| Research Abstract |
Occlusion of the coronary artery produces ischemia of the myocardium, resulting in physiological, biochemical, and hitological alterations of the myocardium. Coronary occlusion also produces acidosis of the myocardium, the exact mechanism for myocardial acidosis remaining unclear, however. One possibility is that ischemia increases breakdown of triglyceride and phospholipids in the myocardium, and releases protons. If this view is correct, the levels of non-esterified fatty acids in the myocardium would increase during ischemia, and a drug that inhibits ischemia-induced myocardial acidosis would attenuate accmulation of non-esterified fatty acids in the myocardium.
In the present study, in the first place, we tried to find a method suitable for detection of non-esterified fatty acids in the myocardium, and found that the method develped by Nimura and Kinoshita using 9-anthryldiazomethane (ADAM) reagent for fluorescent labeling of carboxylic acids was most simple and reliable as well. Th
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e results show that the levels of lauric acid, myristic acid, palmitoleic acid, arachidonic acid, linoleic acid, palmitic acid, oleic acid, and stearic acid in the myocardium were 10.23, 48.29, 7.53, 25.48, 106.61, 135.02, 78.58, and 57.47 nmol/g wet tissue, respectively. Coronary artery occlusion for 90 min increased the levels of these non-esterified fatty acids to 1.70 - 3.38 times, the increase in arachidonic acid being most prominent. This result indicates that there is breakdown of triglyceride and/or phospholipids. An injection of propranolol (1 mg/kg) given intravenously 5 min before coronary occlusion inhibited completely the ischemia-induced increase in non-esterified fatty acids. A dextro-isomer of propranolol (1 mg/kg) also tended to attenuate the increase in non-esterified fatty acids.
These results suggest that coronary artery occlusion produces release of catecholaimnes in the myocardium, and the released catecholamines activate lipases and phospholipases to release non-esterified fatty acids. The membrane stabilizing action of propranolol may also contribute to the inhibitory action of propranolol on the ischemia-induced increase in fatty acids. Less
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