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暴露于深度低温后心脏的完全恢复。

Complete recovery of the heart following exposure to profound hypothermia.

作者信息

Shragge B W, Digerness S B, Blackstone E H

出版信息

J Thorac Cardiovasc Surg. 1981 Mar;81(3):455-8.

PMID:7464207
Abstract

Cold injury has been suggested as a potential limitation to the use of temperatures below 10 degrees to 15 degrees C in clinical myocardial preservation. The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each heart was isolated and stabilized; then initial aortic flow, coronary flow, and heart rate were measured. The heart then was perfused in the Langendorf mode with oxygenated Krebs-Henseleit buffer for 20 minutes at 0.5 degree, 4 degrees, 10 degrees, 15 degrees, or 20 degrees C. After being rewarmed to 37 degrees C, the heart was returned to the working mode for final functional measurements. In a control group, the perfusion was kept at 37 degrees C. Recovery of function in hearts exposed to hypothermic perfusion was not significantly different from that observed in the hearts kept at 37 degrees C. When cold exposure time to 0.5 degree C perfusion was extended to 2 hours, heart function still returned to the same level as that of control hearts maintained at 37 degrees C, and adenosine triphosphate (ATP) and glycogen levels were higher than those in the control group. Thus, under these conditions, cold exposure per se, even for 2 hours at temperatures near 0 degree C, has no deleterious effect upon myocardial function and energy metabolism.

摘要

冷损伤被认为是临床心肌保存中使用低于10摄氏度至15摄氏度温度的一个潜在限制因素。在工作的大鼠心脏标本中研究了深度低温对心肌功能和能量代谢的单独影响。将每颗心脏分离并稳定下来;然后测量初始主动脉流量、冠状动脉流量和心率。然后将心脏以Langendorf模式在0.5摄氏度、4摄氏度、10摄氏度、15摄氏度或20摄氏度下用含氧的Krebs-Henseleit缓冲液灌注20分钟。复温至37摄氏度后,将心脏恢复到工作模式进行最终功能测量。在一个对照组中,灌注保持在37摄氏度。暴露于低温灌注的心脏的功能恢复与保持在37摄氏度的心脏中观察到的情况没有显著差异。当在0.5摄氏度灌注下的冷暴露时间延长至2小时时,心脏功能仍恢复到与维持在37摄氏度的对照心脏相同的水平,并且三磷酸腺苷(ATP)和糖原水平高于对照组。因此,在这些条件下,冷暴露本身,即使在接近0摄氏度的温度下暴露2小时,对心肌功能和能量代谢也没有有害影响。

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