八肽胆囊收缩素逆转内毒素休克大鼠心功能降低的实验研究

目的: 观察八肽胆囊收缩素(CCK-8)改善内毒素休克(ES)大鼠心功能的变化,探讨CCK-8抗ES的作用及机制。方法: 实验分对照组、脂多糖(LPS)组、CCK组及CCK+LPS组;监测左室内收缩压(LVP)、左室收缩与舒张期内压变化的最大速率、心率(HR)和平均动脉压(MAP)的动态变化;分别测定2h血清、心肌组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)和一氧化氮(NO)含量的变化。结果: 静脉注射CCK-8(40μg·kg^-1),引起短时间心率减慢,轻度MAP、LVP和±LVdp/dt_max上升;静脉注时LPS(8mg·kg^-1),引起HR生快后慢双向改变MAP、LVP和±LVdp/dt_max快速持续下降;整体预先注射CCK-8,可明显缓解ES大鼠HR的快速变化,逆转MAP、LVP和±LVdp/dt_max下降,但未恢复至正常水平。CCK-8可提高ES大鼠血清、心肌组织中SOD活性,降低MDA和NO含量。结论: CCK-8可引起短时间心率减慢、轻度MAP上升和心肌收缩力增强;预先应用CCK-8可以减轻ES大鼠心肌氧化损伤,减少NO合成,恢复心肌收缩力,逆转心功能降低及顽固性低血压,是其发挥抗ES的重要机制之一。

Reversion of the decline of cardiac function in endotoxin shock rats by cholecystokinin octapeptide

AIM: To verify the effect of cholecystokinin octapeptide(CCK-8) on cardiac function in endotoxin shock (ES) rats. METHODS: The rats were divided into four groups:control,lipopolysaccharide(LPS),CCK-8 and CCK-8+LPS. The left ventricle pressure(LVP),the maximal/minimum rate of LVP,heart rate (HR) and mean arterial pressure (MAP) were measured. The activity of superoxide dismutase (SOD),the contents of malondialdehyde (MDA) and nitric oxide (NO) in both serum and myocardium were also measured,respectively. RESULTS: CCK-8 (40 μg·kg^-1, iv) elicited bradycardia in short time and gently increase MAP,LVP and ±LVdp/dt_max. Lipopolysaccharide(LPS, 8 mg·kg^-1, iv) caused a variation in heart rate (HR)(a bradycardia following a tachycardia) and rapid decreases in MAP,LVP and ±LVdp/dt_max. The rapid variation of HR and the decline of MAP,LVP and ±LVdp/dt_max were reversed by pretreatment with CCK-8 in ES rats, but didn't restore to normal. The activity of SOD was increased and the contents of MDA and NO were decreased by pretreatment with CCK-8 in ES rats. CONCLUSION: The decline of cardiac function in ES rats could be reversed by pre-administration of CCK-8 and the decrease in NO production may be one of the mechanisms.