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Cardiac function and responsiveness to beta-adrenoceptor agonists in rats with obstructive jaundice
1Department of Pharmacology, Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.
The American Journal of Physiology
|August 1, 1993
Summary
Obstructive jaundice in rats causes cardiac myopathy with impaired contractility. However, cardiac beta-adrenoceptor function, number, and affinity remain normal, suggesting other mechanisms contribute to circulatory failure.
Area of Science:
- Cardiology
- Physiology
- Pharmacology
Background:
- Obstructive jaundice can lead to circulatory failure.
- The role of cardiac beta-adrenoceptors in this condition is not fully understood.
Purpose of the Study:
- To investigate cardiac function and beta-adrenoceptor characteristics in a rat model of obstructive jaundice.
- To determine if beta-adrenoceptor pathways are altered in the pathogenesis of circulatory failure.
Main Methods:
- Utilized pithed rat and isolated working heart preparations to assess cardiac function.
- Employed competitive radioligand binding assays to measure beta-adrenoceptor number and affinity.
- Compared results from bile duct-ligated (BDL) rats with sham-operated (SO) controls.
Main Results:
- Bile duct ligation (BDL) resulted in impaired basal cardiac contractility in both tested preparations.
- Responsiveness to norepinephrine and beta-adrenoceptor agonists (isoproterenol, dobutamine) was unaffected by BDL.
- No significant differences were found in cardiac beta-adrenoceptor affinity or number between BDL and SO rats.
Conclusions:
- The 3-day bile duct-ligated rat exhibits a cardiac myopathy.
- This cardiac myopathy occurs despite preserved responsiveness to beta-adrenoceptor agonists.
- Cardiac beta-adrenoceptor number and affinity remain unchanged, indicating these receptors are not primary contributors to the observed cardiac dysfunction in this model.