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目的 探讨降钙素基因相关肽 (CGRP)在临床肝脏缺血预处理中的保护作用。方法 随机将 40例住院患者分组 ,1缺血预处理组 (2 2例 ) :在持续肝门阻断前先给予一个 5分钟缺血和 5分钟再灌注 ;2常规手术组 (18例 ) :按改良Pringle法常规持续阻断肝门。用放免法观察缺血预处理组和常规组持续肝门阻断前后血清 CGRP水平变化。结果 术前预处理组 CGRP值为 (2 7.41± 8.2 4) pg/ ml,常规组 (2 6 .44± 5 .2 6 ) pg/ ml,两组 CGRP值相近 (P>0 .0 5 ) ;术后预处理组 (48.19±17.98) pg/ m l,常规组 (35 .0 9± 10 .89) pg/ m l,两组均升高 (P<0 .0 1) ,但预处理组升高值与常规组比有极显著差异 (P<0 .0 1)。结论 缺血再灌注可诱发肝脏产生内源性 CGRP,缺血预处理明显增强这一作用 ,减轻了肝脏缺血再灌注损伤。
Objective To investigate the protective effect of calcitonin gene related peptide (CGRP) on clinical liver ischemic preconditioning. Methods Forty inpatients were randomly divided into two groups: one group with ischemic preconditioning (n = 22): one 5-minute ischemia and 5-minute reperfusion after sustained hepatic portal vein occlusion; and two routine operation groups (n = 18) According to the modified Pringle routine blocking the hilar. The level of serum CGRP in the ischemic preconditioning group and the routine group were observed by radioimmunotherapy. Results The preoperative CGRP values were (2 7.41 ± 8.2 4) pg / ml in the pretreatment group and 26.64 ± 5.26 pg / ml in the conventional group (P 0. 05) ; Pretreatment group (48.19 ± 17.98) pg / ml, conventional group (35.0 ± 10.89) pg / ml, both groups were increased (P <0.01) There was a significant difference between high value and conventional group (P <0.01). Conclusion Ischemia / reperfusion can induce endogenous CGRP production in the liver, and preconditioning with ischemic preconditioning can significantly enhance this effect and relieve liver ischemia-reperfusion injury.