生理学报Acta Physiologica Sinica, April

研究论文

八肽胆囊收缩素对家兔内毒素休克时肺动脉张力的影响

段国辰, 凌亦凌*, 谷振勇, 韦鹏, 牛志云, 杨世方

河北医科大学病理生理教研室, 石家庄 050017

摘要: 为探讨八肽胆囊收缩素(CCK-8)缓解内毒素休克(ES)时肺动脉血压(PAP)增高的机制, 观察了CCK-8对脂多糖(LPS)引起家兔ES时PAP变化以及离体肺动脉环(PARs)张力改变的影响。实验用新西兰大耳白雄性家兔40只, 分为颈静脉注入LPS (8 mg/kg i.v.)复制的家兔ES模型、 LPS注入前15 min给CCK-8 (15 μg/kg, i.v.)、 LPS注入前15 min给CCK受体拮抗剂丙谷胺(Pro 1 mg/kg, i.v.)、 单独注入CCK-8 (15 μg/kg, i.v.)和注射生理盐水(对照)共5组。用生理记录仪监测平均动脉压(MAP) 和PAP的变化; 5 h后制备PARs, 应用血管张力测定技术, 检测各组PARs张力。结果为: (1) ES时MAP降低、 PAP升高, CCK-8可完全翻转ES时PAP的增高, 而Pro加剧ES时PAP的增高; (2) LPS组的PARs对苯肾上腺素(PE)的收缩反应增强, 对ACh内皮依赖性舒张反应降低, 而CCK-8可逆转LPS的上述作用。上述结果提示CCK-8可缓解ES时的PAP升高, 这可能与其调节肺动脉张力改变有关。

关键词: 胆囊收缩素; 内毒素休克; 肺动脉; 血管张力

中图分类号: Q463.6; R363

Effects of cholecystokinin-octapeptide on the tension of pulmonary artery in rabbits with endotoxic shock

DUAN Guo-Chen, LING Yi-Ling*, GU Zhen-Yong, WEI Peng, NIU Zhi-Yun, YANG Shi-Fang

Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017

Abstract: For investigation of the regulatory mechanism of cholecystokinin-octapeptide (CCK-8) on pulmonary circulation in rabbits with endotoxic shock (ES) induced by lipopolysaccharides (LPS), mean arterial pressure (MAP) and pulmonary arterial pressure (PAP) were evaluated for 5 h in five groups of rabbits: group of LPS (8 mg/kg, i.v.)-induced ES, group of CCK-8 pretreatment (15 μg/kg, i.v.) 15 min before LPS administration (8 mg/kg, i.v.), group of proglumide pretreatment (1 mg/kg, i.v.) 15 min before LPS administration (8 mg/kg, i.v.), group of CCK (15 μg/kg, i.v.) only, and normal saline (control) group.The pulmonary arterial tension was measured with isolated vascular ring technique.The results showed that LPS-induced pulmonary arterial hypertension was abolished by CCK-8. In contrast, proglumide, a nonspecific antagonist of CCK-8 receptor, potentiated the deleterious effect of LPS. The contractile response of isolated pulmonary artery to α-adrenoceptor agonist phenylephrine (PE) was enhanced and the relaxation response to acetylcholine (ACh) was depressed significantly after LPS was injected, but the effect could be reversed by CCK-8. These results suggest that pulmonary circulation is improved by CCK-8 in ES, and the regulatory effects of CCK-8 may be brought about by modulating the pulmonary arterial tension.

Key words: cholecystokinin-octapeptide; endotoxic shock; pulmonary artery; vascular tension