八肽胆囊收缩素对大鼠心功能的影响及受体机制(英文)  

Effects of cholecystokinin octapeptide on rat cardiac function and the receptor mechanism

作　　者：赵晓云[1] 凌亦凌[1] 孟爱宏[1] 单宝恩[2] 张君岚[1] 

机构地区：[1]河北医科大学病理生理学教研室,石家庄050017 [2]河北医科大学第四医院科研中心

出　　处：《生理学报》2002年第3期239-243,共5页Acta Physiologica Sinica

基　　金：HealthandEducationMinistriesofHebeiProvince (No 2K0 0 2andNo 2 0 0 12 2 )

摘　　要：为探讨八肽胆囊收缩素 (CCK 8)对麻醉大鼠心功能的影响及受体机制 ,实验监测了左心室收缩压(LVP)、左心室收缩与舒张期内压变化的最大速率 (±LVdp/dtmax)、心率 (HR)和平均动脉压 (MAP)。结果如下 :小剂量CCK 8(0 4 μg/kg)可引起心动过速 ,MAP、LVP和±LVdp/dtmax轻度上升 ;中剂量CCK 8(4 μg/kg)和大剂量CCK 8(4 0 μg/kg)可引起心动过缓 ,MAP、LVP和±LVdp/dtmax显著增加 ;应用CCK 受体 (CCK R)拮抗剂丙谷胺 (1 0mg/kg)抑制以上变化 ;由逆转录 聚合酶链反应 (RT PCR)检测到心肌组织有CCK A受体 (CCK AR)和CCK B受体 (CCK BR)mRNA表达。以上结果提示 :CCK 8可激活心肌组织的CCK R ,引起剂量依赖性的心功能增加和心率改变。The aim of this study was to explore the effects of cholecystokinin octapeptide ( CCK-8) on cardiac function and the receptor mechanism in anesthetized rats. The mean arterial pressure (MAP), heart rate (HR), the left ventricle systolic pressure (LVP) and the maximal/minimum rate of LVP (±LV dp/dt max) were measured. The results obtained are as follows. (1) Low dose of CCK-8 (0. 4 μg/kg i.v.) caused tachycardia and slight increase in MAP, LVP and ±LV dp/dt max (P<0.01), while medium dose (4.0 μg/kg i.v.) and high dose of CCK-8 (40 μg/kg i.v.) elicited a bradycardia and marked increase in MAP, LVP and ±LV dp/dt max (P<0.01) . (2) Proglumide (1.0 mg/kg i.v.), a CCK-receptor (CCK-R) antagonist, significantly inhibited the pressor effects of CCK-8, whilst it reversed the bradycardic responses (P<0.01) . (3) Using reverse transcription polymerase chain reaction (RT-PCR), CCK-A receptor (CCK-AR) and CCK-B receptor (CCK-BR) mRNA were expressed in myocardium of rats. The above results indicate that CCK-8 may enhance cardiac function in a dose-dependent manner and elicit a change in HR, which is likely induced by the activation of CCK-R on myocardium.

关 键 词：胆囊收缩素 心功能 受体 

分 类 号：R363[医药卫生—病理学]