Showing papers by "Dipak K. Das published in 1991"

Reduction of cold injury by superoxide dismutase and catalase.

Abstract: The pathophysiology of cold injury was examined by cooling a hind leg of an anesthetized New Zealand white rabbit. A flow probe and a thermocouple were placed in the leg to be cooled to monitor the blood flow and tissue temperature. After baseline measurements, the leg was cooled with a freezing mixture up to 0 degrees C, which was followed by rewarming. The other leg served as control. In the experimental group, liposome-bound superoxide dismutase and catalase were infused through the femoral vein 15 minutes prior to putting the freezing mixture on the leg. Salicylic acid was injected through the femoral vein at the end of some experiments to assay hydroxy radical (OH). Our results demonstrated reduction of local blood flow in cold-exposed leg, indicating development of ischemia. Creatine kinase and lactage dehydrogenase were increased during rewarming in conjunction with hydroxyl radical formation, phospholipid breakdown, and lipid peroxidation. Treatment with superoxide dismutase and catalase reduced OH formation, prevented phospholipid degradation, and decreased creatine kinase, lactate dehydrogenase, and malonaldehyde formation. These results indicate that rewarming of cooled tissue is associated with "rewarming injury" similar to "reperfusion injury", and that oxygen-derived free radicals play a significant role in the pathophysiology of such injury.

Amiloride Enhances Postischemic Ventricular Recovery During Cardioplegic Arrest

Abstract: Intracellular Ca2+ is of primary importance in the pathogenesis of ischemia and reperfusion injury in the myocardium.'p2 Although the exact mechanism of intracellular Ca2+accumulation has not been described, several mechanisms have been proposed, including the Ca2+ transmembrane inflow through the slow channels2 and through the permeable membrane caused by myocardial i~chemia.~Recent studies suggested that massive Ca2+ influx may occur as a consequence of the Na+-Ca2+ exchange during reperfusion, which in turn may be caused by accumulation of Na+ during i~chemia.~ It is known that acidosis induced by anaerobic metabolism leads to enhanced exchange of intracellular H+ for Na+. In addition, inhibition of Na+-K+-ATPase by energy depletion also is known to cause to the accumulation of intracellular Na+. This study proposes to determine if inhibition of H+-Na+ exchange by amiloride can lead to myocardial preservation during cardioplegic arrest as seen during openheart surgery. We used an animal model simulating coronary artery bypass for acute myocardial infarction. The results suggest that amiloride reduces myocardial ischemic reperfusion injury.

Role of Membrane Phospholipids in Nonfreezing Cold Injury

Abstract: Nonfreezing cold injury (NFCI) represents a potential threat to infantry and marine operations carried out in inclement weather conditions.1,2 The term “NFCI” is used to identify the syndrome that results from damage to tissues that have been cooled, usually for prolonged periods, at temperatures between about 288°K (15°C) and their freezing point (272.5°K) (-0.5°C). NFCI reduces man’s mobility at the time, but through cold sensitization it may compromise his ability to fight under similar conditions in the future.