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J Thorac Cardiovasc Surg 1996;112:1064-1072
© 1996 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

DIRECT EFFECTS OF OXYGENATED CRYSTALLOID OR BLOOD CARDIOPLEGIA ON ISOLATED MYOCYTE CONTRACTILE FUNCTION

Supported by National Institutes of Health Grant HL-45024, a Basic Research Grant from Pfizer Inc., a South Carolina American Heart Association Grant, and a Grant-in-Aid from the American Heart Association. F.G.S. is an Established Investigator of the American Heart Association.

Received for publication Jan. 22, 1996 Revisions requested March 13, 1996; revisions received April 26, 1996 Accepted for publication April 26, 1996. Address for reprints: Francis G. Spinale, MD, PhD, Division of Cardiothoracic Surgery, Medical University of South Carolina, 171 Ashley Ave., Charleston, SC 29425.

Abstract

The majority of myocardial protective techniques performed in the United States incorporate hypothermic, hyperkalemic blood or crystalloid cardioplegia. Oxygenated blood cardioplegia has not been compared with oxygenated crystalloid cardioplegia in an isolated myocyte model of hypothermic, hyperkalemic cardioplegic arrest in which direct measurements of contractile function and myocyte swelling can be made. Accordingly, isolated myocyte contractile function and myocyte profile surface area were examined after hypothermic arrest with oxygenated crystalloid or blood cardioplegia. Methods: Isolated left ventricular pig myocytes were randomly assigned to undergo cardioplegic arrest for 2 hours at 4° C. Either oxygenated crystalloid or blood cardioplegia was used. After 2 hours, myocytes were reperfused with standard cell medium at 37° C and contractile function was examined. A control group of myocytes was maintained in cell medium at 37° C for 2 hours. Myocyte velocity of shortening (micrometers per second) was examined at baseline and afterß-adrenergic stimulation (isoproterenol, 25 nmol/L). Velocity of shortening declined equally from baseline control values (65 ± 2µm/sec) in the groups subjected to oxygenated crystalloid cardioplegia and blood cardioplegia (37 ± 2µm/sec and 42 ± 1µm/sec, respectively; p < 0.05). Results: Althoughß-adrenergic stimulation caused a significant increase in velocity of shortening in all myocyte groups, the increase was less pronounced in myocytes subjected to crystalloid cardioplegia (157 ± 6µm/sec) and blood cardioplegia (159 ± 6µm/sec) than in normothermic control myocytes (205 ± 7µm/sec; p < 0.05). Myocyte profile surface area, an index of cell volume, was measured in all myocyte groups. Myocyte surface area increased equally after cardioplegic arrest and rewarming in both cardioplegia groups (crystalloid 4119 ± 53µm²; blood 3924 ± 48µm²); surface areas in both cardioplegia groups were significantly greater than in the normothermic control group (3158 ± 39µm², p < 0.05). Conclusion: Equivalent effects of oxygenated crystalloid and blood cardioplegia were observed with respect to myocyte contractile function, inotropic responsiveness, and intracellular volume regulatory processes. (J THORACCARDIOVASCSURG1996;112:1064-72)

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