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In vitro and in vivo vascular responses to the L‐type calcium channel activator, Bay K 8644, in rats with cirrhosis
Author(s) -
MOREAU RICHARD,
OBERTI FREDERIC,
LAHAYE PHILIPPE,
GADANO ADRIAN,
CAILMAIL STEPHANE,
SOGNI PHILIPPE,
CALES PAUL,
LEBREC DIDIER
Publication year - 1998
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.1998.01789.x
Subject(s) - medicine , splanchnic , vascular resistance , vasodilation , endocrinology , portal hypertension , splanchnic circulation , vascular smooth muscle , portal venous pressure , cirrhosis , hemodynamics , smooth muscle
A substance which increases the entry of extracellular calcium into arterial smooth muscle may decrease cirrhosis‐induced vasodilation. The aim of the present study was to measure the effects of the L‐type Ca 2+ channel activator, Bay K 8644, on the haemodynamics of rats with cirrhosis. Vascular reactivity to this substance was also investigated. Splanchnic and systemic haemodynamic responses to Bay K 8644 (50 μg/kg) were measured in cirrhotic and normal rats. Contraction induced by 0.1 μmol/L Bay K 8644 was measured in arterial rings (aorta and superior mesenteric artery) from cirrhotic and normal rats. In cirrhotic rats, Bay K 8644 significantly decreased portal pressure (15%) and portal tributary blood flow (24%), significantly increased portal territory vascular resistance (54%) and did not significantly change hepatocollateral vascular resistance. Bay K 8644 significantly increased arterial pressure (7%) and systemic vascular resistance (24%) and did not change the cardiac index. In normal rats, Bay K 8644 significantly increased vascular resistance (150%) in portal, hepatocollateral and systemic territories and significantly decreased the cardiac index (44%). Changes in portal territory, hepatocollateral and systemic vascular resistances were significantly less marked in cirrhotic than in normal rats. In rings from the aorta and superior mesenteric artery, Bay K 8644‐induced contraction was significantly lower in cirrhotic than in normal rats. In conclusion, in rats with cirrhosis, Bay K 8644 administration reduced vasodilation in splanchnic and systemic arteries and did not affect hepatocollateral vascular resistance. The Bay K 8644‐induced reduction in splanchnic vasodilation caused a decrease in portal hypertension. This study also shows that Bay K 8644‐induced vascular contraction was less marked in cirrhotic than in normal rats, in systemic and splanchnic vascular beds.