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Improvement of a Closed Chest Porcine Myocardial Infarction Model by Standardization of Tissue and Blood Sampling Procedures
Published on: March 12, 2018
Endothelium-dependent coronary flow in ischemia reperfusion
P A Jorge1, M R Osaki, E de Almeida
1Department of Experimental Medicine, State University of Campinas, São Paulo, Brazil.
Insights
Myocardial infarction reperfusion impairs coronary endothelial function. Following ischemia-reperfusion, acetylcholine no longer increases coronary blood flow, indicating endothelial dysfunction in resistance coronary vessels.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function Research
Background:
- Ischemia-reperfusion injury is a significant complication following myocardial infarction.
- Endothelial cells play a crucial role in regulating coronary blood flow and vascular tone.
Purpose of the Study:
- To investigate the impact of ischemia-reperfusion on the endothelial cell function of coronary vessels.
- To assess changes in coronary blood flow regulation post-myocardial infarction.
Main Methods:
- Twelve adult male dogs underwent surgical instrumentation for hemodynamic monitoring.
- Coronary artery occlusion for 90 minutes followed by 20 minutes of reperfusion.
- Acetylcholine infusion to assess endothelial-dependent vasodilation before and after reperfusion.
Main Results:
- Acetylcholine significantly increased coronary flow by 155% pre-occlusion (p < 0.05).
- Post-reperfusion, acetylcholine failed to induce a significant increase in coronary flow.
- No significant changes in heart rate, aortic, or left ventricular pressures were observed during acetylcholine administration in the reperfusion period.
Conclusions:
- Reperfusion following myocardial infarction leads to endothelial dysfunction in coronary resistance vessels.
- This dysfunction prevents the normal vasodilatory response to acetylcholine, impacting coronary blood flow regulation.
Abstract:
The aim of the present report was to study the effect of ischemia-reperfusion on the endothelial cell function of coronary vessels. Twelve adult male dogs were instrumented for the measurement of aortic and left ventricular pressures, heart rate and coronary blood flow. The left anterior descending coronary artery was occluded for 90 minutes followed by 20 minutes of reperfusion. Acetylcholine was infused into the coronary artery at a rate of 15 micrograms/kg/min. Coronary flow, heart rate and aortic and left ventricular pressures were registered during the pre-occlusion period and after 20 minutes of reperfusion under basal conditions, as well as during acetylcholine administration. These same parameters were also measured during reactive hyperemia following vessel deocclusion. Acetylcholine produced a 155% increasing coronary flow during the pre-occlusion period (p < 0.05). In the reperfusion period, no statistically significant difference was observed between the flows in the presence and absence of this substance, nor were there any differences in the other cardiovascular parameters monitored. Triphenyltetrazolium staining confirmed myocardial infarction in all the hearts examined. The authors conclude that reperfusion following myocardial infarction prevents the increasing in coronary flow in response to acetylcholine as a result of endothelial dysfunction in the resistance coronary vessels.
