Controlled postcardioplegia reperfusion: Mechanism for attenuation of reperfusion injury

Objective: Controlled reperfusion and secondary cardioplegia are used to mi nimize reperfusion injury. The mechanisms for their benefit are incompletel y defined and may include attenuation of myocyte sodium uptake. Methods: Pi gs had 1 hour of cardioplegic arrest followed by reperfusion with blood (co ntrol) or warm cardioplegic solution followed by blood (test). Reperfusion injury in the control and test groups was quantified by measuring changes o f intramyocyte ion content with atomic absorption spectrometry and by analy zing electrophysiologic recovery from recordings of reperfusion arrhythmias . Results: Control animals had an increase in intramyocyte sodium content a t 5 minutes after initiating reperfusion (+20.2 mu mol/g dry weight, P < .0 4), whereas the test group had an insignificant decrease (-14.0 mu mol/g dr y weight, P = .33). The first rhythm after initiating reperfusion was more often ventricular fibrillation in the control group (100% vs 50%, P < .02), and the control group required more defibrillations to establish a nonfibr illating rhythm (4.5 +/- 1.2 vs 1.1 +/- 0.3, P < .03). Conclusions: Control led reperfusion eliminated the increase in intramyocyte sodium that was obs erved in the control group at 5 minutes after cardioplegic arrest. This imp rovement in myocyte ion homeostasis during post-cardioplegia reperfusion wa s associated with fewer reperfusion arrhythmias. These data support the hyp othesis that attenuation of myocyte sodium gain during postischemic reperfu sion is a mechanism by which controlled reperfusion and secondary cardiople gia are beneficial.