H Ao1, J K Moon, M Tashiro, H Terasaki. 1. Department of Anesthesiology, Kumamoto University School of Medicine, Honjo, 860-8556, Kumamoto, Japan. aohushan@hotmail.com
Abstract
UNLABELLED: Mild to moderate hypothermia (33-32 degrees C) is recognized as beneficial for brain protection after brain trauma. However, there are few experimental reports on hemostatic changes during prolonged hypothermia. We compared hemostatic changes during 72 h of mild to moderate hypothermia with data in normothermic dogs. METHOD: Mongolian dogs in a hypothermic group (N=7, 33 degrees C core temperature) and normothermic group (N=6, 37.5 degrees C core temperature) were anesthetized and instrumented to control temperatures and record hemodynamic changes continuously. Hypothermia or normothermia was maintained for 72 h. Platelet count, platelet aggregation, and thromboelastograms (TEG) were measured in each group. RESULTS: Heart rate, blood pressure, pulmonary pressure and blood gas were not significantly different between the two groups. Platelet counts, compared to baseline values, were significantly decreased in both groups (P<0.01). Platelet aggregation was significantly decreased in the hypothermic group after 24 h (P<0.04). CONCLUSION: Long-term hypothermia induced platelet dysfunction, leading to decreased platelet aggregation and prolonged coagulation time (R and K times of TEG).
UNLABELLED: Mild to moderate hypothermia (33-32 degrees C) is recognized as beneficial for brain protection after brain trauma. However, there are few experimental reports on hemostatic changes during prolonged hypothermia. We compared hemostatic changes during 72 h of mild to moderate hypothermia with data in normothermic dogs. METHOD: Mongolian dogs in a hypothermic group (N=7, 33 degrees C core temperature) and normothermic group (N=6, 37.5 degrees C core temperature) were anesthetized and instrumented to control temperatures and record hemodynamic changes continuously. Hypothermia or normothermia was maintained for 72 h. Platelet count, platelet aggregation, and thromboelastograms (TEG) were measured in each group. RESULTS: Heart rate, blood pressure, pulmonary pressure and blood gas were not significantly different between the two groups. Platelet counts, compared to baseline values, were significantly decreased in both groups (P<0.01). Platelet aggregation was significantly decreased in the hypothermic group after 24 h (P<0.04). CONCLUSION: Long-term hypothermia induced platelet dysfunction, leading to decreased platelet aggregation and prolonged coagulation time (R and K times of TEG).
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