Fish oil treatment decreases superoxide anions in the myocardium and coronary arteries of atherosclerotic monkeys.

BACKGROUND: This experiment sought to determine the effects of fish oil on superoxide anion production in the myocardium and coronary arteries of atherosclerotic monkeys. Recent evidence indicates that dietary supplementation with fish oil preserves normal vasomotion of atherosclerotic coronary arteries and reduces damage to the myocardium after ischemia and reperfusion, although the mechanisms remain unclear. METHODS AND RESULTS: Adult male cynomolgus monkeys were fed an atherogenic diet with (n = 15) or without (n = 15) half the fat calories from fish oil. After 12 months, chemiluminescence of lucigenin was used to measure superoxide anion production in coronary arteries and myocardium after 1 hour of ischemia and 2 hours of reperfusion. The signals were calibrated with known quantities of xanthine and xanthine oxidase. Superoxide anion production in ischemic myocardium was (mean +/- SEM, nmol/mg dry wt per minute) 1 +/- 1 and 4 +/- 1 in monkeys fed fish oil and not fed fish oil, respectively (P < .05). Superoxide anion production in coronary arteries not exposed to ischemia and reperfusion was (nmol/mg dry wt per minute) 4 +/- 1 and 8 +/- 2 in monkeys fed fish oil and not fed fish oil, respectively (P < .05). Superoxide anion production in coronary arteries was (nmol/mg dry wt per minute) 5 +/- 2 and 16 +/- 3 in monkeys fed fish oil and not fed fish oil after ischemia and reperfusion, respectively (P < .05). CONCLUSIONS: Dietary supplementation with fish oil reduced vascular superoxide anion production and prevented the increase in vascular and myocardial superoxide anion production that accompanied ischemia and reperfusion. These phenomena may underlie some of the beneficial cardiovascular effects of fish oil.

Hemodynamic effects of long term feeding of sympathomimetic amines to swine.

The hemodynamic effects of long term feeding of sympathomimetic amines (SPMA) to swine were studied. Three groups of female swine (N = 20 for each group) were fed either aminorex fumarate, d-amphetamine sulfate, or dextrose (control) for as long as 8 months in dosages up to 15 mg/kg/day. After 4 months of this feeding regiment, the weight gain of the pigs fed either aminorex or amphetamine was significantly less than the control animals. Hemodynamic measurements on awake swine indicated no elevation of pulmonary arterial blood pressure in the pigs fed SPMA. Measurement of systemic hemodynamics revealed that cardiac index was lower in the treated pigs than in control animals, but that heart rate and systemic arterial blood pressure were not altered by the drugs. In addition to baseline measurements of hemodynamic variables, the animals were exposed to acute hypoxia (12 percent O2 in N2) for 5 minutes. Although pulmonary arterial blood pressure increased similarly in the 3 groups of pigs, total pulmonary resistance increased to a greater extent in the pigs fed SPMA, indicating perhaps an enhancement of the hypoxic pulmonary pressor response after chronic ingestion of either amphetamine or aminorex. In a limited number of pigs, SPMA were fed for a period of 8 months, of which the last 3 months were during pregnancy. Hemodynamic measurements on sedated (metomidate, IV) swine revealed no difference in pulmonary arterial blood pressures between treated and control animals. We conclude that chronic ingestion of large doses of aminorex or amphetamine in swine does not lead to pulmonary arterial hypertension, but that slight reductions in cardiac output and subtle alterations in the pulmonary pressor response to acute hypoxia may occur.

Hemodynamic effects of acute hypoxia and minute amounts of endotoxin in awake swine.

Hemodynamic measurements and arterial blood gases were determined from awake swine (n = 8) during acute hypoxia (12% O2, balance N2 for 5 minutes) and following injection of Escherichia coli endotoxin (4 microgram/kg of body weight) into the pulmonary artery. Comparison of baseline data with these treatments indicated: (1) swine exhibited a marked pulmonary pressor response to acute hypoxia (deltaBPpul = 9 to 12 mm of Hg): (2) injection of minute amounts of endotoxin led to a marked increase of pulmonary arterial blood pressure 10 to 20 minutes following the injection (deltaBPpul = 15 mm of Hg); and (3) the pulmonary pressor response to a 2nd exposure of acute hypoxia was unaffected by the intervening endotoxin injection.

Cardiopulmonary effects of mechanical distension of the rumen in nonanesthetized sheep.

The cardiopulmonary effects of mechanical distension of the rumen were studied in nonanesthetized sheep. Results in group I ewes indicated that simply increasing intraruminal pressure by compressed air insufflation did not seriously affect cardiopulmonary hemodynamics. Changes were more serious in group II ewes when water injection was followed by ruminal insufflation with compressed air. Heart rate, total peripheral resistance, and total pulmonary resistance increased, with a concommitant increase in arterial and pulmonary blood pressure and decrease in stroke volume. Infusion of water alone increased heart rate and cardiac output. The blood gas data indicated a definite arterial hypoxemia and hypercapnia, suggesting impaired ventilation during ruminal distension. The increase in total pulmonary resistance was thought to be due to alveolar hypoxia caused by a significant decrease in ventilation.

Effect of exercise on cardiac output and distribution of uterine blood flow in pregnant ewes.

This study was designed to determine what effect physical training has on heart rate and stroke volume responses to exercise stress and to determine if exercise altered the distribution of uterine blood flow. Measurements were made in ten pregnant ewes at rest and immediately following exercise on a treadmill. Five ewes underwent physical training for 3 wk prior to measurement. An increase in heart rate with no change in stroke volume was observed following exercise in both trained and untrained ewes. Total uterine blood flow was not changed following exercise, but distribution was altered in favor of the placenta. Blood flow was evenly distributed within the placenta before and after exercise. The redistribution of flow to the placenta that occurs after exercise. tphe redistribution of flow to the placenta that occurs after exercise might represent a compensatory mechanism for the fetus.