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
Sm. Jacinto et Bs. Jandhyala, 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, Free radical biology & medicine, 17(2), 1994, pp. 171-179
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.