PATHOPHYSIOLOGIC, BIOCHEMICAL CHANGES OF THERMAL INJURY

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Studies of the mechanisms of fluid and electrolyte translocation, protracted erythrocyte destruction, cardiac (hyper- and hypo-) function and identification of immunoglobulin-suppressive substance following major burn injury are being undertaken. Serial measurements of transmembrane potentials (TM) and micromuscle electrolyte analysis coupled with metabolic balance studies are done in thermally injured patients with injuries exceeding 35% total body surface area (TBSA). Methods are being developed for rapid determination of exchangeable sodium mass and animal models developed for study of the mechanism of electolyte transport abnormalities. Erythrocyte destruction has been identified as produced by toxic levels of free fatty acids and studies of fat metabolism initiated. Currently lipoprotein metabolism and liver metabolism of mobilized adipose is being pursued by the development of a three compartment model for oxidation studies of high density lipoprotein metabolism and hepatcyte culture for the role of carnitine and HMG-Ac activity. Forty percent TBSA scald burn in guina pigs have been developed for the future study of the myocardial abnormalities and therapeutic interventions in nutrition and metabolism of fat. Purification chromatography techniques have been accomplished for the isolation of alpha-globulin associated immunosuppressive factors which are currently being tested on a lymphocyte and leukocyte in vitro model.