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为探讨八肽胆囊收缩素 (CCK 8)缓解内毒素休克时肺动脉高压的作用机制 ,应用离体血管环张力测定技术及扫描电镜方法 ,观察了CCK 8对肿瘤坏死因子α (TNF α)引起的肺动脉反应性及肺动脉内皮细胞超微结构变化的影响。结果显示 :离体肺动脉经TNF α (4 0 0 0U/ml)孵育 2h对苯肾上腺素 (PE)的收缩反应、对乙酰胆碱(ACh)及硝普钠 (SNP)的内皮依赖性及非内皮依赖性舒张反应均无明显影响。TNF α (4 0 0 0U/ml,孵育 7h或 14h)可降低离体肺动脉对ACh介导的内皮依赖性舒张反应 ;CCK 8(0 5 μg/ml)逆转了TNF α的上述作用。CCK 8(0 5μg/ml)本身对正常肺动脉舒缩反应无明显影响。扫描电镜显示 ,CCK 8(0 5 μg/ml)对TNF α (4 0 0 0U/ml,7h)损伤的肺动脉内皮细胞有保护作用。结果提示 ,CCK 8可逆转TNF α对内皮依赖性舒张反应的抑制作用 ,减轻内皮细胞结构损伤 ,这可能是CCK 8抗内毒素休克时肺动脉高压并具有细胞保护作用的机制之一。
To investigate the mechanism of cholecystokinin octapeptide (CCK 8) in relieving pulmonary hypertension induced by endotoxin shock, the effect of CCK 8 on tumor necrosis factor α (TNFα) induced by endotoxin shock was observed by means of in vitro vascular ring tension measurement and scanning electron microscopy Pulmonary arterial reactivity and ultrastructure changes of pulmonary artery endothelial cells. The results showed that the contraction of phenylephrine (PE), the endothelium-dependent and non-endothelium-dependent effects of acetylcholine (ACh) and sodium nitroprusside (SNP) in pulmonary arteries incubated with TNFα (4000U / ml) No significant effect of sexual relaxation response. TNFα (4 000 μU / ml, 7 h or 14 h incubation) decreased ACh-mediated endothelium-dependent vasodilation in isolated pulmonary arteries; CCK 8 (0 5 μg / ml) reversed the effects of TNFα. CCK 8 (0 5μg / ml) itself has no significant effect on the normal pulmonary artery contractile response. Scanning electron microscopy showed that CCK 8 (0 5 μg / ml) had a protective effect on pulmonary artery endothelial cells damaged by TNFα (400 000 U / ml, 7 h). The results suggest that CCK 8 can reverse the inhibitory effect of TNFα on endothelium-dependent vasorelaxation and reduce the structural damage of endothelial cells, which may be one of the mechanisms of CCK 8 against pulmonary hypertension and endocytosis during endotoxic shock.