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为探讨调节肽CGRP在休克中的发病学意义,本工作在结扎大鼠盲肠加穿孔的败血症休克模型上,观察了CGRP的变化及外源性CGRP对败血症休克过程的影响。结果发现,败血症休克时,血浆中CGRP显著增加(14.3±4.0 vs 5.5±1.8 Pg/ml,P<0.01)。在休克早期、晚期运用CGRP治疗(5μg/kg CGRP ⅳ)都能明显改善动物的低血压状态(分别是14.8±0.8,15.5±0.9 vs休克组10.3±1.6kPa,P<0.05),减轻心肌组织病理损伤,减少血浆中酶(LDH,CD)的漏出。同时,也可抑制休克动物血浆中AGT-Ⅱ含量的增加,提高血浆6-kcto-PGF_1α/TXB_2的比值(早期:69.1±5.3,晚期:65.8±4.1 vs休克组51.0±4.7%,P<0.05)。结果提示,CGRP可能参与败血症休克的代偿调节,适当应用CGRP治疗败血症休克是有益的。
To investigate the pathogenesis of CGRP in shock, this study was to observe the changes of CGRP and the effect of exogenous CGRP on the process of septic shock in rats by ligating the cecal and perforation septic shock model in rats. The results showed that in septic shock, plasma CGRP increased significantly (14.3 ± 4.0 vs 5.5 ± 1.8 Pg / ml, P <0.01). In the early stage of shock, late application of CGRP (5μg / kg CGRP ⅳ) significantly improved the hypotensive state of animals (14.8 ± 0.8,15.5 ± 0.9 vs 10.3 ± 1.6kPa in shock group, P <0.05) Pathological damage, reduce the plasma enzyme (LDH, CD) leakage. At the same time, it also inhibited the increase of plasma AGT-Ⅱ level and increased the ratio of plasma 6-kcto-PGF_1α / TXB_2 (69.1 ± 5.3, 65.8 ± 4.1 vs 51.0 ± 4.7%, P <0.05 ). The results suggest that CGRP may be involved in the compensatory regulation of septic shock, appropriate treatment of sepsis with CGRP is beneficial.