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八肽胆囊收缩素对脂多糖诱导离体兔肺动脉反应性变化的影响 |
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谷振勇 凌亦凌 孟爱宏 丛 斌 黄善生
摘 要 目的与方法：为探讨胆囊收缩素(CCK)缓解内毒素休克时肺动脉压增高的作用机制，应用离体血管环技术观察CCK对内毒素主要成分脂多糖(LPS)诱导兔肺动脉反应性变化的影响。结果：LPS(4 μg/mL, 2h)引起离体肺动脉对α受体激动剂苯肾上腺素(PE)的收缩反应增强，降低对乙酰胆碱(ACh)介导的内皮依赖性舒张反应；CCK-8(0.1 μg/mL和0.5 μg/mL)逆转了LPS的上述作用；CCK-8( 0.5 μg/mL, 2h)本身对正常肺动脉舒缩反应无明显影响。结论：CCK通过保护肺内皮细胞、增强肺动脉内皮依赖性舒张反应而拮抗收缩反应，可能是发挥抗肺动脉压增高的机制之一。
主题词 缩胆囊素；肺动脉；脂多糖类；兔
Effects of cholecystokinin octapeptide on the response of
rabbit pulomonary artery induced by LPS in vitro
GU Zhen-Yong, LING Yi-Ling, MENG Ai-Hong, CONG Bin, HUANG Shan-Sheng
Department of Pathophysiology, Hebei Medical University, Shijiazhuang(050017)
Abstract AIM and METHODS：To elucidate the mechanism of cholecystokinin (CCK) for attenuation of pulmonary hypertension in the early stage of endotoxin shock in vitro, effects of CCK-8, an important functional fragment of endogenous CCK, on the responses of rabbit pulmonary artery induced by lipopolysaccharides (LPS) in vitro were observed with isolated artery ring technique. RESULTS：The exposure of pulmonary artery to LPS (4μg/mL, 2h) 1ed to enhancement of its contractile response to α-adrenoceptor agonist phenylephrine (PE) but reduction of its relaxation response to acetylcholine, an endothelium-dependent vasodilator, both of which were reversed by the concomitant exposure to CCK-8(0.1 μg/mL and 0.5 μg/mL), whereas incubation of pulmonary artery with CCK-8 (0.5 μg/mL) had no effect on the responses. CONCLUSION：CCK can protect pulmonary artery endothelia against detrimental effects by LPS, which may be one of mechanisms underlying anti-pulmonary hypertension of CCK.
MeSH Cholecystokinin; Pulmonary artery; Lipopolysaccharides; Rabbits
内毒素休克是一种危重病征，肺动脉压增高而平均动脉压降低是其发病早期的特征性病理变化。研究显示，肺动脉压增高的程度及其维持的时间是休克并发急性呼吸窘迫综合征，导致休克难治的重要因素［1］。探索内源性抗休克物质及其作用机制一直就是研究休克的热点课题。研究表明，胆囊收缩素(cholecystokinin,CCK)具有抗休克的作用［2，3］，并可防止内毒素主要成分脂多糖(LPS)诱导的大鼠肺动脉压增高［4］。然而，CCK对[1] [2] [3] 下一页
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