The effect of magnesium sulfate infusion on systemic and renal prostacyclin production

Recent in vitro studies have suggested that magnesium sulfate (MgSO4) infusions may increase prostacyclin production. We studied the effect of MgSO4 infusion on prostacyclin (PGI2) metabolite excretion in women with either pregnancy induced hypertension or preterm labor. Excretion of renal and systemic metabolites of PGI2 was measured prior to and following the start of MgSO4 infusion in the two groups. An increased in renal PGI2 metabolite preterm labor excretion was noted in the hypertension group but no change was noted in systemic PGI2 excretion in either group. These data fail to support a generalized, short term increase in endothelial cell PGI2 production as the basis for the beneficial effect of MgSO4.     

Effects of glucose ingestion on postprandial lipemia and triglyceride clearance in humans

To determine whether the metabolism of diet-derived triglycerides (TG) is acutely regulated by the consumption of insulinogenic carbohydrates, we measured the effects of glucose ingestion on oral and intravenous fat tolerance, and on serum triglyceride concentrations obtained during duodenal fat perfusion. Postprandial lipemia was diminished by the ingestion of 50 g (148 +/- 121 mg.dl-1 x 7 h-1 vs 192 +/- 124 mg.dl-1 x 7 h-1, P less than 0.05) and 100 g (104 +/- 106 mg.dl-1 x 7 h-1 vs 171 +/- 104 mg.dl-1 x 7 h-1, P less than 0.05) glucose. Peak postprandial TG concentrations occurred later after meals containing glucose and fat than after meals containing fat alone. This effect could be reproduced when an iso-osmotic quantity of urea was substituted for glucose in the test meal. Starch ingestion had no discernible effect on postprandial lipemia. Intravenous fat tolerance was similar before (4.9 +/- 1.2%.min-1) and 2 h (4.4 +/- 1.3%.min-1) and 4 h (4.8 +/- 1.5%.min-1) after 50 g glucose ingestion. During duodenal fat perfusion, glucose ingestion caused a progressive decrease in plasma triglyceride concentrations. These data suggest that glucose ingestion diminishes postprandial lipemia in a dose-dependent manner, but that this effect is not due to increased clearance of triglyceride from the circulation. The hypotriglyceridemic effects of glucose appear to reflect delayed gastric emptying and decreased hepatic secretion of triglyceride.     

Effect of magnesium sulfate administration on subendocardial and subepicardial perfusion

The objective of this study was to determine the effect of systemic MgSO₄ infusion on subendocardial and subepicardial perfusion. Seventeen spontaneously breathing piglets were examined. Myocardial perfusion was measured using radiolabeled microspheres at baseline, 30 and 60 min after either MgSO₄ (80 mg/kg) or saline infusion. Blood pressure, heart rate, and cardiac output were also measured at these time intervals. Comparison of the magnesiuminduced changes in systemic blood pressure and on subendocardial and subepicardial perfusion at 30 and 60 min with values obtained with saline solution at 30 and 60 min, yielded no statistically significant difference (Tables 1–3). The ratio of subendocardial/subepicardial blood flow and subendocardial and subepicardial coronary vascular resistance at 30 and 60 min revealed no statistically significant differences between the magnesium and the control group (Table 3). There were no statistically significant difference in cardiac output and heart rate during any of the measured periods (Table 2). Our results suggest that the administration of MgSO₄ does not alter the ratio of subendocardial/subepicardial blood flow and the ratio of subendocardial/subepicardial coronary vascular resistance.     

Apolipoprotein effects on the lipolysis of perfused triglyceride by heparin-immobilized milk lipase

Bovine milk lipase was noncovalently bound to a heparin-Sepharose support and a [3H]glycerol/[14C]triolein emulsion was circulated through it. This system, more closely simulating in vivo conditions than the standard lipoprotein lipase assay, was employed to determine the effect of human apo-E and apo-C-II on the lipolysis of the circulating substrate. Both apo-C-II and apo-E produced enhanced lipolysis in comparison to unsupplemented emulsions, at appropriate enzyme densities on the heparin-Sepharose. With high enzyme densities the stimulation produced by apo-E was lost but that of apo-C-II persisted. When apo-E and apo-C-II were added together they produced significantly more lipolysis than when either was added separately. The enhancement of lipolysis produced by apo-E was correlated with the increased binding of triglyceride to the heparin-Sepharose enzyme complex. The effect of additions of both apoproteins to rat intestinal chylomicrons resulted in data quite similar to the triglyceride emulsions. Heparin-Sepharose columns with high and low zones of enzyme density produced greater lipolysis than when the enzyme was distributed more uniformly throughout the column. Perfusions of substrate supplemented with sufficient apo-E to produce maximal binding and lipolysis resulted in a progressive elution of the triglyceride substrate from the column during the perfusion. Free fatty acid:albumin molar ratios greater than 2 resulted in desorption of substrate from the column. This suggests the possibility of regulation of the lipolytic process by the products of lipolysis.     

Effect of intravenous epinephrine infusion on plasma renin activity in adrenalectomized dogs

Previous experiments have shown that circulating epinephrine stimulates renin secretin and increases plasma renin activity (PRA) when it is infused intravenously, but not when it is infused directly into the renal artery at similar infusion rates. The present experiments were designed to test the hypothesis that the adrenal glands mediate the PRA response to intravenous epinephrine infusion. Accordingly, anesthetized dogs were prepared with either an acute bilateral adrenalectomy or a sham-adrenalectomy procedure. Epinephrine was then infused intravenously into each animal for 45 minutes at a rate of 25 ng X kg-1 X min-1. Time control experiments in which epinephrine was not infused were also conducted. In sham-adrenalectomized dogs, PRA (in nanograms per ml h-1) rose from 4.1 +/- 1.4 in the control period to 13.0 +/- 3.0 during intravenous epinephrine infusion (means +/- SE; p less than 0.01). In adrenalectomized dogs, PRA rose from 2.1 +/- 0.4 during the control period to 5.5 +/- 0.9 during intravenous epinephrine infusion (p less than 0.01). Neither the absolute increments in PRA nor the percent increases in PRA were significantly different between the two groups receiving epinephrine. PRA remained unchanged in time control experiments. These data demonstrate that the adrenal glands need not be present in order for intravenous epinephrine infusion to elicit an increase in PRA. The data do not support the hypothesis, therefore, that epinephrine-induced increases in PRA are initiated by receptors located within the adrenal glands.     

Effect of intrarenal arterial infusion of magnesium on renin release in dogs.

Magnesium chloride was infused into the renal artery of anesthetized dogs in order to determine its effect on renal function. Natriuresis and diuresis were observed during MgCl2 infusion, but there appeared to be no effect on glomerular filtration rate (GFR), or plasma sodium or potassium concentrations. Although mean arterial blood pressure and renal plasma flow (RPF) decreased throughout the experiment, the fall was not significant until after stopping MgCl2 infusion. A significant stimulation of renin secretion occurred during magnesium administration.