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Captopril in cardioplegia and reperfusion: protective effects on the ischemic heart
J Gurevitch1, D Pevni, I Frolkis
1Department of Thoracic and Cardiovascular Surgery, Elias Sourasky-Tel-Aviv Medical Center, Tel-Aviv University, Israel.
Insights
Captopril protects isolated rat hearts from ischemia and reperfusion injury. Administering captopril during cardioplegia and reperfusion significantly improves heart function and reduces damage.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Myocardial Ischemia
Background:
- Long-term captopril use improves survival post-myocardial infarction.
- Limited data exists on immediate captopril effects during global ischemia and reperfusion.
Purpose of the Study:
- Investigate captopril's direct impact on reperfused myocardium.
- Assess captopril's effects when given during cardioplegia or after ischemia.
Main Methods:
- Isolated rat hearts subjected to warm cardioplegic arrest.
- Global ischemia (1 hour) followed by 30 minutes of reperfusion.
- Modified Langendorff model used for functional assessment.
Main Results:
- Captopril improved hemodynamic performance, including higher pressure and pressure-time integral.
- Enhanced coronary flow and oxygen consumption observed with captopril treatment.
- Combined cardioplegia and reperfusion captopril administration yielded superior recovery and reduced creatine kinase levels.
Conclusions:
- Captopril demonstrates a protective and additive effect on ischemic and reperfused rat hearts.
- Improved hemodynamic function, increased coronary flow, and reduced myocardial damage were noted.
- Captopril is beneficial when administered both in cardioplegia and during reperfusion.
Background:
Previous studies have shown that long-term treatment with the angiotensin-converting enzyme inhibitor captopril attenuates left ventricular dilatation and improves survival after extensive myocardial infarction. However, there is only sparse evidence of the immediate effects of the drug on hearts undergoing global ischemia and reperfusion. The purpose of this study was to investigate the direct effect of captopril, given in cardioplegia or after ischemia, on the functional recovery of the reperfused myocardium.
Methods:
Isolated rat hearts undergoing warm cardioplegic arrest followed by 1 hour of global ischemia and 30 minutes of reperfusion were studied using the modified Langendorff model.
Results:
After ischemia, hearts receiving captopril (360 mumol/L) either in the cardioplegic solution (n = 9) or during reperfusion (n = 9) developed higher pressure (p < 0.001), greater first derivative of the rise in left ventricular pressure (p < 0.01 and p < 0.001, respectively), greater first derivative of the fall in left ventricular pressure (p < 0.001 and p < 0.002), higher pressure-time integral (p < 0.001), greater coronary flow (p < 0.001), and higher oxygen consumption values (p < 0.001 and p < 0.003) compared with the control group (n = 9). Hearts receiving captopril both in the cardioplegia and during reperfusion (n = 9) had the best recovery of all three groups and lower levels of creatine kinase (47.8 +/- 5.9 U/L versus 73.3 +/- 5.6 U/L; p < 0.01) compared with the control group.
Conclusions:
Captopril given in cardioplegia and in reperfusion has a favorable, protective, and additive effect on the recovery of isolated rat hearts undergoing global ischemia and reperfusion; hemodynamic performance improves, coronary flow and oxygen consumption increase, and myocardial damage decreases.