[Experimental study on changes of the pulmonary vessels in the cirrhotic rats]

Gut-liver-lung axis hypothesis in the pulmonary hypertension complicated with the cirrhosis, that some humonal factors escaping the hepatic inactivation caused by the liver cirrhosis were responsible for the changes in the lung vessels and caused the pulmonary hypertension, was set up. To determine the relation between the pulmonary hypertension and the liver cirrhosis, the author studied experimentally the hemodynamics and the pathological changes in the lung in the cirrhotic rats induced with carbon tetrachloride and in the rats with the portacaval anastomosis. Pathologically the intimal and medial thickness of the small lung arteries were created in both grous. The right ventricular systolic pressure in the cirrhotic rats (25.6 +/- 1.4 torr) was higher than that of the rats with the portacaval anastomosis (21.3 +/- 2.0 torr), but the rate of the extrahepatic portasystemic shunt in the cirrhotic rats (3.3 +/- 1.2%), which was measured with using gamma-labelled microsphere, was conversely lower than that in the rats with the portacaval shunt (17.8 +/- 3.9%). The same pathological changes were also created in another cirrhotic rats induced with dimethylnitrosamine. The right ventricular systolic pressure increased as the liver function became severe. It was suggested that not only the extrahepatic portasystemic shunt but also the dysfunction of the reticuloendothelial system in the liver, was responsible for the mechanism of the pulmonary hypertension in the cirrhosis.