Role of prostacyclin in hemodynamic alterations in conscious rats with extrahepatic or intrahepatic portal hypertension
✍ Scribed by Frederic Oberti; Philippe Sogni; Stephane Cailmail; Richard Moreau; Bernard Pipy; Dr. Didier Lebrec
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 673 KB
- Volume
- 18
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
Although prostaglandins are thought to be involved in the hyperdynamic circulation of portal hypertension, the role of this substance has not been elucidated. Dose-response curves, the hemodynamic effects of prostacyclin (20 k e g ) and its inhibitor indomethacin and measurements of plasma and urinary levels of 6-keto-prostaglandin F,, were compared in three groups of six rats each: normal, with portal vein stenosis and with secondary biliary cirrhosis. Plasma and urinary levels of 6-keto-prostaglandin F,, were higher in rats with portal vein stenosis and cirrhotic rats than in normal rats. Dose-response curves showed similar maximal decreases in arterial pressure in the three groups, whereas the maximal increase in portal pressure was less marked in cirrhotic rats than in normal rats and rats with portal vein stenosis. In normal rats, prostacyclin increased cardiac output by 21% and portal pressure by 41%. Similar increases were observed in rats with portal vein stenosis. In contrast, prostacyclin did not affect cardiac output and portal pressure in cirrhotic rats. Indomethacin induced a more marked vasoconstrictive effect in normal rats than in cirrhotic rats. This study shows that prostacyclin plays a role in the hemodynamic alterations in portal hypertension. Moreover, the hyporeactivity observed in cirrhotic rats suggests that prostacyclin plays a major role in the circulatory changes of portal hypertension due to chronic liver disease. (HEPATOLOGY 1993: 18~62 1-627.) Although many studies have been conducted on the alterations of the splanchnic and systemic circulation in portal hypertension, the exact mechanisms of these changes have not been elucidated. Because systemic and splanchnic vasodilatation occurs in portal hypertension,