Abstract
In our studies of the effects of perfusing the rabbit hearts with Ringer-Locke solution to which various amino-acids were added, 1 we were struck by the fact that infarction of the myocardium caused a sharp drop in the pH of the perfusate. This was apparently due to the liberation of a non-volatile acid metabolite giving the qualitative test for lactic acid. The inevitable result of the drop in pH was earlier failure, and, furthermore, low heart muscle creatine values. These findings seemed to be a corollary of our previous observation 2 that myocardial infarction in the dog leads to a creatinuria.
We therefore decided to undertake chemical studies of the infarcted as compared with the normal heart muscle of the dog. In addition to the creatine content we thought it worth while to determine the glycogen content, since Riesser and Brentano, we found, had demonstrated a close relationship between creatine mobilization and glycogenolysis. 3 Himwich and Goldfarb have demonstrated a decrease in glycogen content and an increase in lactic acid in infarcted heart muscle coincident with a rise in blood lactic acid. 4
Dogs were anesthetized with barbiturates intraperitoneally and the chest opened under artificial pressure respiration. A nick was made in the pericardium over the first part of the main anterior descending branch of the left coronary artery. The artery was isolated and tied off, and the pericardium and chest closed. The heart was then allowed to continue beating for periods varying from 15 minutes to 12 hours. The infarcted beating heart was removed and sections of infarcted and normal muscle were minced in cold alcohol for glycogen determinations; similar portions were removed for creatine and total solid determinations.
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