Objective:To investigate the effects of CCK-8 on mean pulmonary artery pressure in rats with endotoxic shock.Methods:Male SD rats were randomized into seven groups(n=6):control group,model group,LPS+CCK-8 group,CCK-8 ...Objective:To investigate the effects of CCK-8 on mean pulmonary artery pressure in rats with endotoxic shock.Methods:Male SD rats were randomized into seven groups(n=6):control group,model group,LPS+CCK-8 group,CCK-8 group,CCK-1R antagonist group,CCK-2R antagonist group,DFSO+PF group.The rats were induced to lethal endotoxic shock by an injection of LPS(30 mg.kg-1).CCK-8(50μg.kg-1)was administered 30 min after LPS injection.Either a specific CCK-1R antagonist or CCK-2R antagonist was injected before CCK-8 treatment.The mean arterial pressure(MAP)and mean pulmonary artery pressure(MPAP)were collected by a multi-channel data physiological recorder.As well as the 8h mortality was recorded.Results:Compared with control group,the MAP were significantly continuously lower and the MPAP significantly higher in model group.Administration of CCK-8 significantly delayed the LPS-induced not only decreases in MAP but also rises in MPAP,while reduceing the mortality.In addition,the specific antagonist at the CCK-2 receptor(CCK-2R)abrogated the action of CCK-8 significantly.Conclusion:while the LPS-induced hypotension delayed,CCK-8 could effectively alleviate the LPS-induced rises in MPAP via the CCK-2 receptor in ES rat model,while reduceing the mortality.展开更多
目的研究松果菊苷对低氧性肺动脉高压大鼠的作用。方法大鼠随机分为正常对照组、模型组、大花红景天口服液组[1.78 m L/(kg·d)]、松果菊苷高、中、低剂量组[50、25、12.5 mg/(kg·d)],每组12只。除正常对照组外其余各组置于模...目的研究松果菊苷对低氧性肺动脉高压大鼠的作用。方法大鼠随机分为正常对照组、模型组、大花红景天口服液组[1.78 m L/(kg·d)]、松果菊苷高、中、低剂量组[50、25、12.5 mg/(kg·d)],每组12只。除正常对照组外其余各组置于模拟海拔5000 m高原环境的人工实验舱中饲养4周后再灌胃给药4周。观察各组大鼠血流动力学改变,免疫组化法检测血管生长因子(VEGF)的表达,Western Blot法检测VEGF蛋白的表达。结果松果菊苷高、中、低剂量组和大花红景天组均能降低高原肺动脉高压大鼠平均肺动脉压、右心室收缩压及右心室肥厚指数(P<0.01);抑制低氧性肺动脉高压大鼠肺组织VEGF及蛋白的表达(P<0.01)。结论松果菊苷能够治疗低氧性肺动脉高压,可能与其抑制VEGF的表达有关。展开更多
基金Research Project of Hebei Administration of Traditional Chinese Medicine(No.2017005)Youth Fund of Hebei University of Chinese Medicine(No.QNZ2014036)
文摘Objective:To investigate the effects of CCK-8 on mean pulmonary artery pressure in rats with endotoxic shock.Methods:Male SD rats were randomized into seven groups(n=6):control group,model group,LPS+CCK-8 group,CCK-8 group,CCK-1R antagonist group,CCK-2R antagonist group,DFSO+PF group.The rats were induced to lethal endotoxic shock by an injection of LPS(30 mg.kg-1).CCK-8(50μg.kg-1)was administered 30 min after LPS injection.Either a specific CCK-1R antagonist or CCK-2R antagonist was injected before CCK-8 treatment.The mean arterial pressure(MAP)and mean pulmonary artery pressure(MPAP)were collected by a multi-channel data physiological recorder.As well as the 8h mortality was recorded.Results:Compared with control group,the MAP were significantly continuously lower and the MPAP significantly higher in model group.Administration of CCK-8 significantly delayed the LPS-induced not only decreases in MAP but also rises in MPAP,while reduceing the mortality.In addition,the specific antagonist at the CCK-2 receptor(CCK-2R)abrogated the action of CCK-8 significantly.Conclusion:while the LPS-induced hypotension delayed,CCK-8 could effectively alleviate the LPS-induced rises in MPAP via the CCK-2 receptor in ES rat model,while reduceing the mortality.
