EXPERIMENTAL HYPOTHERMIA AND REWARMING - CHANGES IN MECHANICAL FUNCTION AND METABOLISM OF RAT HEARTS

Rewarming from accidental hypothermia is associated with fatal circula tory derangements. To investigate potential pathophysiological mechani sms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a sign ificant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum r ate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remain ed unchanged. After rewarming, heart rate returned to control value, w hereas LV systolic pressure, cardiac output, and stroke volume all rem ained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1,643 mmHg/s. The posthypothermic myocardi al lactate content was significantly increased (to 13.3 +/- 3.2 nmol/m g from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen rem ained significantly lowered. Creatine phosphate or energy charge did n ot change significantly during the experiment. The finding of deterior ated myocardial mechanical function and a shift in energy metabolism s hows that the heart could be an important target during hypothermia an d rewarming in vivo, thus contributing to the development of a posthyp othermic circulatory collapse.