COMPARATIVE-EVALUATION OF THE ACUTE EFFECTS OF OXYGEN-FREE RADICALS ON MYOCARDIAL-CONTRACTILITY IN ANESTHETIZED DOGS WITH THOSE OCCURRING IN THE EARLY STAGES OF SPLANCHNIC ARTERY-OCCLUSION AND HEMORRHAGIC-SHOCK

Oxygen free radicals are cytotoxic and generated in excessive quantiti es during reoxygenation of ischemic organs. It has been demonstrated t hat oxygen free radicals impair cardiac contractile mechanisms in in v itro studies as well as depress myocardial contractility in in vivo ex periments. The objectives of the present studies are to evaluate alter ations in cardiac contractility and hemodynamics in two canine models of shock, namely, Wigger's model of hemorrhage and splanchnic artery o cclusion (SAG) model. The data obtained in these models are comparativ ely evaluated with that caused by oxygen free radicals. Pentobarbital anesthetized dogs were instrumented to record blood pressure, heart ra te, left ventricular pressure, (LVP & LVEDP) and LVdp/dt. Contractilit y index was evaluated as max dp/dt p. In the Wigger's model, during th e period of hemorrhage or after reinfusion of the shed blood despite m arked variations in preload and afterload, index of contractility was not altered. Similarly, in the SAG model also, during the period of oc clusion or after release, contractility index was not depressed. Howev er, in both the models, after reinfusion of the blood (Wigger's) or af ter release of splanchnic arteries, there were gradual deteriorations of stroke volume, cardiac output, and arterial blood pressure. In cont rast, after generation of free radicals by exogenous administration of xanthine plus xanthine oxidase, cardiac contractility was significant ly depressed leading to decreases in stroke volume, cardiac output, an d blood pressure. Using identical procedures evaluate contractility, w e have demonstrated that the initial depression of myocardial contract ility was not the causative factor for circulatory failure in the two models of shock. It is possible that the nature and the time course of generation of free radicals may be entirely different in the models o f shock. It is also likely that various physiological compensatory pro cesses that would occur in the early stages of shock may have masked o r neutralized the effects of free radicals on the myocardium. Therefor e, enhanced venous compliance and venous pooling would account for ini tiating circulatory failure in the present shock models.