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Updated: Aug 29, 2026

Evaluation of Coronary Flow Reserve After Myocardial Ischemia Reperfusion in Rats
Published on: June 28, 2019
Effects of statins on myocardial and coronary artery response to ischemia-reperfusion
Stephen V Rendig1, J David Symons, Ezra A Amsterdam
1Department of Internal Medicine, University of California, Davis 95616, USA.
Insights
Statins did not affect ventricular recovery after myocardial ischemia-reperfusion in pigs. However, statin treatment improved endothelium-dependent vasodilation in coronary arteries, potentially enhancing blood flow to ischemic regions.
Area of Science:
- Cardiovascular Science
- Pharmacology
Background:
- Statins are widely used to manage hypercholesterolemia.
- Their effects on myocardial ischemia-reperfusion injury and coronary vasodilation are not fully understood.
- Lipophilic statins may have different effects than hydrophilic statins due to cell permeability.
Purpose of the Study:
- To investigate if lipophilic statins impair ventricular recovery from ischemia-reperfusion compared to a hydrophilic statin.
- To determine if statins enhance endothelium-dependent vasodilation in coronary arteries from ischemic regions.
Main Methods:
- Farm pigs were treated with atorvastatin, pravastatin, simvastatin, or no statin for 3 weeks.
- Left ventricular function was assessed during ischemia-reperfusion.
- Coronary artery vasodilation and vasoconstriction were measured in isolated arteries from the ischemic region.
Main Results:
- No significant differences in ventricular function recovery were observed among statin-treated groups and controls.
- Bradykinin-induced vasorelaxation of coronary conductance vessels was greater in statin-treated pigs.
- Acetylcholine-induced vasoconstriction was reduced in simvastatin-treated animals.
Conclusions:
- Three weeks of atorvastatin, pravastatin, or simvastatin treatment did not alter ischemia-induced myocardial stunning in pigs.
- Statin treatment appears to enhance endothelium-dependent vasodilation in coronary conductance vessels but not resistance vessels.
- These findings suggest a potential benefit of statins in improving coronary blood flow to jeopardized myocardial regions.
Abstract:
This study tested the hypotheses that (i) lipophilic statins (atorvastatin and simvastatin) impair ventricular recovery from myocardial ischemia-reperfusion, owing to their greater myocyte permeability, compared with a hydrophilic statin (pravastatin), and (ii) statins enhance endothelium-dependent vasodilation of isolated coronary arteries from the ischemic region. Farm pigs consumed chow supplemented with atorvastatin (2.5 mg.kg(-1).d(-1); n=6), pravastatin (10 (n=3) or 20 (n=2) mg.kg(-1).d(-1)), simvastatin (5 mg.kg(-1).d(-1); n=6), or no statin (control; n=6) for 3 weeks. Animals were anesthetized and instrumented to measure regional (% segment shortening) and global (dP/dt max) left ventricular (LV) function during coronary artery occlusion (10 min) and reperfusion (30 min). Coronary resistance (i.d. = 119 +/- 3 microm) and conductance (i.d. = 487 +/- 11 microm) arteries were isolated from the ischemic region to measure receptor-dependent (acetylcholine (ACh)) and -independent (KCl) vasoconstriction, and endothelium-dependent (bradykinin (BK)) and -independent (sodium nitroprusside (SNP)) vasodilation. At 30 min reperfusion, neither percent recovery of regional ventricular function (atorvastatin, 24% +/- 15%; pravastatin, 36% +/- 13%; simvastatin, 29% +/- 13%; control, 36% +/- 13%) nor percent recovery of global LV cardiac function differed among groups. However, BK-induced vasorelaxation of coronary conductance vessels was greater (P<0.05) in statins versus controls, and ACh-induced vasoconstriction was less in simvastatin-treated animals, suggesting the potential for enhanced coronary arterial blood flow to the jeopardized region. In conclusion, our data suggest that ischemia-induced myocardial stunning is similar among pigs treated for 3 weeks with atorvastatin, pravastatin, or simvastatin, even though statin treatment appears to augment endothelium-dependent vasodilation of conductance, but not resistance, vessels subjected to ischemia-reperfusion.
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