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Ward V. Houck
James L. Zellner
Fred A. Crawford, Jr
Francis G. Spinale
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Ann Thorac Surg 1998;65:1279-1283
© 1998 The Society of Thoracic Surgeons

Normothermic Versus Hypothermic Hyperkalemic Cardioplegia: Effects on Myocyte Contractility

Ward V. Houck, MDa, Scott B. Kribbs, BSa, James L. Zellner, MDa, Melissa A. Doscher, BSa, Jignesh D. Joshi, BSa, Fred A. Crawford, Jr, MDa, Francis G. Spinale, MD, PhDa

a Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, South Carolina, USA

Accepted for publication December 11, 1997.

Address reprint requests to Dr Spinale, Cardiothoracic Surgery, Medical University of South Carolina, Rm 418 CSB, Charleston, SC 29425

Background. This study was designed to determine the effects of prolonged hyperkalemic cardioplegic arrest under normothermic or hypothermic conditions with respect to left ventricular myocyte contractile performance and ß-adrenergic responsiveness.

Methods. Isolated left ventricular porcine myocytes were randomly assigned to one of three groups: (group 1) normothermic control, (group 2) hypothermic cardioplegic arrest, or (group 3) normothermic cardioplegic arrest. Myocyte contractility was evaluated by high-speed video microscopy at baseline and after ß-adrenergic stimulation with isoproterenol (25 nmol/L).

Results. Myocyte velocity of shortening was decreased after both hypothermic and normothermic cardioplegic arrest (68 ± 2 and 69 ± 2 µm/s, respectively) compared with normothermic control values (96 ± 2 µm/s; p < 0.05). This relative reduction in baseline contractile function was equivalent in both cardioplegia groups (p = 0.5356). With ß-adrenergic stimulation, myocyte velocity of shortening was 186 ± 4 µm/s in the hypothermic and 176 ± 3 µm/s in the normothermic cardioplegia groups (p = 0.0563). However, myocyte contractility with ß-adrenergic stimulation was reduced in both cardioplegia groups compared with normothermic controls (205 ± 4 µm/s; p < 0.05, respectively).

Conclusions. Hyperkalemic cardioplegic arrest under either normothermic or hypothermic conditions resulted in an equivalent reduction in baseline myocyte contractile function with reperfusion/rewarming. Hypothermic cardioplegic arrest may have provided mild protective effects on ß-adrenergic responsiveness. Nevertheless, these results suggest that an important contributory factor for diminished myocyte contractility after simulated cardioplegic arrest was prolonged exposure to a hyperkalemic environment.






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