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Function of Isolated Hearts from Septic, Saline‐Infused, and Septic, Alcohol‐Infused Rats
Author(s) -
Muniz Antonio E.,
McDonough Kathleen H.
Publication year - 1991
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1991.tb05213.x
Subject(s) - preload , medicine , inotrope , sepsis , saline , cardiac output , anesthesia , stroke volume , septic shock , alcohol , cardiac function curve , cardiology , myocardial infarction , heart rate , hemodynamics , heart failure , blood pressure , biology , biochemistry
The aim of the present study was to determine whether hearts that demonstrate depressed myocardial reserves as a result of sustained hypermetabolic sepsis would show a potentiation of the dysfunction after an infusion of high doses of alcohol. We have previously shown that myocardial depression is present in hearts removed from hy permetabolic septic rats. Acute alcohol administration has also been shown to have a negative inotropic effect on the heart. In this study, myocardial function was assessed under in vitro conditions in which preload could be varied and aortic outflow resistance controlled and thus heart function could be determined under both low and high workloads. The alcohol‐infused group increased cardiac perform ance as a function of increasing preload similarly to the controls. Heart rate, however, was significantly elevated compared with con trol. Isolated hearts from septic, saline‐infused animals showed depressed cardlac performance both in terms of stroke volume and myocardial work over a range of preloads. The septic, alcohol‐infused animals did not show this depression. Thus, a loss of myocardial reserve was demonstrable in hearts isolated from septic, saline‐infused rats but not in septic, alcohol‐infused rats. Alcohol, at least acutely, seemed to reverse or ameliorate the loss of myocardial reserve induced by sepsis possibly by increasing the ability of the heart to fill during diastole and thus perform volume work.