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延迟预处理保护在去神经支配骨骼肌的微循环中很明显。

Late-preconditioning protection is evident in the microcirculation of denervated skeletal muscle.

作者信息

Wang W Z, Tsai T M, Anderson G L

机构信息

Center for Applied Microcirculatory Research, University of Louisville, and Christine M. Kleinert Institute for Hand and Micro Surgery, Kentucky 40292, USA.

出版信息

J Orthop Res. 1999 Jul;17(4):571-7. doi: 10.1002/jor.1100170416.

DOI:10.1002/jor.1100170416
PMID:10459764
Abstract

We investigated whether ischemic preconditioning induces microvascular protection in skeletal muscle at the late phase (after 24 hours) when the same muscles are subjected to prolonged warm global ischemia. The cremaster muscle of the male Sprague-Dawley rat underwent vascular isolation and was subjected to 4 hours of ischemia and 60 minutes of reperfusion. Early preconditioning consisted of 45 minutes of ischemia followed by 15 minutes of reperfusion before prolonged ischemia/reperfusion; late preconditioning also consisted of 45 minutes of ischemia but was done 24 hours (24-hour period of reperfusion) before the prolonged ischemia/reperfusion. Arteriole diameters and capillary perfusion were measured with use of intravital microscopy. Four groups were compared: rats that underwent early preconditioning, their controls, rats that underwent late preconditioning, and their controls. Early and late preconditioning significantly attenuated vasospasm and capillary no-reflow compared with the controls for each. Average arteriole diameter was significantly larger in the rats that underwent late preconditioning than in any other rats; it was also significantly larger in the controls for late preconditioning than in those for early preconditioning. We introduce a model of the rat cremaster muscle that has been isolated from its vascular supply as a useful preparation to study the effects of late preconditioning on microcirculation in skeletal muscle. Late preconditioning provided better microvascular protection than did early preconditioning. The mechanism for this preconditioning protection is being investigated because it should provide a means for therapeutic intervention.

摘要

我们研究了在同一肌肉遭受长时间温暖性全身缺血的晚期阶段(24小时后),缺血预处理是否能诱导骨骼肌微血管保护。雄性Sprague-Dawley大鼠的提睾肌进行血管分离,然后经历4小时缺血和60分钟再灌注。早期预处理包括在长时间缺血/再灌注之前进行45分钟缺血,接着15分钟再灌注;晚期预处理同样包括45分钟缺血,但在长时间缺血/再灌注前24小时(24小时再灌注期)进行。使用活体显微镜测量小动脉直径和毛细血管灌注。比较了四组:接受早期预处理的大鼠及其对照、接受晚期预处理的大鼠及其对照。与各自的对照组相比,早期和晚期预处理均显著减轻了血管痉挛和毛细血管无复流。接受晚期预处理的大鼠的平均小动脉直径显著大于其他任何一组大鼠;晚期预处理组的对照大鼠的平均小动脉直径也显著大于早期预处理组的对照大鼠。我们介绍了一种从其血管供应中分离出来的大鼠提睾肌模型,作为研究晚期预处理对骨骼肌微循环影响的有用制剂。晚期预处理比早期预处理提供了更好的微血管保护。目前正在研究这种预处理保护的机制,因为它应为治疗干预提供一种手段。

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