Barner H B, Standeven J W, Jellinek M, Menz L J, Hahn J W
J Thorac Cardiovasc Surg. 1977 Jun;73(6):856-67.
We compared moderate (29 degrees C.) and profound (5 degrees C.) (ice chips) cardiac hypothermia for myocardial preservation during aortic cross-clamping for 30 or 60 minutes in a canine right heart bypass preparation. Ventricular function deteriorated significantly at 29 degrees C. but not at 5 degrees C. Maximum dp/dt declined only after 60 minutes of ischemia at 29 degrees C., and Vmax decreased after one hour at either temperature. Lactate and pyruvate washout were greater after 29 degrees C., and pyruvate production persisted after 60 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C., and total coronary flow remained elevated after 60 minutes of ischemia at 29 degrees C. Coronary flow distribution was not altered by hypothermia. Ultrastructural changes were primarily time dependent and not temperature dependent. Ice-induced subepicardial injury was not evident in the ultrastructure or by flow distribution. Sixty minutes of profound topical cardiac hypothermia is moderately well tolerated by the canine heart, but functional and structural alterations are evident.
在犬类右心旁路制备中,我们比较了中度(29摄氏度)和深度(5摄氏度)(冰屑)心脏低温对主动脉交叉钳夹30或60分钟期间心肌保护的作用。在29摄氏度时心室功能显著恶化,但在5摄氏度时未出现。最大dp/dt仅在29摄氏度缺血60分钟后下降,在任一温度下一小时后Vmax降低。29摄氏度后乳酸和丙酮酸清除更多,且在29摄氏度缺血60分钟后丙酮酸仍持续产生。29摄氏度缺血30分钟后反应性充血更明显。29摄氏度缺血30分钟后反应性充血更明显,且在29摄氏度缺血60分钟后冠状动脉总血流量仍升高。低温未改变冠状动脉血流分布。超微结构变化主要取决于时间而非温度。冰诱导的心外膜下损伤在超微结构或血流分布中不明显。犬心对60分钟的深度局部心脏低温耐受性中等,但功能和结构改变明显。