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Objective: To examine the effect of hydrogen peroxide on the function and ultrastructure of cardiac muscle and the coronary vasculature in an isovolumic rat heart preparation perfused at constant flow., Design: Ventricular function was monitored via a balloon placed in the left ventricle and the response of the coronary vessels to vasodilators was assessed in hearts arrested with 35 mM potassium and treated with 5 microM phenylephrine to contract the coronary resistance vessels. Changes in coronary perfusion pressure reflect changes in resistance vessel tone. SETTING/ANIMALS: This experimental study consisted of 14 heart preparations, six control and eight treated hearts., Interventions: Hydrogen peroxide was included in the perfusate at a final concentration of 250 microM for 20 mins., Main Results: Hydrogen peroxide reduced rate-pressure product by 42%, caused a fivefold increase in end-diastolic pressure and increased coronary perfusion pressure by 33%. Also, the response of the coronary vasculature to the endothelium-dependent vasodilator, histamine, and endothelium-independent vasodilator, sodium nitrite, was decreased by 55% and 53%, respectively. Electron microscopy of hydrogen peroxide-treated hearts showed damage to both capillaries and arterioles. Endothelial cells were distorted and contained pinocytotic vesicles, endothelial cell junctions were disrupted and blood vessels were detached from surrounding tissue. A comparatively small amount of injury was seen in the myocyte population., Conclusions: The greater amount of ultrastructural damage seen in blood vessels compared with cardiac muscle suggests that the smooth muscle and endothelial cells of the vasculature are more susceptible to oxidant injury than the myocytes.

The marine natural product, halistanol trisulfate, has a relatively low critical micelle concentration of 0.001% m/v (14.5 microM) and strong hemolytic potency with an EC50 of 0.00046% m/v (6.67 microM). As expected of a detergent, it inhibits the growth of gram-positive but not gram-negative bacteria. The hemolytic activity of halistanol trisulfate and other detergents has been shown to correlate with critical micelle concentration. This correlation may have important implications in the mechanism of membranolytic bioactivity.

Mice were exposed to concentrations of 20, 40 and 200 ppm ozone in air for 30 min. Ozone exposure decreased lung ascorbic acid levels and increased lung weight by up to 50% in a dose related manner. On incubation in Krebs-phosphate solution, lung slices from mice exposed to 200 ppm ozone released a smaller fraction of their content of ascorbic acid into the medium than did lung slices from control mice, suggesting that there was a preferential loss of extracellular ascorbic acid during oxone exposure. These results are consistent with the proposed function of ascorbic acid as an extracellular antioxidant in lungs.

Isolated hearts repleted with calcium after a short period of perfusion with a calcium-free medium undergo the injury of the calcium paradox and release cellular protein. In the present experiments, 15 min perfusion with a calcium containing HEPES solution subsequent to 10 min calcium-free perfusion resulted in the loss of 42.7 +/- 3.9 mg of protein/g heart. If hearts were repleted with calcium for 30 s only, then returned to calcium-free perfusion, resultant protein loss was the same. When calcium repletion was further decreased to 20 s, 23.9 +/- 1.3 mg/g of protein was lost. This critical period coincided with the onset of contracture but was prior to major ion movements. It is concluded that the transition to irreversible injury occurs within 30 s of calcium repletion and that subsequent removal of extra-cellular calcium does not alter the course of events leading to cell death.

Clinical proton NMR imaging uses magnetic field strengths in the range 0.1 to 0.5 T. In addition to the large static magnetic field, patients are exposed to magnetic field gradients during imaging and under extreme conditions, such as power failure or quenching, the field may collapse precipitously. A potential source of hazard to patients under these conditions is the induction of thoracic currents which may trigger ventricular fibrillation. In the present experiments, a 0.16 T resistive magnet with a time constant of 60 ms, powered by a programmable power supply, was used to examine any possible effects of static and changing magnetic field on the ECG and arterial blood pressure of anesthetized rats and guinea pigs. Animals were exposed to the following field conditions: static fields of 0.16 T; sine, triangular, and square wave modulated fields from 0.1 to 2 Hz; rapid field switches in excess of 2.0 T/s for 25 ms timed to occur at different stages of the cardiac cycle, including the vulnerable period during ventricular repolarization; and AC fields of 50 Hz. No change was observed in the blood pressure, heart rate, or ECG under any of the field conditions examined.

Although the importance of proper management of acute epiglottitis has been well recognized, little attention has been paid to the vulnerable period of time before the patient reaches the hospital. The courses of 23 children with acute epiglottitis were reviewed to determine prehospitalization management and morbidity.