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J Thorac Cardiovasc Surg 2003;126:1442-1448
© 2003 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

A new role for cardioplegic buffering: should acidosis or calcium accumulation be counteracted to salvage jeopardized hearts?

^a Department of Surgery, Divisions of Cardiothoracic Surgery, University of California, Los Angeles, School of Medicine, Los Angeles, Calif, USA,
^b Department of Nephrology, University of California, Los Angeles, School of Medicine, Los Angeles, Calif, USA,
^c Department of Physiology, University of California, Los Angeles, School of Medicine, Los Angeles, Calif, USA

Received for publication May 2, 2002; revisions received May 15, 2002; accepted for publication March 12, 2003.

^* Address for reprints: Gerald D. Buckberg, MD, Division of Cardiothoracic Surgery, 62-258 Center for the Health Sciences, Los Angeles, CA 90095-1701, USA
gbuckberg{at}mednet.ucla.edu

OBJECTIVES:: Thirty minutes of unprotected ischemia produced a jeopardized heart that was treated with a blood cardioplegic solution containing the natural erythrocyte and protein buffers. Cardioplegic pH was changed to 7.7 (buffered) or 7.2 (nonbuffered), and this was tested alone and after pretreatment with Na⁺-H⁺ exchange blockade (cariporide) to define their protective effects.

METHODS: Twenty-four Yorkshire-Duroc pigs (27-34.5 kg) underwent 30 minutes of normothermic global ischemia, followed by 30 minutes of aortic clamping during protection with buffered (n = 12) or nonbuffered (n = 12) glutamate-aspartate–enriched blood cardioplegic solution. Twelve hearts (6 buffered and 6 nonbuffered) were pretreated with intravenous cariporide (5 mg/kg) 15 minutes before ischemia.

RESULTS: Severe and comparable left ventricle dysfunction followed buffered or nonbuffered cardioplegia: Preload recruitable stroke work recovered to 56% ± 21% and 45% ± 20% of baseline levels; creatine kinase MB, conjugated dienes, and myeloperoxidase activity markedly increased; moderate myocardial edema occurred; and endothelin-1 increased 2-fold more than baseline values. Cariporide pretreatment caused a similar return of preload recruitable stroke work to 86% ± 9% and 90% ± 6% after buffered or nonbuffered cardioplegia (P < .05 vs nonpretreated groups), allowed only minor creatine kinase MB and conjugated diene changes, and reduced endothelin-1 release 3-fold compared with hearts without sodium-hydrogen exchange blockage.

CONCLUSIONS: The severe ischemia-reperfusion injury of 30 minutes of normothermic ischemia is not altered by an acidic or alkalotic pH cardioplegic solution. Correction of damage is achieved by adding Na⁺-H⁺ exchange blocker therapy before treatment with buffered and nonbuffered solutions; thus, sodium-hydrogen exchange inhibition plays a more vital role in recovery than pH management.

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				G. D. Buckberg Stroke and extra-cardiac perfusion: new vantage points in brain protection Eur. J. Cardiothorac. Surg., December 1, 2004; 26(Suppl_1): S62 - S67. [Abstract] [Full Text] [PDF]