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Endogenous cannabinoids mediate hypotension after experimental myocardial infarction
J A Wagner1, K Hu, J Bauersachs
1Department of Medicine, University of Würzburg, Würzburg, Germany. j.wagner@medizin.uni-wuerzburg.de
Journal of the American College of Cardiology
|December 12, 2001
Summary
Endocannabinoids contribute to hypotension following myocardial infarction (MI). Blocking cannabinoid(1) receptors (CB(1)) in rats with MI improved blood pressure but increased mortality, suggesting impaired endothelial function.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Endocrinology
Background:
- Hypotension and cardiogenic shock are frequent complications of acute myocardial infarction (MI).
- Cannabinoids are potent vasodilators, and endocannabinoids play a role in hypotension during hemorrhagic and septic shock.
Purpose of the Study:
- To investigate the influence of endocannabinoids on hemodynamic variables in experimental models of acute myocardial infarction (MI).
Main Methods:
- Rats underwent left coronary artery ligation to induce MI.
- Hemodynamic variables were measured in rats pretreated with a selective cannabinoid(1) receptor (CB(1)) antagonist (SR141716A) or vehicle.
- Endocannabinoids in monocytes and platelets were quantified, and their effects on blood pressure and vascular reactivity were assessed.
Main Results:
- MI induced a significant drop in mean arterial pressure (MAP) in control rats, which was attenuated by CB(1) antagonist pretreatment.
- CB(1) receptor blockade increased heart rate and 2-hour mortality post-MI, while MI size remained unchanged.
- Endocannabinoids anandamide and 2-arachidonyl glycerol were detected in monocytes and platelets after MI.
- Endothelium-dependent arterial relaxation was impaired in rats treated with the CB(1) antagonist.
Conclusions:
- Endocannabinoids produced in monocytes and platelets contribute to hypotension in acute MI.
- CB(1) receptor blockade can restore MAP but may increase mortality by impairing endothelial function.