HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Hajime Otani Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ko, T. Articles by Inagaki, C. Search for Related Content PubMed PubMed Citation Articles by Ko, T. Articles by Inagaki, C.

J Thorac Cardiovasc Surg 1995;110:103-110
© 1995 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Role of sodium pump activity in warm induction of cardioplegia combined with reperfusion of oxygenated cardioplegic solution

Osaka, Japan

Received for publication May 26, 1994. Accepted for publication Nov. 15, 1994. Address for reprints: Tokumitsu Ko, MD, Department of Thoracic and Cardiovascular Surgery, Kansai Medical University, Fumizono-cho 1, Moriguchi City, Osaka 570, Japan.

Abstract

Na^+/K⁺adenosinetriphosphatase (sodium pump) may play a key role in the prevention of reperfusion injury caused by Ca²⁺overload. The present study was undertaken to investigate the role of sodium pump activity in warm induction of cardioplegia combined with reperfusion of oxygenated cardioplegic solution. Isolated and perfused rat hearts were subjected to 15 minutes of normothermic ischemia to produce a model of severely failing heart. The hearts then received myocardial preservation. Warm (37º C) or cold (4º C) oxygenated modified St. Thomas' Hospital solution was given for 5 minutes before and after 120 minutes of hypothermic cardioplegic arrest. Reduced myocardial pH during normothermic ischemia was adjusted toward the baseline level by administration of cold or warm oxygenated cardioplegic solution without a significant intergroup difference. Myocardial adenosine triphosphate levels decreased to less than 30% of the preischemic level during 15 minutes of normothermic ischemia, but were increased partly by induction of cold or warm oxygenated cardioplegia. Thus these metabolic indices failed to demonstrate the superiority of warm over cold oxygenated cardioplegia. Na^+/K⁺adenosinetriphosphatase activity in the membrane fraction was significantly stimulated by a cardioplegic dose of K⁺with maximum activity at 16 mEq/L. The enzyme activity of the heart measured after normothermic ischemia was reduced to less than 50% of that in the nonischemic heart. Although warm induction of cardioplegia and reperfusion of oxygenated cardioplegic solution maintained Na^+/K⁺adenosinetriphosphatase activity at the preischemic level, the enzyme activity was abolished at 4º C, which is the temperature used in cold cardioplegia. A subtoxic dose of ouabain (0.1 mmol/L) inhibited the enzyme activity of the heart undergoing this preservation regimen to approximately 50%. Warm induction and reperfusion of oxygenated cardioplegic solution showed significantly better recovery of isovolumic left ventricular function during reperfusion compared with that obtained with cold oxygenated cardioplegia. However, the beneficial effect of warm oxygenated cardioplegia on left ventricular function was compromised by inclusion of 0.1 mmol/L ouabain without a significant effect on myocardial metabolic parameters. These results suggest that stimulation of Na⁺pump activity may account for the beneficial effect of warm induction and reperfusion of oxygenated cardioplegic solution in the energy-depleted heart. (J THORACCARDIOVASCSURG1995;110:103-10)

This article has been cited by other articles:

				T. Sumida, H. Otani, S. Kyoi, T. Okada, H. Fujiwara, Y. Nakao, M. Kido, and H. Imamura Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580 Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2726 - H2734. [Abstract] [Full Text] [PDF]

				S. L. Hale and R. A. Kloner Myocardial temperature reduction attenuates necrosis after prolonged ischemia in rabbits Cardiovasc Res, December 1, 1998; 40(3): 502 - 507. [Abstract] [Full Text] [PDF]

				V. D. Schepkin, I. O. Choy, and T. F. Budinger Sodium alterations in isolated rat heart during cardioplegic arrest J Appl Physiol, December 1, 1996; 81(6): 2696 - 2702. [Abstract] [Full Text] [PDF]