Pathophysiological Investigations on the Myocardial Carbohydrate Metabolism in Liver Cirrhosis : (II) Myocardial Carbohydrate Metabolism during Induced Hypoxemia

Abstract

Since BING's description of the coronary venous catheterization technique in 1949, studies on myocardial carbohydrate metabolism mainly in patients with cardiopathy have been reported by GOODALE, MIKAMO, KOBAYASHI, and, from our Department, by HAYASHI et al. WUHRMANN reported that non-inflammatory myocardial disturbance is elicited in association with protein metabolic disturbance in hepatopathy. NANGU in our Department, made clear the relation between electrocardiographic findings and dysproteinemia quantitatively, and YAJIMA described the disturbance of coronary circulation and myocardial oxygen metabolism in relation to the S-T deviation of liver cirrhosis. However, the metabolism of the energy source of the myocardium in liver cirrhosis has not been explained. In this paper, the actualities of disturbance of myocardial carbohydrate metabolism in liver cirrhosis is clarified by means of coronary catheterization in room air and under 10 per cent oxygen gas inhalation, and it will be compared with HAYASHI'S data of our Department which is studied mainly in patients with compensatory cardiopathy, in order to contribute to the pathophysiology of liver cirrhosis. Materials and Methods Fifteen patients who apparently had no primary cardiovascular lesion but had a diagnosis of liver cirrhosis established by general clinical laboratory examinations, laparoscopy, and liver biopsy were subjected to coronary venous catheterization, and their myocardial carbohydrate metabolic values were determined in room air respiration and subsequently in 10 per cent oxygen gas inhalation for 20 minutes. Results and Discussion I. Myocardial carbohydrate metabolism in room air respiration (a) Glucose : Ten of the 15 cases showed myocardial uptake of glucose, 2 showed no coronary arteriovenous difference, and 5 showed glucose release. The incidence of glucose release was higher in the above series than in normal subjects. At the arterial carbohydrate level of about 100 mg%, no case exhibited glucose release. At lower levels of arterial carbohydrate, cases of glucose release were also noted, and were found to be about fifty-fifty with the cases showing glucose uptake. Myocardial glucose uptake in liver cirrhosis did not show a significant correlationship to the arterial glucose levels, and the amount of its uptake was less than known in other diseases.