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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Main Authors: Dong Zhang, Bin Cong
Format: Article
Language:English
Published: Editorial Board of Journal of Hainan Medical University 2020-07-01
Series:Journal of Hainan Medical University
Subjects:
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Online Access:http://www.hnykdxxb.com/PDF/202014/05.pdf
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spelling 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
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