Zinc supplements and serum lipids in young adult white males.

A 12-wk double-blind study was conducted to determine the effect of oral zinc supplementation upon serum total cholesterol, lipoprotein-cholesterol fractions, and serum triglycerides in white males. The subjects were randomly assigned to one of three treatment groups and consumed either a placebo tablet (n = 9), 50 mg Zn/d (n = 13), or 75 mg Zn/d (n = 9) as Zn gluconate. Serum total cholesterol, low-density-lipoprotein (LDL) cholesterol, very-low-density-lipoprotein (VLDL) cholesterol, and triglycerides were not affected by Zn supplements. However, serum high-density-lipoprotein (HDL)-cholesterol levels in subjects assigned to the 75 mg Zn/d group were significantly lower at weeks 6 and 12 than those for the placebo group and lower at weeks 6, 8, and 12 than at baseline; subjects assigned to the 50 mg Zn/d group had lower serum HDL-cholesterol levels at week 12 than did the placebo group and lower at week 12 than at base line.

Myocardial failure with altered response to adrenaline in endotoxin shock.

1 There is a growing concensus that myocardial performance in the early stages of experimental endotoxic and septic shock is relatively normal; however, recent reports have identified an intermediate phase of shock when myocardial dysfunction is clearly apparent.2 The mechanism of dysfunction has become a subject of intense investigation. A current view is that altered myocardial responsiveness to circulating catecholamines may play an important role in the dysfunction observed after endotoxin administration. The present studies, in which an isolated working heart preparation of the dog was used, were designed to test this hypothesis. This particular experimental preparation was selected to provide an adequate interpretation of results; cardiac output, afterload, and concentrations of adrenaline reaching the coronary vascular bed were controlled in all experiments. Responses to infusions of adrenaline were recorded in the ;steady-state' condition. Control (non-shocked) heart responses to adrenaline were highly reproducible in terms of inotropic, chronotropic and coronary vascular behaviour.3 Results from the study document myocardial dysfunction within 4-6 h following an LD(70) endotoxin administration on the basis of increased left ventricular end diastolic pressure (LVEDP), decreased cardiac power and myocardial efficiency, and depressed negative and positive dP/dt parameters.4 Findings suggest significantly altered responsiveness of the myocardium to infused adrenaline at rates of 1, 2, and 5 mug/min with concentrations between 10 and 1 ng/ml blood. LVEDP was elevated while calculated power and efficiency parameters remained significantly below control values during infusion of adrenaline in endotoxin-treated hearts. Depressions of responsiveness were interpreted to occur on the basis of failure to restore positive and negative dP/dt to normal values and depressed coronary blood flow responses during adrenaline administration. Increases in coronary flow were regularly less in experimental hearts than the controls. Heart rate responses to adrenaline in both failing and non-failing hearts were identical.5 In conclusion, it is suggested that myocardial contractile and relaxation characteristics and coronary vascular responses to adrenaline infusion are depressed in endotoxin shock during the period of demonstrated myocardial dysfunction. No distinct causal relationships were observed between the altered myocardial responsiveness and pathogenesis of heart dysfunction since myocardial dysfunction and altered responsiveness to adrenaline were generally observed together. Myocardial oedema formation after endotoxin as previously reported by this laboratory may bear a relationship to the depressed negative dP/dt response to adrenaline.

Effects of coronary hypotension on myocardial substrate utilization.

Changes in myocardial substrate utilization were studied after experimental coronary hypotension in the isolated dog heart perfused with the blood of a large donor animal. After a control period (100 mmHg) the afterload of the isolated heart was adjusted to 50 mmHg and kept at that level for 4 h. After this period, a second control observation was made at a 100-mmHg afterload. Coronary sinus blood flow and oxygen consumption decreased during hypotension and returned to normal during the second control period. Myocardial free fatty acid (FFA) uptake and oxidation did not change significantly. Lactate uptake and the percentage of CO2 derived from myocardial lactate utilization were both diminished during hypotension. These changes were not present during the second control period. Glucose uptake and myocardial respiratory quotient were decreased during the hypotensive period. Half the hearts exhibited elevated end-diastolic pressure after hypotension, but no metabolic differences were detectable between the failing and nonfailing hearts. Thus, prolonged severe hypotension caused a relative preference of FFA oxidation and diminished lactate and glucose uptakes by the myocardium. These changes were quite different from those obtained during experimental hemorrhagic or endotoxic shock.