Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats
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....
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doaj-a81d53db0f8042f28bbd10be8a2d75392020-11-25T03:35:47ZengEditorial Board of Journal of Hainan Medical UniversityJournal of Hainan Medical University1007-12371007-12372020-07-0126142226Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock ratsDong Zhang0Bin Cong1College of Forensic Medicine, Hebei Medical University, Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular IdentificationsCollege of Forensic Medicine, Hebei Medical University, Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular IdentificationsObjective: 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 (50 μg. 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 LPSinduced 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.http://www.hnykdxxb.com/PDF/202014/05.pdfcholecystokininlipopolysaccharideendotoxin shockmapmpap |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Dong Zhang Bin Cong |
spellingShingle |
Dong Zhang Bin Cong Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats Journal of Hainan Medical University cholecystokinin lipopolysaccharide endotoxin shock map mpap |
author_facet |
Dong Zhang Bin Cong |
author_sort |
Dong Zhang |
title |
Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats |
title_short |
Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats |
title_full |
Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats |
title_fullStr |
Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats |
title_full_unstemmed |
Effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats |
title_sort |
effect of cholecystokinin octapeptide on mean pulmonary artery pressure in endotoxic shock rats |
publisher |
Editorial Board of Journal of Hainan Medical University |
series |
Journal of Hainan Medical University |
issn |
1007-1237 1007-1237 |
publishDate |
2020-07-01 |
description |
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 (50 μg. 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 LPSinduced
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. |
topic |
cholecystokinin lipopolysaccharide endotoxin shock map mpap |
url |
http://www.hnykdxxb.com/PDF/202014/05.pdf |
work_keys_str_mv |
AT dongzhang effectofcholecystokininoctapeptideonmeanpulmonaryarterypressureinendotoxicshockrats AT bincong effectofcholecystokininoctapeptideonmeanpulmonaryarterypressureinendotoxicshockrats |
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