Anesthetized dogs were cooled to a core body temperature of 26°C or maintained at a body temperature of 37°C during periods of 5 and 10 hours of LAD coronary artery occlusion. Subsequent macroscopic dehydrogenase enzyme mapping showed that ischemic injury was 25 per cent less after 5 hours of coronary occlusion and 20 per cent less after 10 hours of occlusion in hypothermic dogs than in normothermic controls. The heart rate and left ventricular minute work in hypothermic dogs decreased to roughly half the levels measured in normothermic animals, while left ventricular contractility was 10 to 40 per cent lower in hypothermic dogs than in normothermic dogs. However, cardiac index and left ventricular end-diastolic pressure were unchanged by whole body cooling. Thus, hypothermia appeared to diminish the oxygen requirements of the ischemic myocardium without reducing the performance of the heart as a pump. Hypothermia may be useful as a therapeutic adjunct to myocardial revascularization or pharmacologrc interventions.


This is the author accepted manuscript of Abendschein D.R., Tacker W.A., Babbs C.F., Protection of ischemic myocardium by whole-body hypothermia after coronary artery occlusion in dogs, American Heart Journal 96, 772-780, 1978. Copyright Elsevier, it is made available here CC-BY-NC-ND, and the version of record can be found at http://dx.doi.org/10.1016/0002-8703(78)90010-8.


acute myocardial infarction, India ink, myocardial protection, nitrobluetetrazolium

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