Author + information
- Received April 15, 1987
- Revision received July 23, 1987
- Accepted August 11, 1987
- Published online January 1, 1988.
- Michael R Courtois, MA,
- Peter B Kurnik, MS, MD, FACC and
- Philip A Ludbrook, MB, BS, FACC∗
- ↵∗Address for reprints: Philip A. Ludbrook, MB, BS, Washington University School of Medicine, Cardiovascular Division, 660 South Euclid, Box 8086, St. Louis, Missouri 63110.
Effects of moderate spontaneous hypothermia on left ventricular systolic and diastolic function during acute myocardial infarction were documented in 17 anesthetized dogs with micromanometric pressure and ventriculographic dimension recordings acquired at baseline and at 1 and 3 h after coronary occlusion. In Group 1 (n = 5), core temperature was allowed to decline spontaneously. In Groups 2 (n = 6) and 3 (n = 6), core temperature was maintained at normothermic levels. Hypothermia impaired isovolumic relaxation markedly despite its lack of effect on ventricular volumes or ejection fraction. At 32.3 °C, τ1/2, defined as the time needed for the left ventricular pressure at the time of peak negative rate of change of left ventricular pressure (dPdt) to fall by 50%, was increased by 129% 3 h after occlusion. In addition, at this temperature significant changes were found in heart rate, cardiac output, minute work, peak positive and peak negative dPdt, systolic ejection time, mean velocity of circumferential fiber shortening, mean aortic pressure and end-diastolic pressure.
Thus, hypothermia evolving under conditions of general anesthesia profoundly alters left ventricular function in the setting of acute myocardial infarction, a phenomenon that requires consideration and control in studies of myocardial ischemia and left ventricular function in experimental animals.
☆ This study was supported in part by National Heart, Lung, and Blood Institute Grant R01 HL25430 and SCOR in Ischemia Heart Disease, Grant HL17646, National Institutes of Health, Bethesda, Maryland. It was presented in part at The American Federation for Clinical Research National Meeting, May 4, 1986. Washington, D C.
- Received April 15, 1987.
- Revision received July 23, 1987.
- Accepted August 11, 1987.