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
Objective:To investigate the effects of CCK-8 receptor on lung injury in endotoxemia rats. Methods: Male SD rats were randomized into four groups (n=6): control group (LPS+CCK-8 group), CCK-1R antagonist group, CCK-2R...Objective:To investigate the effects of CCK-8 receptor on lung injury in endotoxemia rats. Methods: Male SD rats were randomized into four groups (n=6): control group (LPS+CCK-8 group), CCK-1R antagonist group, CCK-2R antagonist group, DFSO+PF group. The rats were injected by LPS (5 mg.kg-1). CCK-8 (20 μg.kg-1) was administered 30 min after LPS injection. Either a specific CCK-1R antagonist or CCK-2R antagonist (0.5.kg-1) was injected before CCK-8 treatment (after LPS 20min). The tidal volume (TV) was collected by a multi-channel data physiological recorder. The lung injury was observed by light and electron microscopy. The concentrations of TNF-α、IL-1 and IL-6 in lung homogenates were measured by ELISA kits.Rresults: Compared with control group, the TV were significantly lower and the lung injuries were more serious in CCK-2R antagonist group. As well as the concentrations of TNF-α、IL-1 and IL-6 in lung homogenates were higher.Conclusion: CCK-2 receptor plays a major role in the effect of CCK-8 on lung injury in ETM rats.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.
基金Research Project of Hebei Administration of Traditional Chinese Medicine(2017005)Youth Fund of Hebei University of Chinese Medicine(QNZ2014036)
文摘Objective:To investigate the effects of CCK-8 receptor on lung injury in endotoxemia rats. Methods: Male SD rats were randomized into four groups (n=6): control group (LPS+CCK-8 group), CCK-1R antagonist group, CCK-2R antagonist group, DFSO+PF group. The rats were injected by LPS (5 mg.kg-1). CCK-8 (20 μg.kg-1) was administered 30 min after LPS injection. Either a specific CCK-1R antagonist or CCK-2R antagonist (0.5.kg-1) was injected before CCK-8 treatment (after LPS 20min). The tidal volume (TV) was collected by a multi-channel data physiological recorder. The lung injury was observed by light and electron microscopy. The concentrations of TNF-α、IL-1 and IL-6 in lung homogenates were measured by ELISA kits.Rresults: Compared with control group, the TV were significantly lower and the lung injuries were more serious in CCK-2R antagonist group. As well as the concentrations of TNF-α、IL-1 and IL-6 in lung homogenates were higher.Conclusion: CCK-2 receptor plays a major role in the effect of CCK-8 on lung injury in ETM rats.