Key result
Endotoxin shows no direct toxic effect on myocardial performance or metabolism during hypotension.
Why the study?
The study aimed to determine possible direct adverse effects of endotoxin toxicity on myocardial tissue.
Endotoxin may directly impair isolated canine myocardium; leaves open mechanisms of septic cardiomyopathy in vivo.
The purpose of the present study was to determine possible direct adverse effects of endotoxin toxicity on canine myocardial tissue. Experiments were designed to assay cardiac performance, hemodynamics and metabolism in an isolated working left ventricle removed from a donor dog, exchanging blood with an intact support animal. Aortic pressure and cardiac output of the heart were decreased by pump adjustment in the experimental group to follow the support animal's mean systemic pressure after endotoxin or in the control group to mimic the previous cardiac endotoxin response. Three hours of systemic hypotension and depressed cardiac output followed by restoration of pressure and flow to control values by pump adjustment revealed insignificant differences between the endotoxin and control groups. Left ventricular end diastolic pressure, myocardial contractility, cardiac power (work/sec), dP/dT, O2 uptake and CO2 production were statistically unaltered from zero time control values after the sustained period of hypotension in both control and experimental groups. Findings indicate the absence of a direct toxic action of endotoxin on the myocardium.
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Lb et al. (1971) studied Endotoxin toxicity. Endotoxin vs. Control group (mimicking previous cardiac response without endotoxin) was evaluated on Left ventricular end diastolic pressure, myocardial contractility, cardiac power, dP/dT, O2 uptake and CO2 production. Endotoxin exhibited no direct toxic action on the canine myocardium, with cardiac performance and metabolism remaining statistically unaltered from control values after 3 hours of hypotension.
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