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（４μｇ／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（０１μｇ／ｍＬ和０５μｇ／ｍＬ）逆转了ＬＰＳ的上述作用；ＣＣＫ－８（０５μｇ／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。
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.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第6期484-487,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
关键词
肺动脉
脂多糖
兔
内毒素休克
胆囊收缩素
Cholecystokinin
Pulmonary artery
Lipopolysaccharides
Rabbits
