Tveita T, Mortensen E, Hevrøy O, Refsum H, Ytrehus K
Department of Medical Physiology, University of Tromsø, Norway.
Anesth Analg. 1994 Aug;79(2):212-8. doi: 10.1213/00000539-199408000-00002.
Conflicting results have been reported as to the extent that cardiovascular function can be reestablished after rewarming from hypothermia. We measured hemodynamic function, myocardial metabolism and tissue water content in dogs core-cooled to 25 degrees C and later rewarmed. At 25 degrees C left ventricular (LV) systolic pressure (LVSP) was 54% +/- 4%, maximum rate of LV pressure rise (LV dP/dtmax) 44% +/- 5%, aortic pressure (AOP) 50% +/- 6%, heart rate (HR) 40% +/- 0%, cardiac output (CO) 37% +/- 5%, myocardial blood flow (MBF) 34% +/- 5%, and myocardial oxygen consumption (MVO2) 8% +/- 1%, compared to precooling. Stroke volume (SV) and LV end-diastolic pressure (LVEDP) were unchanged. As normothermia (37 degrees C) was reestablished, the depression of cardiac function and myocardial metabolism remained the same as that at 25 degrees C: LVSP 71% +/- 6%, LV dP/dtmax 73% +/- 7%, SV 60% +/- 9%, AOP 70% +/- 6%, CO 57% +/- 9%, MBF 53% +/- 8%, and MVO2 44% +/- 8% HR, in contrast, recovered to precooling values. The arterial concentrations of glucose and free fatty acids (FFA) did not change significantly during the experimental period, whereas an increase in lactate of nonmyocardial origin appeared after rewarming. Increased myocardial contents of creatine phosphate and water were found during both hypothermia and rewarming. The present study demonstrates a persistent depression of cardiac function after hypothermia and rewarming in spite of adequate energy stores. Thus, a direct influence on myocardial contractile function by the cooling and rewarming process is suggested.
关于低温复温后心血管功能能够恢复的程度，已有相互矛盾的报道。我们对核心体温降至25摄氏度后再复温的犬类进行了血流动力学功能、心肌代谢和组织含水量的测量。在25摄氏度时，与降温前相比，左心室（LV）收缩压（LVSP）为54%±4%，左心室压力最大上升速率（LV dP/dtmax）为44%±5%，主动脉压（AOP）为50%±6%，心率（HR）为40%±0%，心输出量（CO）为37%±5%，心肌血流量（MBF）为34%±5%，心肌耗氧量（MVO2）为8%±1%。每搏输出量（SV）和左心室舒张末期压力（LVEDP）未发生变化。当恢复至正常体温（37摄氏度）时，心脏功能和心肌代谢的抑制情况与25摄氏度时相同：LVSP为71%±6%，LV dP/dtmax为73%±7%，SV为60%±9%，AOP为70%±6%，CO为57%±9%，MBF为53%±8%，MVO2为44%±8%。相比之下，心率恢复到了降温前的值。实验期间，动脉血中葡萄糖和游离脂肪酸（FFA）的浓度没有显著变化，而复温后出现了非心肌来源的乳酸增加。在低温和复温过程中均发现心肌中磷酸肌酸和水的含量增加。本研究表明，尽管有充足的能量储备，但低温复温后心脏功能仍持续受到抑制。因此，提示降温及复温过程对心肌收缩功能有直接影响。
