Acute sleep deprivation preconditions the heart against ischemia/ reperfusion injury: the role of central GABA-A receptors

Parsa, Hoda and Imani, Alireza and Faghihi, Mahdieh and Riahi, Esmail and Badavi, Mohammad and Shakoori, Abbas and Rastegar, Tayebeh and Aghajani, Marjan and Rajani, Sulail Fatima (2017) Acute sleep deprivation preconditions the heart against ischemia/ reperfusion injury: the role of central GABA-A receptors. Iranian Journal of Basic Medical Sciences, 20 (11). pp. 1232-1241.

[img]
Preview
Text
IJBMS_Volume 20_Issue 11_Pages 1232-1241.pdf

Download (1MB) | Preview
Official URL: http://ijbms.mums.ac.ir/article_9539.html

Abstract

Objective(s): Central γ-aminobutyric acid (GABA) neurotransmission modulates cardiovascular functions and sleep. Acute sleep deprivation (ASD) affects functions of various body organs via different mechanisms. Here, we evaluated the effect of ASD on cardiac ischemia/reperfusion injury (IRI), and studied the role of GABA-A receptor inhibition in central nucleus of amygdala (CeA) by assessing nitric oxide (NO) and oxidative stress. Materials and Methods: The CeA in sixty male Wistar rats was cannulated for saline or bicuculline (GABA-A receptor antagonist) administration. All animals underwent 30 min of coronary occlusion (ischemia), followed by 2 hr reperfusion (IR). The five experimental groups (n=12) included are as follows: IR: received saline; BIC+IR: received Bicuculline; MLP+IR: received saline, followed by the placement of animals in an aquarium with multiple large platforms; ASD+IR: underwent ASD in an aquarium with multiple small platforms; and BIC+ASD+IR: received bicuculline prior to ASD. Results: Bicuculline administration increased the malondialdehyde levels and infarct size, and decreased the NO metabolites levels and endothelial nitric oxide synthase (eNOS) gene expression in infarcted and non-infarcted areas in comparison to IR group. ASD reduced malondialdehyde levels and infarct size and increased NO metabolites, corticosterone levels and eNOS expression in infarcted and non-infarcted areas as compared to the IR group. Levels of malondialdehyde were increased while levels of NO metabolites, corticosterone and eNOS expression in infarcted and non-infarcted areas were reduced in the BIC+ASD+IR as compared to the ASD+IR group. Conclusion: Blockade of GABA-A receptors in the CeA abolishes ASD-induced cardioprotection by suppressing oxidative stress and NO production.

Item Type: Article
Subjects: QV pharmacology
Divisions: Journals > Iranian J Basic Medical Sciences
Depositing User: ijbms ijbms
Date Deposited: 04 Nov 2017 15:47
Last Modified: 04 Nov 2017 15:47
URI: http://eprints.mums.ac.ir/id/eprint/8512

Actions (login required)

View Item View Item