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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Effects of calcium entry blockade on myocardial blood flow
1Department of Medicine, University of Minnesota, Minneapolis 55455.
Insights
Calcium entry blockers aid anti-ischemia by preventing coronary artery vasoconstriction and enhancing blood flow to the subendocardium. Diltiazem specifically improves collateral blood flow in chronic coronary occlusion models.
Area of Science:
- Cardiovascular Pharmacology
- Ischemic Heart Disease
Background:
- Calcium entry blockers impact coronary vasculature, suggesting anti-ischemia potential.
- These drugs minimally affect basal epicardial arteries but counter vasoconstriction during exercise and spasm.
Purpose of the Study:
- To evaluate the anti-ischemia effects of calcium entry blockers on coronary vasculature.
- To understand their impact on coronary blood flow regulation and collateral circulation.
Main Methods:
- Review of pharmacological effects on coronary arteries (epicardial and resistance vessels).
- Analysis of impact on vasoconstriction, vasodilation, and reactive hyperemia.
- Examination of effects on coronary collateral vessels in acute and chronic occlusion models.
Main Results:
- Calcium blockers prevent vasoconstriction exacerbating stenosis and interrupt variant angina spasms.
- They cause transient vasodilation of resistance vessels, reducing responsiveness to ischemia and reactive hyperemia.
- These agents enhance subendocardial perfusion distal to stenoses by preventing excessive vasodilation.
- Limited effect on acute collateral vessels, but diltiazem improves collateral flow in chronic occlusion models.
Conclusions:
- Calcium entry blockers offer anti-ischemia benefits by modulating coronary vascular tone and improving perfusion.
- Their differential effects on resistance vessels and collaterals highlight specific therapeutic applications in ischemic heart disease.
Abstract:
The calcium entry-blocking drugs produce effects on the coronary vasculature that might be expected to exert anti-ischemia activity. Although these agents cause little vasodilation of the epicardial coronary arteries during basal conditions, they block vasoconstriction that can increase stenosis severity during isometric exercise and interrupt coronary artery spasm in patients with variant angina. Administration of the calcium blockers causes transient vasodilation of the coronary resistance vessels, followed by decreased responsiveness to a brief ischemic stimulus. This results in decreased coronary reactive hyperemia after transient coronary occlusion. By preventing excessive ischemic vasodilation of the resistance vessels, these agents can enhance perfusion of the subendocardium distal to a flow-limiting coronary stenosis. The calcium entry blockers have relatively little effect on the immature coronary collateral vessels that exist at the time of acute coronary occlusion. Diltiazem, however, has been demonstrated to increase collateral blood flow in animals in which chronic coronary occlusion has resulted in growth of moderately well-developed collateral vessels.
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