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Intravenous injections of ionic contrast media increase extravascular lung water in patients with elevated left atrial pressure, particularly in the presence of myocardial ischemia. The authors compared bolus injections of sodium methylglucamine diatrizoate and iopamidol on extravascular lung water at several levels of left atrial pressure in dogs. Methylglucamine increased lung water by a maximum of approximately 25-30% above baseline levels at low (less than 3 mm Hg), moderate (approximately equal to 15 mm Hg), and elevated left atrial pressures (greater than or equal to 25 mm Hg). At matched pressures, the peak change in lung water in the dogs given iopamidol was +4%, +7%, and +6%, respectively. In dogs with myocardial ischemia, the differences were even more pronounced (+45%, +60%, and +70%, respectively, for ionic media, and +7%, +12%, and +21% for iopamidol). The authors caution against using ionic contrast media in patients with left ventricular dysfunction, particularly associated with ischemia. In such cases, non-ionic media appear safer.

In order to assess the sensitivity of nuclear magnetic resonance (NMR) in detecting acute renal vascular insufficiency, in vitro NMR spectroscopy (at 0.25 T) was performed on rabbit renal cortices following 45 min of unilateral renal artery (RAO) or renal vein occlusion (RVO). Data were obtained both with and without paramagnetic enhancement with gadolinium-DTPA (Gd-DTPA). In the absence of contrast material, RVO was distinguished by markedly elevated spin-lattice (T1) and spin-spin (T2) relaxation times when compared to the contralateral control kidney [mean increase of 29% in T1 (p less than 0.001) and 19% in T2 (p less than .001)]. RAO produced no change in T1 (p = N.S.) and a small change in T2 (mean increase of 11%, p less than .01). Five min following injection of 0.05 mM/kg of Gd-DTPA, relaxation times of control kidneys were markedly shortened [mean decrease 75% in T1 (p less than .001) and 12% in T2 (p less than 0.01)]. With Gd-DTPA, kidneys with RVO continued to have elevated T1 and T2 relaxation time, and kidneys with RAO maintained their essentially normal pre-contrast relaxation time values. We conclude that non-contrast NMR tissue analysis clearly differentiated normal from congested (RVO) kidneys, but not from acutely ischemic (RAO) kidneys. Paramagnetic enhancement with Gd-DTPA allows the differentiation of normally perfused from acutely ischemic or congested kidneys.

Congenitally athymic nude mice have recognized reproductive defects, accompanied by decreased pituitary gonadotropin and hypothalamic LRF concentrations at 3 weeks of age, compared to their normal heterozygous littermates. To determine if these hormonal changes are due to decreased secretion of thymic peptides, we measured pituitary concentrations of LH and FSH and hypothalamic LRF content at 21 days of age in 122 congenitally athymic nude (nu/nu) mice and in 190 heterozygous (nu/+) littermates administered daily injections of a crude thymic extract, semipurified thymosin fraction 5, or a synthetic thymic protein preparation. All animals receiving crude thymic protein extract, and some receiving either thymosin or synthetic thymic factor, had reduced levels of hypothalamic LRF. The changes in concentrations of gonadotropins were more variable. All mice receiving crude thymic extract (with reduced hypothalamic LRF content) appeared to have increased pituitary concentrations of LH, FSH, or both when compared to control animals, although statistical significance was not achieved in all groups. A similar but less marked trend toward increased pituitary gonadotropins was also noted in mice receiving thymic factor. These preliminary results suggest that thymus-derived peptides can affect hypothalamic-pituitary function and support our hypothesis that thymic hormones may play a role in programming the hypothalamic-pituitary axis in the prepubertal period in rodents.

Uniformly excellent myocardial protection during global ischemia in cardiac procedures requiring cessation of aortic root perfusion remains an elusive goal. This study establishes the importance of the preischemic inotropic state of the left ventricle and the arterial blood glucose concentration ([glucose]) immediately prior to an elective period of myocardial ischemia. Thirty-one experiments were performed on dogs subjected to 90 minutes of global ischemia on cardiopulmonary bypass at 28 degrees C with perfusion pressure constantly maintained at 90 mm Hg. The maximum rate of development of left ventricular pressure (LVdp/dtmax) at constant arterial and left atrial (LAP) pressures was used as a measure of contractility prior to ischemia. In a group of 18 of these dogs undergoing anoxic cardiac arrest, arterial blood [glucose], in conjunction with the preischemic LVdp/dtmax and the cross-clamp to asystole time interval (metabolic supply/demand index), significantly predicted (p less than 0.01) the functional result following the standard ischemic insult. In 13 other dogs with [glucose] greater than 120 mg/100 ml and treated with potassium cardioplegia, "normal" preischemic LVdp/dtmas (N = 7) was associated with a good functional result, but an elevated preischemic LVdp/dtmax (N = 6) produced severe functional impairment following ischemia. Optimum myocardial protection thus involves minimizing metabolic demands and maximizing metabolic supply immediately prior to and during the period of aortic cross-clamping.

Intravenous injections of ionic contrast media are widely used in the performance of radiographic techniques. The effects of ionic contrast media on lung water are unclear in the setting of elevated left atrial pressure, particularly in the presence of myocardial ischemia. In this study, we examined the effects of bolus injections of intravenous sodium meglumine diatrizoate (Renografin 76, 1 ml/kg, injected at 20 ml per second) on measures of extravascular lung water (EVLW) at several levels of left atrial pressure and in the presence of myocardial ischemia. Bolus injections of Renografin 76 produced significant increases in EVLW, with similar mean peak increases of approximately 26% EVLW at low (initial pressure less than 3 mm Hg), moderate (approximately 15 mm Hg), and elevated left atrial pressures (approximately 25 mm Hg). At matched pressures, the peak change in EVLW in the ischemic dogs was +45%, +60%, and +70%, respectively (all P less than .001 vs. the nonischemic dogs). Thus, use of intravenous ionic media precipitated acute transient increases in lung water, which were exaggerated by myocardial ischemia. While the effects were time limited in this experimental model, caution is advised in using intravenous ionic media in patients who have left ventricular dysfunction, particularly if underlying ischemia is present.

The increase in serum testosterone levels generally observed with intense, short-term exercise remains unexplained since most investigators have not reported any increase in the levels of luteinizing hormone, the pituitary glycoprotein most responsible for testicular steroidogenesis. Hemoconcentration and decreased metabolic clearance have been suggested as mechanisms to explain the exercise-associated testosterone increase. Such non-specific mechanisms should apply to other steroid hormones as well as to testosterone. To investigate whether the exercise-induced changes in other steroid hormones were similar to that of testosterone, we measured serum levels of testosterone, androstenedione, dehydroepiandrosterone, and cortisol as well as gonadotropins, luteinizing hormone and follicle-stimulating hormone, and prolactin at 5-15 min intervals throughout progressive maximal intensity exercise on a cycle ergometer. Significant increases were observed with all hormones with exercise. The increase in serum testosterone began prior to exercise, peaked at 20 min after the beginning of exercise, and fell to baseline within 10 min. The serum luteinizing hormone increase was synchronous with that of testosterone, suggesting that gonadotropin stimulation was not responsible for the testosterone increment. The increments in serum cortisol, androstenedione, dehydroepiandrosterone, and prolactin levels were simultaneous but began 25-30 min after that of testosterone in all subjects. These findings, therefore, suggest that, contrary to previous evidence, the exercise-associated increase in serum testosterone results predominantly from a specific mechanism, presumably involving increased testicular production without gonadotropin stimulation.

In order to assess the potential sensitivity of nuclear magnetic resonance for the assessment and detection of renal vascular insufficiency, nuclear magnetic resonance spectroscopy was performed on rabbit renal cortices following 45 minutes of unilateral renal artery or vein occlusion with and without the injection of a paramagnetic contrast material (manganese chloride). Renal vein occlusions produced a marked increase in T1 and T2 relaxation times when compared to the contralateral control kidney (mean increase of 18 per cent in T1 and 27 per cent in T2). Renal artery occlusions produced no change in T1 and only a slight increase in T2 (mean increase of 5 per cent). After the intravenous injection of 0.03 mM/kg. of manganese chloride, T1 of the control kidneys was reduced by almost 50 per cent. Relaxation parameters from the kidneys undergoing arterial occlusion did not change after manganese injection when compared to the occluded kidneys without contrast. In the kidneys undergoing venous occlusion, a moderate decrease in T1 resulted from manganese chloride. We conclude that in the absence of a paramagnetic contrast material, nuclear magnetic resonance discriminates well between normal and (venous occlusion) congested kidneys, but not between normal and acutely ischemic (arterial occlusion) kidneys. In the presence of a renal paramagnetic contrast material, NMR aids in the differentiation of acute unilateral arterial insufficiency, as relaxation times from the normal kidney decline while the ischemic kidney does not change.

The purpose of this study was to evaluate the effects of acute and chronic ischemic injury on myocardial spin-lattice relaxation times (T1) in dogs. Ligation of the left anterior descending coronary artery was performed on 23 dogs which were divided into four experimental groups and killed at 3 hours (n = 6), 4 days (n = 6), 21 days (n = 5), and 56 days (n = 6) after coronary occlusion. T1 was measured in vitro with a 2.5 kg nuclear magnetic resonance (NMR) spectrometer using tissue from ischemic and control areas of the myocardium. Both the 3-hour and 4-day groups showed prolongations in T1 (p less than 0.01) for tissue from the ischemic area. In the 21-day group, two infarcts showed an increase in T1, two showed a decrease in T1, and one showed no significant change. The 56-day old infarcts had a lower mean value for T1 than control myocardium (p less than 0.01). The differences in myocardial water content between control and infarcted myocardium were found to parallel changes in T1 values in each experimental group. Pathologic examination of the myocardial scar from 21- and 56-day-old infarcts revealed extensive fibrosis in the infarcts with lower T1 values and tissue water contents than control myocardium. We conclude that myocardial edema in 3-hour and 4-day-old infarcts results in association with prolongations in T1. Twenty-one-day-old infarcts may be edematous (with increased T1) or fibrotic (with T1 values lower than normal myocardium), while 56-day-old infarcts are fibrotic and have shorter T1 values than normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

The purposes of this study were to evaluate the effects of acute myocardial ischemia with reperfusion on T1 (spin-lattice) nuclear magnetic resonance (NMR) relaxation times in a canine model and correlate these changes with bulk myocardial water content (%H2O). In 15 dogs the left anterior descending coronary artery was occluded for either 40 minutes (n = 5), 1 hour (n = 5), or 2 hours (n = 5). In 15 additional dogs, matched occlusion periods were followed by 3 hours of reperfusion. T1 of tissue from normal and ischemic myocardium was measured in vitro with a 2.5 kg NMR spectrometer. In the reperfusion animals, the 2-hour group showed significant increases in %H2O and T1 when the ischemic segment of myocardium was evaluated (both p less than 0.01). All but one animal in the 1-hour (reperfusion) group showed increases in both %H2O or T1 in the ischemic segment of myocardium when compared to control segments. The mean values from the ischemic myocardium in the 1-hour group were significantly higher than the values from the matched control segment for %H2O (p less than 0.05) and T1 (p less than 0.05). In the group undergoing 40 minutes of ischemia followed by 3 hours of reperfusion, neither %H2O nor T1 changed significantly. In the nonreperfused animals, neither T1 nor %H2O content increased significantly after 40 minutes. Significant increases were seen in the 1-hour (p less than 0.05) and 2-hour groups (without reperfusion) (p less than 0.01). In addition, the 2-hour occlusion followed by reperfusion animals had significantly greater T1 relaxation times and %H2O than control ischemic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of transient ischemia and reperfusion on regional myocardial function, salvage and swelling have been systematically analyzed in experimental canine preparations. The results of these interventions on myocardial in vitro measurements of magnetic relaxation times (T1 = magnetization recovery, T2 = spin echo) are of significant importance with respect to future nuclear magnetic resonance tomographic imaging. Thus, using a pulsed magnetic resonance spectrometer (10.7 MHz), myocardial tissue samples from two groups of dogs were evaluated. In group 1 (n = six dogs), the left anterior descending artery was occluded for 3 hours before sacrifice; in group 2 (six dogs), 3 hours of occlusion was followed by 1 hour of reperfusion. Multiple tissue samples from normal and ischemic (or ischemic and reperfused) myocardium were obtained for measurement of T1, T2 and % water content (wet weight--dry weight/wet weight). Water content increased with ischemia (78 +/- 4%) and reperfusion (81 +/- 4%) (both p less than 0.01 versus control values). Values for T1 increased with ischemia (598 +/- 39 versus 487 +/- 23 ms in normal tissue from the same heart, p less than 0.01). Even greater T1 changes occurred in the animals with reperfusion (654 +/- 52 ms, p less than 0.01 versus the intra-animal control values). Changes in T2 were similar but less marked (ischemic zone 43.9 +/- 1.0 versus 41.2 +/- 1.0 ms in nonischemic tissue in the corresponding heart, p less than 0.05; reperfusion zone 48.3 +/- 3.5 versus 41.9 +/- 2.3 ms in the normal zone, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)