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Ann Thorac Surg 1998;65:1235-1240
© 1998 The Society of Thoracic Surgeons

Glucose and Fatty Acid Oxidation by the In Situ Dog Heart During Experimental Cooling and Rewarming

Terje K. Steigen, MD, PhDa, Torkjel Tveita, MDa, Olav Hevrøy, MD, PhDb, Thomas V. Andreasena,b, Terje S. Larsen, PhDa

a Department of Medical Physiology, Institute of Medical Biology, University of Tromsø, Tromsø, Norway
b Department of Anesthesiology, Institute of Clinical Medicine, University of Tromsø, Tromsø, Norway

Accepted for publication November 21, 1997.

Address reprint requests to Dr Steigen, Department of Medical Physiology, Institute of Medical Biology, University of Tromsø, 9037 Tromsø, Norway

Background. Reduced myocardial function after hypothermia may be metabolic in origin, but the relationship between myocardial metabolism and the various components of hypothermia-mediated dysfunction has not been thoroughly investigated.

Methods. In the present study we measured myocardial uptake and oxidation of glucose and oleate in mongrel dogs undergoing cooling to 25°C followed by rewarming to 37°C, using radiolabeled substrates.

Results. Segment work index declined from 39.3 ± 5.1 to 15.1 ± 2.4 mm Hg in response to cooling from 37° to 25°C and did not recover completely on rewarming (27.2 ± 4.2 mm Hg, p < 0.05). Oleate uptake declined from 3,251 ± 619 to 1,043 ± 356 nmol · min-1 · 100 g-1 (p < 0.05) when the dogs were cooled from 37° to 25°C. Simultaneously, oxidation rate fell from 1,089 ± 158 to 354 ± 83 nmol · min-1 · 100 g-1 (p < 0.05). On rewarming, oleate uptake was restored to prehypothermic values, whereas its rate of oxidation remained depressed (480 ± 129 nmol · min-1 · 100 g-1; p < 0.05). Uptake and oxidation of glucose also declined significantly during cooling. However, both uptake and oxidation of glucose recovered fully on rewarming.

Conclusions. The results of the present study demonstrate a reduced capacity to oxidize fatty acids by the myocardium during rewarming after hypothermia.






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