SUPEROXIDE RADICAL INVOLVEMENT IN THE PATHOGENESIS OF BURN SHOCK
- 1 January 1984
- journal article
- research article
- Vol. 12 (4) , 229-239
Abstract
The pathogenesis of burn shock syndrome involves the production of superoxide radicals which are first generated in the burned skin. They are responsible for an increase in vascular permeability with loss of plasma, which results in hemoconcentration and hypovolemia. The resulting systemic hypoperfusion leads to a generalized production of superoxide radicals and subsequent cellular damage. Prior administration of allopurinol or superoxide dismutase increases the survival rates of mice subjected to burn shock.This publication has 21 references indexed in Scilit:
- Oxygen Metabolism and the Toxic Properties of PhagocytesAnnals of Internal Medicine, 1980
- Glucose and lactate kinetics in burn shock.American Journal of Physiology-Endocrinology and Metabolism, 1977
- EFFECT OF BURN INJURY ON GLUCOSE TURNOVER IN GUINEA-PIGS1977
- Cardiovascular and metabolic responses during burn shock in the guinea pigAmerican Journal of Physiology-Legacy Content, 1976
- Metabolic studies of allopurinol, an inhibitor of xanthine oxidaseBiochemical Pharmacology, 1966
- Sympathetic Nerve Depletion in Severe Thermal InjuryAnnals of Surgery, 1965
- A LIGHT AND ELECTRON MICROSCOPIC ANALYSIS OF VASCULAR INJURY*Annals of the New York Academy of Sciences, 1964
- Role of Infection in the Delayed Deaths of Mice Following Extensive Burn InjuryExperimental Biology and Medicine, 1961
- Hemodynamic Response of the Dog to Thermal RadiationJournal of Applied Physiology, 1956
- Effects of Shock and Gold on Mouse Liver Sulfhydryl.Experimental Biology and Medicine, 1952