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Background. We studied hemodynamic alterations in normal and three models of portal hypertension
at rest, after hemorrhage, and after resuscitation to determine the role of hepatic
dysfunction in the splanchnic vascular response to hemorrhage in portal hypertension.
Methods. One noncirrhotic and two cirrhotic models of portal hypertension were produced in
rabbits: partial prehepatic portal vein ligation, common bile duct ligation, and carbon
tetrachloride-induced cirrhosis. Animals were subjected to isovolemic hemorrhage followed
by reinfusion of shed blood. Portal, central, and aortic pressures, superior mesenteric
artery blood flow, and portosystemic shunt were measured.
Results. Histologic examination showed parenchymal damage was absent in normal and portal
vein ligation, severe in common bile duct ligation, and moderate in carbon tetrachloride-induced
cirrhosis. All portal hypertensive animals exhibited diminished splanchnic vasoconstrictive
response to hemorrhage compared with normal. The carbon tetrachloride cirrhosis group
had severe cirrhotic changes, minimal portosystemic shunt, and mildly diminished constrictive
response. In contrast, the portal vein ligation and common bile duct ligation animals
had larger portosystemic shunts, markedly diminished constrictive response, and less
severe parenchymal damage. A direct correlation existed between magnitude of rise
in portal venous pressure or degree of portosystemic shunt and the fall in mesenteric
resistance or diminution of vasoconstrictive response to hemorrhage.
Conclusions. We concluded that the abnormal splanchnic vascular response in portal hypertension
is relatively independent of the degree of hepatic parenchymal injury, but it is related
to the degree of portal hypertension and possibly to splanchnic hyperemia.
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Article info
Publication history
Accepted:
October 3,
1994
Footnotes
1Supported by American Heart Association grant no. 92009340 and the National Institutes of Health grant no. 1 RO1 DK47067-O1A1.
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© 1995 Mosby-Year Book, Inc. Published by Elsevier Inc.
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