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Original Research Article | OPEN ACCESS

Effect of different doses of dexmedetomidine on lung function and tissue cell apoptosis in a rat model of hyperoxic acute lung injury

Yan Yang1, Xian Qin1, Chuangang Han1, Yan Huang1, Lei Jin1, Qingqing Liu1, Quan Hu2

1Department of Anesthesiology; 2Intensive Care Unit, The First People's Hospital of Jiangxia District, Wuhan, PR China.

For correspondence:-  Quan Hu   Email: u40pct@163.com

Accepted: 27 April 2020        Published: 31 May 2020

Citation: Yang Y, Qin X, Han C, Huang Y, Jin L, Liu Q, et al. Effect of different doses of dexmedetomidine on lung function and tissue cell apoptosis in a rat model of hyperoxic acute lung injury. Trop J Pharm Res 2020; 19(5):1093-1098 doi: 10.4314/tjpr.v19i5.27

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To study the effect of different doses of dexmedetomidine on lung function and lung tissue cell apoptosis in a rat model of hyperoxic acute lung injury.
Methods: Five groups of healthy male Sprague-Dawley rats were used: normal rats, untreated hyperoxic rats, and hyperoxic rats given 3 different doses of dexmedetomidine, with 20 rats in each group. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined using enzyme-linked immunosorbent assay (ELISA). Parietal paraffin cuts were taken from the right upper lobe for measurement of apoptosis using in situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and the apoptosis index was calculated.
Results: At 24 and 48 h, the levels of IL-6 and TNF-α in the hyperoxia model group were significantly higher than those in the normal control group, and their levels in the middle- and high-dose groups were markedly lowered, relative to untreated hyperoxia rats (p < 0.05). Apoptosis index in the hyperoxia model rats significantly increased, relative to normal rats (p < 0.05). The apoptosis index in the medium- and high-dose groups decreased significantly (p < 0.05).
Conclusion: Dexmedetomidine inhibits inflammatory responses caused by high concentration of oxygen inhalation, minimizes lung injury, improves lung function and inhibits lung apoptosis. 

Keywords: Dexmedetomidine, Hyperoxia, Acute lung injury, Lung function, Apoptosis

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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