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Coronary autoregulation protects against harmful effects of commonly used cardioplegia delivery pressure
1Department of Surgery, University of Tromsø, Regionsykehuset i Tromsø, Norway.
Insights
Coronary vasodilation before cardioplegic solution infusion impairs heart protection. This leads to reduced coronary flow and impaired cardiac function during reperfusion, highlighting the importance of pre-infusion conditions.
Area of Science:
- Cardiology
- Cardiovascular Surgery
- Biomedical Engineering
Background:
- Hearts often experience ischemia and coronary vasodilation before cardioplegic solution administration.
- The impact of pre-infusion coronary vasodilation on cardioprotection remains incompletely understood.
Purpose of the Study:
- To investigate whether coronary vasodilation prior to cardiac arrest induction influences cardioprotection.
- To assess the effect of pre-infusion vasodilation on myocardial recovery after hypothermic ischemia.
Main Methods:
- Isolated buffer-perfused rat hearts were subjected to hypothermic ischemia and reperfusion.
- Coronary vasodilation was induced in one group using Papaverine before cardioplegic solution infusion.
- Cardiac function, coronary flow, and biochemical markers were assessed during ischemia and reperfusion.
Main Results:
- The vasodilation group exhibited increased coronary resistance during ischemia.
- During reperfusion, the vasodilation group showed significantly lower coronary flow, reduced left ventricle developed pressure, and elevated creatine kinase release.
- Biochemical analysis revealed lower adenosine-triphosphate and creatine phosphate levels, and a greater increase in dry/wet weight ratio in the vasodilation group.
Conclusions:
- Pre-infusion coronary vasodilation, even with a safe cardioplegic solution pressure, can impair myocardial protection.
- These findings suggest that managing coronary bed status before cardioplegia is crucial for optimizing cardioprotection.
Objective:
Hearts or parts of hearts are often ischemic prior to infusion of the cardioplegic solution and have a more or less dilated coronary bed. We made an investigation whether coronary dilation just prior to induction of cardiac arrest by aortic clamping and infusion of crystalloid cardioplegic solution would influence cardioprotection.
Methods:
Isolated buffer-perfused rat hearts (100 cm H2O pressure (= 73.5 mmHg), 37 degrees C) were used. After a stabilization period the perfusion of 8 rats (group 1) was stopped and the hearts arrested with 5 ml CS (100 cm H2O, 12 degrees C). Equal amounts of cardioplegic solution were then delivered every 20 minutes for the entire 3 1/2 hour hypothermic ischemic period. Following ischemia the hearts were reperfused for 60 minutes. In group 2 (n = 8) 1 ml 10(-2) mmol Papaverine was given into the aortic root just prior to the first cardioplegic solution infusion in order to induce coronary vasodilation. The procedure was identical in the two groups during ischemia and reperfusion.
Results:
During the ischemic period coronary resistance increased in group 2. During reperfusion group 2 had lower coronary flow (P = 0.001), left ventricle developed pressure (P = 0.002) and a higher creatine kinase release (P = 0.003) than group 1 hearts. Group 2 also had a lower adenosine-triphosphate (6.51 +/- 0.40 mumol.g-1 and 14.03 +/- 0.59 mumol.g-1, respectively, P = 0.011), creatine phosphate (24.70 +/- 1.02 mumol.g-1 and 36.50 +/- 1.31 mumol.g-1, respectively, P = 0.020) and a larger fall in dry/wet-weight ratio (1.7 +/- 0.4 and 0.8 +/- 0.5, respectively, P = 0.043).
Conclusions:
Vasodilation (i.e. ischemia) just prior to infusion of crystalloid cardioplegic solution may impair myocardial protection even when the cardioplegic solution is delivered at a relatively low and presumably safe pressure.