【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 ( 8mg/kgi v )复制的家兔ES模型、LPS注入前 15min给CCK 8( 15 μg/kg ,i v )、LPS注入前 15min给CCK受体拮抗剂丙谷胺 (Pro 1mg/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 ;5h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更多还原

【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.更多还原