Abstract

It is known that coronary insufficiency is chiefly due to coronary sclerosis, but gradual coronary occlusion does not cause a myocardial infarction. On the course of clinico-pathological studies on myocardial infarction, about a half of cases showed only a narrowing of corresponding coronary artery. The present investigation is a histochemical and pathologic study of myocardial infarction produced by acute coronary constriction.Method : Twenty-three adult mongrel dogs were used. Coronary constriction was produced by U-shaped silver clamp (0.7-1.0 mm in inner diameter) to clip the same artery as reported in the preceding paper. Animals were killed after 3 hours to 131 days of ischemia. Histochemical, histological and electrocardiographic methods were the same as in the first report.Results : 1. In histochemical studies, loss of glycogen and appearance of fatty droplets in muscle fibers were seen in early stage, but these changes seemed to be reversible as 3 to 5 days later most of the myocardial fibers regained their normal staining paralleled with the recovery from edema and degeneration. On the other hand, loss of succinic dehydrogenase, ATP-ase and acid phosphatase activity, and appearance of acid mucopolysaccharide reaction in muscle fibers, were accompanied with the destruction of their fine structures and seemed to be irreversible changes.2. After one day, a slight degeneration of muscle fibers was seen in full layers of the anterior wall of the left ventricle, but two to three days later, most myocardial fibers recovered from degeneration, and only a part of subendocardial muscle layer and a border of muscle bundles (deep sinospiral and deep bulbospiral) showed a minor degree of myocardial necrosis. This indicated that a collateral circulation could develop within two to three days following coronary constriction.3. Coronary arteries showed marked edema of its wall in early stage, then regenerative processes took place gradually and intimal hyperplasia such as fibroelatosis narrowed the lumen. These changes formed a contrast to histolytic changes seen in coronary artery ligation. Fibrinoid necrosis was seen in the arteries beyond the occluded area in two cases.4. In most cases, early changes of myocardial necrosis were seen in posterior wall, especially in subepicardial layer or a border of muscle bundles. These were seen in old infarction which showed only a interstitial fibrosis in the anterior wall. These findings could indicate the presence of functional circulatory disturbance and intercoronary reflex mechanism.5. Electrocardiogram taken directly from epicardial surface revealed the following : The elevation of RS-T segment was seen 1/2 to two minutes after the constriction, reaching its maximum in two to five minutes. After sixty to ninety minutes, RS-T segment returned to former level, then turned into the coronary T inversion. The coronary T inversion became positive around three to four days. Neither QRS changes nor extrasystoles were seen. Depressed RS-T segment was seen in 3 cases. In 2 cases of marked subendocardial infarction, electrocardiographic abnormalities were not observed.

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