Home General Physiology and Biophysics 2016 General Physiology and Biophysics Vol.35, No.3, p.353–362, 2016

Journal info

Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

Aims and Scope
Editorial Info
Abstracting and Indexing
Submission Guidelines

Select Journal

Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

General Physiology and Biophysics Vol.35, No.3, p.353–362, 2016

Title: Could nitric oxide be a mediator of action of oxytocin on myocardial injury in rats? (Biochemical, histological and immunohistochemical study)
Author: Noha I. Hussien, Ayman M. Mousa

Abstract: Oxytocin (OT) was revisited recently as a hormone of cardiovascular system with several new functions in cardiovascular regulation. But less is known about its role in acute myocardial injury (MI). The aim of our study was to investigate the possible protective effect of OT on the biochemical, histological and immunohistochemical changes of MI induced by isoprenaline (ISO) in adult male albino rats and studying the possible role of nitric oxide (NO) in its action. Forty male albino rats were divided into 5 groups: control rats (Group I), acute MI rats (Group II), rats pretreated with OT prior to induction of MI (Group III), rats injected with a combination of OT and atosiban (ATO, OT receptor antagonist) prior to induction of MI (Group IV). In Group V, a combination of OT and nitric oxide synthase inhibitor (L-NAME) were injected to the rats prior to induction of MI. The heart wall in all groups were taken and processed for histological, immunohistochemical, morphometrical and biochemical studies. We concluded that OT has antioxidant, anti-inflammatory and anti-apoptotic effects on MI and its effects is mediated through NO.

Keywords: Myocardial injury — Isoprenaline — Oxytocin — Atosiban — Nitric oxide — Apoptosis
Published online: 13-Jun-2016
Year: 2016, Volume: 35, Issue: 3 Page From: 353, Page To: 362

download file

© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.