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Paper Information

Title: 

OPIOID BLOCKADE IMPROVES MESENTERIC RESPONSIVENESS IN CIRRHOTIC RATS

Type: POSTER
Author(s): MOEZI L.*,EBRAHIMKHANI M.R.,KIANI S.,MERAT SH.,DEHPOUR A.R.
 
 *DEPARTMENT OF PHARMACOLOGY, SCHOOL OF MEDICINE, TEHRAN UNIVERSITY OF MEDICAL SCIENCES, TEHRAN, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Arterial vasodilation with concomitant hyperdynamic circulation is common findings in cirrhotic subjects. Elevated levels of plasma endogenous opioid peptides have been reported in cholestasis and cirrhosis. Increased opioid peptides contribute to different manifestations of chronic liver disease such as pruritis, ascitis and hepatic encephalopathy. In this study the potential role of opioid system in cirrhosis-induced vascular hyporesponsiveness was investigated. Bile duct ligated (BDL) and sham operated animals received daily subcutaneous administration of naltrexone, an opioid receptor antagonist (20mg/kg/day), or saline for 28 days. After 4 weeks the superior mesenteric artery was cannulated and was perfused according to McGeorge method and then phenylephrine vasoconstrictor response of mesenteric vessels (10-10 to 10-6 mol) was examined. Plasma level of nitrite/nitrate as an indicator for nitric oxide production was measured. Biliary cirrhosis was accompanied with a decrease in baseline perfusion pressure in mesenteric vascular bed (P<0.01). Chronic opioid receptor blockade significantly increased this parameter (P<0.01). The maximum pressure response to phenylephrine was decreased significantly in cirrhosis while naltrexone treatment completely improved it (P<0.01). Chronic opioid receptor blockade did not modulate the increased nitrite/nitrate levels following cholestasis. This study provided evidences on the contribution of endogenous opioid system to vascular hyporesponsiveness in cirrhosis. Opioid-induced vascular hyporespnsiveness is independent of NO production in this model.

 
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