Kanemoto Shinya, Matsubara Muneaki, Noma Mio, Leshnower Bradley G, Parish Landi M, Jackson Benjamin M, Hinmon Robin, Hamamoto Hirotsugu, Gorman Joseph H, Gorman Robert C
Harrison Department of Surgical Research, Glenolden Research Laboratory, University of Pennsylvania, Glenolden, Pennsylvania 19036, USA.
Ann Thorac Surg. 2009 Jan;87(1):157-63. doi: 10.1016/j.athoracsur.2008.08.012.
Hypothermia during ischemia has been shown to reduce myocardial reperfusion injury. We sought to establish the cardioprotective effect of very mild total-body hypothermia (<or= 2.5 degrees C) and to determine whether the application of hypothermia at different points during the ischemia-reperfusion period influenced the degree of myocardial salvage.
Rabbits were subjected to 30 minutes of myocardial ischemia followed by 3 hours of reperfusion. Twenty-five animals were maintained at normal temperature (39.5 degrees C) throughout the experiment (W-W-W group). All other animals were cooled to reduce left atrial temperature 2.0 degrees C to 2.5 degrees C. Eleven animals reached goal temperature before coronary occlusion (C-C-C group), in 14 animals cooling was initiated at coronary occlusion (W-C0-C group), in 8 animals cooling was initiated 15 minutes after coronary occlusion (W-C15-C group), in 5 animals cooling was initiated 25 minutes after coronary occlusion (W-C25-C group), and in 13 animals cooling was started concurrently with reperfusion (W-W-C group). Infarct size as a percentage of the risk area (I/AR) was determined by a double staining-planimetry technique.
Goal temperature was achieved before reperfusion in the C-C-C and W-C0-C groups but was not achieved until the reperfusion period in the other treatment groups. Infarct size was 59.0 +/- 1.2% in the W-W-W group and was reduced in all cooling groups (C-C-C = 30.4 +/- 4.9%; W-C0-C = 33.4 +/- 5.0%; W-C15-C = 42.4 +/- 1.4%; W-C25-C = 44.1 +/- 2.3%; W-W-C = 50.5 +/- 4.1%). The temperature at reperfusion correlated most strongly with infarct size (r = 0.72, p < 1 x 10(-12)).
Very mild hypothermia affords a significant cardioprotective effect. Temperature at the time of reperfusion most strongly correlates with the degree of myocardial salvage.
缺血期间的低温已被证明可减轻心肌再灌注损伤。我们试图确立极轻度全身低温（≤2.5℃）的心脏保护作用，并确定在缺血-再灌注期间不同时间点应用低温是否会影响心肌挽救的程度。
对兔子进行30分钟的心肌缺血，随后进行3小时的再灌注。25只动物在整个实验过程中维持正常体温（39.5℃）（W-W-W组）。所有其他动物被冷却以使左心房温度降低2.0℃至2.5℃。11只动物在冠状动脉闭塞前达到目标温度（C-C-C组），14只动物在冠状动脉闭塞时开始冷却（W-C0-C组），8只动物在冠状动脉闭塞后15分钟开始冷却（W-C15-C组），5只动物在冠状动脉闭塞后25分钟开始冷却（W-C25-C组），13只动物在再灌注时同时开始冷却（W-W-C组）。通过双染色-平面测量技术确定梗死面积占危险区域的百分比（I/AR）。
C-C-C组和W-C0-C组在再灌注前达到目标温度，但其他治疗组直到再灌注期才达到目标温度。W-W-W组的梗死面积为59.0±1.2%，所有冷却组的梗死面积均减小（C-C-C组 = 30.4±4.9%；W-C0-C组 = 33.4±5.0%；W-C15-C组 = 42.4±1.4%；W-C25-C组 = 44.1±2.3%；W-W-C组 = 50.5±4.1%）。再灌注时的温度与梗死面积相关性最强（r = 0.72，p < 1×10⁻¹²）。
极轻度低温具有显著的心脏保护作用。再灌注时的温度与心肌挽救程度相关性最强。
