Preliminary reports of portions of this work were presented at the 42nd Annual Meeting of the American Association for the Study of Liver Diseases, Chicago, November 2–5, 1991.
Vasoactive effect of endothelin-1 on rat liver in vivo†
Article first published online: 5 DEC 2005
Copyright © 1994 American Association for the Study of Liver Diseases
Volume 19, Issue 1, pages 155–161, January 1994
How to Cite
Okumura, S., Takei, Y., Kawano, S., Nagano, K., Masuda, E., Goto, M., Tsuji, S., Michida, T., Chen, S.-S., Kashiwagi, T., Fusamoto, H., Kamada, T. and Sato, N. (1994), Vasoactive effect of endothelin-1 on rat liver in vivo. Hepatology, 19: 155–161. doi: 10.1002/hep.1840190125
- Issue published online: 5 DEC 2005
- Article first published online: 5 DEC 2005
- Manuscript Accepted: 29 JUL 1993
- Manuscript Received: 27 JAN 1993
The purpose of this study was to evaluate the role of endothelin-1 in modulating hepatic microcirculation and liver damage. Rats were infused with endothelin-1 at doses ranging from 30 to 1,000 pmol/kg over 1 min through an indwelling cannula placed in the portal vein. In control rats, saline solution was infused at the same rate. Alterations in hepatic microcirculation were measured with an in vivo microscopy system. Serum lactate dehydrogenase activity, an indicator of hepatic damage, was measured 1 hr after endothelin-1 infusion. Immediately after infusion of endothelin-1, we noted a rapid increase in portal pressure, which remained increased for up to 30 min after endothelin-1 infusion. In contrast, systemic blood pressure remained unchanged, even at 1,000 pmol/kg of endothelin-1. Sinusoidal width was reduced and sinusoidal erythrocyte velocity was diminished in a dose-dependent manner. Oxygen saturation of blood in sinusoids was decreased in a dose-dependent manner, reaching values around 40 of control with 1,000 pmol/kg endothelin-1. The degree of decrease in oxygen saturation of blood in sinusoids had an excellent correlation with the calculated blood flow in the liver tissue. Serum lactate dehydrogenase levels were three to four times control values when endothelin-1 was administered at 1,000 pmol/kg. Thus endothelin-1 decreased hepatic tissue oxygenation associated with sinusoidal vasoconstriction. At high concentrations of endothelin-1, this decrease results in hepatocellular damage. (Hepatology 1994;19:155–161).