AJP - Gastrointestinal and Liver Physiology, Vol 268, Issue 1 47-G53, Copyright © 1995 by American Physiological Society
Changes in circulatory status and transport function of the liver induced by reactive oxygen species
S. Kawamoto, S. Tashiro, Y. Miyauchi and M. Inoue
Department of Surgery, Kumamoto University School of Medicine, Japan.
To elucidate the pathogenesis of microcirculatory disturbance of the liver
after ischemia and reperfusion, the effect of reactive oxygen species on
hepatic circulatory status and transport function for a cholephilic
compound was studied in an isolated perfused rat liver. Perfusion of the
liver with a medium containing hypoxanthine and xanthine oxidase
significantly increased the portal pressure, with concomitant decrease in
intrahepatic vascular volume and hepatic uptake of bromosulfophthalein
(BSP). Similar changes were also elicited by infusion of serotonin, which
induces contraction of sinusoidal endothelial cells. Either superoxide
dismutase or catalase added in the perfusion medium partially inhibited the
oxidase-induced changes in portal pressure, vascular volume of hepatic
sinusoid, and BSP transport. In the presence of superoxide dismutase,
either catalase or erythrocytes inhibited the oxidase-induced changes
completely. These results indicated that superoxide anion and hydrogen
peroxide might induce contraction of hepatic resistance vessels,
capacitance vessels, and/or sinusoidal endothelial cells and that this
contraction decreased the vascular bed in the liver and the time for
interaction of circulation substrates with hepatocytes, thereby decreasing
hepatic transport for cholephilic ligands such as BSP.
