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J Thorac Cardiovasc Surg 2000;119:1093-1101
© 2000 The American Association for Thoracic Surgery

SURGERY FOR CONGENITAL HEART DISEASE

CONTROLLED POSTCARDIOPLEGIA REPERFUSION: MECHANISM FOR ATTENUATION OF REPERFUSION INJURY

From the Departments of Surgery,^a Pathology,^b and Medicine^c in the School of Medicine, and the Department of Biomedical Engineering^d in the School of Engineering, University of Alabama at Birmingham, Birmingham, Ala.

This work was performed with support from American Heart Association Grant-in-Aid No. 96006390 (W.L.H.) and National Institutes of Health grants HL 09493 (J.L.S.) and HL 28429 (R.E.I.).

Address for reprints: William L. Holman, MD, Department of Surgery, University of Alabama at Birmingham, Birmingham, AL 35294-0007 (E-mail: wholman{at}holman.cvsr.uab.edu ).

Objective: Controlled reperfusion and secondary cardioplegia are used to minimize reperfusion injury. The mechanisms for their benefit are incompletely defined and may include attenuation of myocyte sodium uptake.
Methods: Pigs had 1 hour of cardioplegic arrest followed by reperfusion with blood (control) or warm cardioplegic solution followed by blood (test). Reperfusion injury in the control and test groups was quantified by measuring changes of intramyocyte ion content with atomic absorption spectrometry and by analyzing electrophysiologic recovery from recordings of reperfusion arrhythmias.
Results: Control animals had an increase in intramyocyte sodium content at 5 minutes after initiating reperfusion (+20.2 µmol/g dry weight, P < .04), whereas the test group had an insignificant decrease (–14.0 µmol/g dry 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 nonfibrillating rhythm (4.5 ± 1.2 vs 1.1 ± 0.3, P < .03).
Conclusions: Controlled reperfusion eliminated the increase in intramyocyte sodium that was observed in the control group at 5 minutes after cardioplegic arrest. This improvement in myocyte ion homeostasis during postcardioplegia reperfusion was associated with fewer reperfusion arrhythmias. These data support the hypothesis that attenuation of myocyte sodium gain during postischemic reperfusion is a mechanism by which controlled reperfusion and secondary cardioplegia are beneficial.

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