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Effect of intracoronary captopril on coronary blood flow and regional myocardial function in dogs
Insights
This study investigated the cardiac effects of captopril, an angiotensin-converting enzyme inhibitor. Intracoronary captopril did not directly affect cardiac function, suggesting no direct cardiac impact.
Area of Science:
- Cardiovascular physiology
- Pharmacology
Background:
- Angiotensin-converting enzyme (ACE) inhibitors are widely used in cardiovascular medicine.
- Understanding the direct cardiac effects of ACE inhibitors is crucial for clinical application.
Purpose of the Study:
- To evaluate the direct cardiac effects of intracoronary captopril.
- To assess captopril's influence on coronary blood flow and regional myocardial function.
Main Methods:
- Anesthetized open-chest dog model.
- Continuous measurement of left circumflex coronary artery (LCX) blood flow, left ventricular pressure (LVP), aortic pressure (AoP), and myocardial segment length.
- Administration of intravenous and intracoronary captopril, angiotensin I, and bradykinin.
Main Results:
- Intravenous captopril reduced AoP, increased myocardial shortening, and decreased coronary vascular resistance.
- Intracoronary captopril attenuated angiotensin-induced LCX flow reduction and augmented bradykinin-induced LCX flow increase.
- Intracoronary captopril infusion did not alter hemodynamic variables or myocardial shortening.
Conclusions:
- Captopril administered intravenously exhibits systemic cardiovascular effects.
- Direct intracoronary administration of captopril does not appear to have a direct cardiac effect on hemodynamics or myocardial function.
- Captopril modifies vascular responses to angiotensin I and bradykinin within the coronary circulation.
Abstract:
To evaluate the cardiac effect of an inhibitor of angiotensin-converting enzyme, the effect of intracoronary (i.c.) captopril on coronary blood flow and regional myocardial function was examined in the anesthetized open-chest dog. Blood flow of the left circumflex coronary artery (LCX), left ventricular pressure (LVP), aortic pressure (AoP) and regional myocardial segment length were measured continuously. Captopril i.v. (0.3 mg/kg) produced an immediate reduction in AoP and an increase in percent shortening of myocardial segments followed by a decrease in coronary vascular resistance and increases in heart rate and LVdP/dt. Reductions in LCX flow induced by i.c. angiotensin were attenuated and i.c. bradykinin-induced increases in LCX flow were augmented after captopril. On the contrary, i.c. infusion of captopril (0.01 mg/min) into the LCX caused no change in hemodynamic variables and myocardial shortening although responses to angiotensin I and bradykinin were markedly modified. These results suggest that captopril may have no direct cardiac effect.