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J Thorac Cardiovasc Surg 1994;107:233-241
© 1994 Mosby, Inc.


CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Effects of fatty acids on myocardial calcium control during hypothermic perfusion

Terje K. Steigen, MD, Ellen Aasum, MS, Truls Myrmel, MD, PhDa, Terje S. Larsen, PhD


Tromsø, Norway

Supported by The Norwegian Council on Cardiovascular Diseases, the Norwegian Research Council for Science and the Humanities (the "Cold Climate Program"), and The Laerdal Foundation for Acute Medicine.

Received for publication Jan. 13, 1993. Accepted for publication April 12, 1993. Address for reprints: Terje K. Steigen, MD, Department of Medical Physiology, Institute of Medical Biology, University of Tromsø, 9037 Tromsø, Norway.

Abstract

Although hypothermia is regarded as providing protection of the myocardium during cardiac operations, rapid cooling of the myocardium in the nonarrested state may have detrimental effects on the function of the myocardial cell membrane as a permeability barrier. We therefore measured total cellular calcium in isolated working rat hearts, receiving either glucose (11.1 mmol/L) or glucose plus palmitate (1.2 mmol/L), before, during, and after a 40-minute hypothermic arrest (10° C, Langendorff perfusion). In both groups a rise in total cellular calcium, measured by45Ca2+ technique, was observed during hypothermia, followed by a decline on rewarming. However, the rise in total cellular calcium during hypothermia was significantly (p < 0.05) higher in hearts perfused with palmitate (from 1.0 ± 0.2 to 3.5 ± 0.2 nmol/mg dry weight) compared with that in glucose-perfused hearts (from 1.1 ± 0.13 to 2.6 ± 0.2 nmol/mg dry weight). Palmitate-perfused, but not glucose-perfused, hearts showed arrhythmias and delayed pressure development 1 to 2 minutes after rewarming. In addition cardiac output of these hearts was significantly lower (p < 0.025) than that of glucose-perfused hearts 5 to 10 minutes after rewarming. These data show that hypothermia per se causes a net calcium uptake in isolated rat hearts and that this effect is aggravated by high concentrations of fatty acids. Thus the impaired recovery of myocardial function in palmitate-perfused hearts can possibly be related to a distorted calcium handling. (J THORAC CARDIOVASC SURG 1994;107:233-41)




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