Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.

術後急性肺水腫に関する実験的研究 第3編 術後急性肺水腫の発生に及ぼす生理的食塩水大量輸液の影響に関する実験的研究

坂本 昌士 岡山大学医学部第1外科教室
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As one of the experiments to clarify the causes of the development of the post-operative acute pulmonary edema, 50 cc/kg saline solution was injected intravenously to 16 normal dogs and 6 dogs with hypoproteinemia at the rapid rate of 20 cc/m. These dogs were killed 2 hours after the transfusions and the influences of these transfusions on the development of the acute pulmonary edema were examined with following results. 1) In normal dogs, the changes of circulatory blood volume and cardiac output and those of pulmonary arterial pressure by transfusions had a parallel relationship. Electrocardiographically, no disturbances of the heart muscle were observed. Histologically, pulmonary congestion and hemorrhages were found, but no lung edema. 2) On the contrary, the following findings were observed by transfusions in the dogs with hypoproteinemia; decrease of circulatory blood volume, upset of pulmonary circulation caused by an abnormal rise in the pulmonary arterial pressure and a decrease in the cardiac output, signs of heart muscle disturbances in the E.K.G., and the picture of lung edemas in the microscopic examination. 3) Congestion and hemorrhages were the main findings in the group of normal dogs. On the contrary, lung edemas were marked while congestion and hemorrhages were slight in the group of the hypoproteinemia-induced dogs. 4) These findings suggested that the capillary permeability had increased more in the hypoproteinemia-induced dogs than in the normal dogs. 5) A slight increase in the pulmonary arterial pressure and cardiac output had already been observable before transfusions in the hypoproteinemia-induced dogs, comparing with the normal dogs. 6) It is considered from these results that hypoproteinemia which reduces the power of resistence to abrupt circulatory burden is in a preparatory state to the development of the pulmonary edema.