in the last part of pregnancy. A comparison with analogous data in other species demonstrates that the pregnant rabbit, like the guinea pig, has a much lower rate of uterine blood flow than does the pregnant sheep. These interspecies differences in the perfusion rate and oxygen extraction of the pregnant uterus are related to differences in placental structure.

Newborn infants born after a term gestation appear to have an adequate capacity for small intestinal digestion and absorption of carbohydrate. Premature infants do not have a mature level of intestinal lactase activity. Apparently, in the premature infant, colonic fermentation serves an important, if not the only major route, for lactose carbon absorption, and it also appears that signs of fermentation activity such as increased BH2 are not indicative of disease. Important questions remaining in the premature infant relate to developmental aspects of colonic fermentative activity, effects of systemic antibiotic treatment on colonic salvage, the effects of various fermentation pathways on energy balance, the capacity for absorption of sugars, SCFA, and electrolytes by colonic epithelia, and the effects of fermentation products on metabolism and on the mucosal cells of the intestine or colon. Research addressing these questions may have relevance in the following areas: further development of formula diets for healthy premature infants and for patients of all ages with intestinal or colon dysfunction; the effects of colonic disease or surgical resection; the nutritional or clinical effects of dietary fiber; and the effects of antibiotic therapy on intestinal and colon function.

To determine whether salivary amylase of premature infants can function as a surrogate for pancreatic amylase, we evaluated its production in the infant, acid resistance, and hydrolytic potency in a simulated oropharyngeal, gastric, and intestinal environment. The activity of salivary amylase in 11 prematures varied between 1 and 33 U/ml; the isozymic profile and acid resistance of the premature salivary amylase were identical to those of the enzyme of adults. A "modular" formula containing 7 g/dl of a 14C labeled long chain glucose polymer with degrees of polymerization ranging between 18 and 29 glucose units was prepared. Salivary amylase, 1.1 U/ml, was added to this formula. The progressive breakdown of the 14C polymers as the milk was subjected to oropharyngeal, gastric, and intestinal phase environments was evaluated by quantifying the liberation of short-chain oligomers from the 14C labeled substrates. The gastric pH was varied between 2 and 5 and the gastric incubation time was either 5 or 180 min. Substantial gastric phase breakdown only occurred after 3 h of exposure at the higher pHs of 4 (12%) and 5 (32%). During the intestinal phase, salivary amylase activity resumed. Prior gastric phase pH affected ultimate intestinal phase breakdown, p less than 0.001; after 5-min gastric phases at pHs ranging from 2 to 5, the intestinal phase breakdown ranged from 17 to 55%. We conclude that the limited salivary amylase in the saliva of premature infants can produce significant glucose polymer digestion in both the stomach and small intestine but the digestion falls substantially short of that accomplished by usual concentrations of pancreatic amylase.

Alterations in the urinary excretion rate of kallikrein (UKKV) have frequently been assumed to reflect alterations in the intrarenal generation of kinins. Since other factors such as urinary pH and the activity of renal kininases may affect the intrarenal concentration of kinins, we investigated the effect of urinary alkalinization on kinin excretion in the presence and absence of kininase II inhibition. Urine was collected from the ureters of rats during control (ctl) (0.15 M NaCl infusion) and experimental (exp) periods. During exp periods, group I (time control) was infused with 0.15 M NaCl, group II with 0.3 M NaCl, and groups III and IV with 0.3 M NaHCO3, all at 0.12 ml/min. Prior to the ctl period, group IV was pretreated with the kininase II inhibitor captopril (40 mg/kg). During the exp period, urinary kinin excretion (UKiV) increased significantly in all groups ([exp - ctl] UKiV = 21 +/- 7, 27 +/- 9, 52 +/- 14, and 70 +/- 9 pg X min-1 X kg-1 in groups I, II, III, and IV, respectively). Urinary pH increased significantly in groups II, III, and IV. The increases in UKiV and pH were significantly greater in the bicarbonate-infused rats than in control. Partial correlation coefficients show that UKiV correlates with a high degree of significance only with urinary pH (r = 0.6). During the ctl period, UKiV in the captopril-pretreated rats was not different from that in other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

This study was designed to examine: (a) the effects of adenosine and its analogues on renin release in the absence of tubules, glomeruli, and macula densa, and (b) whether adenosine may be involved in a macula densa-mediated renin release mechanism. Rabbit afferent arterioles (Af) alone and afferent arterioles with macula densa attached (Af + MD) were microdissected and incubated for two consecutive 30-min periods. Hourly renin release rate from a single arteriole (or an arteriole with macula densa) was calculated and expressed as ng AI X h-1 X Af-1 (or Af + MD-1)/h (where AI is angiotensin I). Basal renin release rate from Af was 0.69 +/- 0.09 ng AI X h-1 X Af-1/h (means +/- SEM, n = 16) and remained stable for 60 min. Basal renin release rate from Af + MD was 0.20 +/- 0.04 ng AI X h-1 X Af + MD-1/h (n = 6), which was significantly lower (P less than 0.0025) than that from Af. When adenosine (0.1 microM) was added to Af, renin release decreased from 0.72 +/- 0.16 to 0.24 +/- 0.04 ng AI X h-1 X Af-1/h (P less than 0.025; n = 9). However, when adenosine was added to Af + MD, no significant change in renin release was observed. N6-cyclohexyl adenosine (an A1 adenosine receptor agonist) at 0.1 microM decreased renin release from Af from 0.69 +/- 0.14 to 0.39 +/- 0.12 ng AI X h-1 X Af-1/h (n = 5, P less than 0.05). However, 5'-N-ethylcarboxamide adenosine (an A2 adenosine receptor agonist) either at 0.1 microM or at 10 microM had no effect. Theophylline, at a concentration (10 microM) that does not block phosphodiesterase but does block adenosine receptors, increased renin release from Af + MD from 0.21 +/- 0.03 to 0.46 +/- 0.08 ng AI X h-1 X Af + MD-1/h (P less than 0.05; n = 8). The results are consistent with the hypotheses that adenosine decreases renin release via the activation of A1 adenosine receptors, and that adenosine may be an inhibitory signal from the macula densa to juxtaglomerular cells.

Coagulation profiles (platelet count, prothrombin time, partial thromboplastin time) obtained as part of predelivery screening were examined in patients who presented for delivery with a history of previous cesarean section. Coagulation test results (N = 1439) were reviewed from charts of 482 patients. No change in patient management occurred and no cesarean sections or vaginal deliveries were deferred as a result of the laboratory tests. There were no hemorrhagic complications. No blood products were transfused as a result of the tests. Routine coagulation evaluation is not justified for subsequent delivery of patients who had a previous cesarean section.

Autoregulatory responses of renal plasma flow (RPF) and glomerular filtration rate (GFR) to reductions in renal artery pressure (RAP) were studied in both kidneys of two-kidney, one-clamp dogs and in dogs treated with deoxycorticosterone acetate (DOCA; 25 mg/kg) plus high sodium diets with and without renal arterial clamping. In non-DOCA-treated animals, unilateral renal artery constriction resulted in a significant difference (P = 0.004) in renal renin activity (RRA) between the clamped (171 +/- 37 ng AI.mg-1.h-1) and the contralateral (57 +/- 23 mg AI.mg-1.h-1) kidneys with no change in their relative autoregulatory ability. In dogs treated with DOCA/high sodium there were no differences in RRA between the clamped and contralateral kidneys. The dogs treated with DOCA/high sodium were able to autoregulate both RPF and GFR even though their RRA was only 5.4 ng AI.mg-1.h-1. DOCA/high sodium treatment, however, reduced basal RPF (22%) and GFR (23%) below those in non-DOCA-treated animals. Analysis of the autoregulatory ability of individual kidneys showed no relationship to either RRA or renin secretory rates. These results support the conclusion that the renin-angiotensin system is not necessary component in the autoregulation of RPF or GFR.