Related Experiment Video
Updated: Aug 15, 2026
Evaluation of Coronary Flow Reserve After Myocardial Ischemia Reperfusion in Rats
Published on: June 28, 2019
Coronary vasoconstriction in experimental myocardial ischemia
Insights
Myocardial ischemia activates the renin-angiotensin system, causing coronary constriction, not maximal dilation. This study shows captopril benefits experimental myocardial ischemia by acting as a coronary vasodilator.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Pharmacology
Background:
- Myocardial ischemia is often assumed to cause maximal coronary vasodilation.
- The role of the renin-angiotensin system in regulating coronary tone during ischemia is not fully understood.
Purpose of the Study:
- To investigate the coexistence of coronary arteriolar constriction mediated by the renin-angiotensin system and myocardial ischemia.
- To evaluate the therapeutic potential of ACE inhibitors in experimental myocardial ischemia.
Main Methods:
- Coronary stenosis was simulated by perfusing the left anterior descending coronary artery at varying pressures.
- Myocardial ischemia was identified by lactate production.
- Effects of adenosine, indomethacin, saralasin, and captopril on coronary conductance and infarct size were assessed.
Main Results:
- Low coronary pressure induced myocardial ischemia with coronary constriction, not maximal dilation.
- Plasma renin activity increased during ischemia.
- Saralasin and captopril demonstrated coronary vasodilator effects.
- Captopril reduced infarct size, improved flow, and preserved function during ischemia.
Conclusions:
- Myocardial ischemia does not lead to maximal coronary vasodilation.
- The renin-angiotensin system is activated during ischemia and contributes to coronary constriction.
- Captopril exhibits beneficial effects in experimental myocardial ischemia, suggesting a therapeutic role for ACE inhibitors.
Abstract:
The possibility of a coexistence of coronary arteriolar constriction mediated by the renin-angiotensin system and myocardial ischemia was evaluated. Left anterior descending coronary artery was cannulated and perfused at normal (mean aortic), intermediate (50 mm Hg), and low (30-40 mm Hg) pressure in analogy to a progressive coronary stenosis. Lactate production was present at low coronary pressure indicating myocardial ischemia. In control animals (n = 18), mean coronary conductance was higher (p less than 0.005) at intermediate than at high coronary pressure consistent with autoregulation at coronary flow. Coronary conductance was lower (p less than 0.05) at low than at intermediate coronary pressure, indicating coronary constriction during myocardial ischemia. Adenosine (20 micrograms/kg per min i.c., n = 6) resulted in higher coronary conductance, suggesting coronary vasodilator reserve even at low coronary pressure. Indomethacin (5 mg/kg i.v., n = 12) resulted in low coronary conductance; however, the increase at intermediate (autoregulation) and the decrease (constriction) at low pressure was maintained. Plasma renin activity increased, and saralasin (0.1 microgram/kg per min i.c.) and captopril (0.25 mg/kg i.v.) acted as coronary vasodilators in various models of myocardial ischemia. Captopril limited myocardial infarct size at 6 hours of coronary occlusion, diminished flow repayment and prevented lactate production after 30 s of coronary occlusion, and abolished the deterioration of myocardial function during myocardial ischemia induced by coronary hypoperfusion and atrial pacing. Thus, myocardial ischemia does not generally represent a state of maximal coronary dilatation. The renin-angiotensin system is activated by myocardial ischemia and may exert a coronary constrictive tone. Captopril was beneficial in experimental myocardial ischemia.
