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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。
To investigate the effects of cholecystokinin octapeptide (CCK 8) on cardiac function in anesthetized rats and its receptor mechanism, the maximal rates of left ventricular systolic pressure (LVP), left ventricular systolic and diastolic pressure changes (± LVdp / dtmax), heart rate (HR) and mean arterial pressure (MAP). The results were as follows: A small dose of CCK 8 (0 4 μg / kg) caused a slight increase in tachycardia, MAP, LVP and ± LVdp / dtmax; middle dose of CCK 8 (4 μg / kg) and high dose of CCK 8 μg / kg) can cause bradycardia, MAP, LVP and ± LVdp / dtmax increased significantly; CCK receptor antagonist valproate (10 mg / kg) inhibited the above changes; by reverse transcription polymerase chain The mRNA expression of CCK A receptor (CCK AR) and CCK B receptor (CCK BR) was detected in myocardium by RT PCR. The above results suggest that CCK 8 activates CCK R in cardiac muscle tissue, causing a dose-dependent increase in cardiac function and heart rate.