| Project/Area Number |
03807080
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
ICHIKAWA Tohru Hiroshima University Hospital Assistant Professor, 医学部附属病院, 講師 (70142338)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAMOTO Katsunari Hiroshima University Hospital Fellow, 医学部附属病院, 医員
KODAMA Takashi Hiroshima University Hospital Assistant Professor, 医学部附属病院, 講師 (20161945)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1992: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1991: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Liver cirrhosis / Pulmonary hypertension / Carbon - tetrachloride / Dimethynitrosamine / Porta - systemic shunt / GutーLiverーLung axis |
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| Research Abstract |
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 was 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 groups. 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 ratio 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 suspected that the mechanism of the pulmonary hypertension in the cirrhosis was responsible for not only the extrahepatic portasystemic shunt, but also the dysfunction of the reticulo-endothelial system in the liver, for example the functional damage of the kuppfer cells and/or the intrahepatic portasystemic shunt.
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