CAJ | 학술논문

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(±LV dp/dtmax)、心率(HR)和平均动脉压(MAP).结果如下:小剂量CCK-8(0.4μg/kg)可引起心动过速,MAP、LVP和±LV dp/dtmax轻度上升;中剂量CCK-8(4μg/kg)和大剂量CCK-8(40μg/kg)可引起心动过缓,MAP、LVP和±LV dp/dtmax 显著增加;应用CCK-受体(CCK-R)拮抗剂丙谷胺(1.0 mg/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.
위탐토팔태담낭수축소(CCK-8)대마취대서심공능적영향급수체궤제,실험감측료좌심실수축압(LVP)、좌심실수축여서장기내압변화적최대속솔(±LV dp/dtmax)、심솔(HR)화평균동맥압(MAP).결과여하:소제량CCK-8(0.4μg/kg)가인기심동과속,MAP、LVP화±LV dp/dtmax경도상승;중제량CCK-8(4μg/kg)화대제량CCK-8(40μg/kg)가인기심동과완,MAP、LVP화±LV dp/dtmax 현저증가;응용CCK-수체(CCK-R)길항제병곡알(1.0 mg/kg)억제이상변화;유역전록-취합매련반응(RT-PCR)검측도심기조직유CCK-A수체(CCK-AR)화CCK-B수체(CCK-BR)mRNA표체.이상결과제시:CCK-8가격활심기조직적CCK-R,인기제량의뢰성적심공능증가화심솔개변.
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/dtmax) 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/dtmax( 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/dtmax ( 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.