Related Experiment Video

Updated: Mar 27, 2026

Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System
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Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System

Published on: June 11, 2020

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Nitric oxide mediated effects of nebivolol in myocardial infarction: the source of nitric oxide

G Mercanoglu1, N Safran, B Ahishali B

  • 1Department of Pharmacology, Biruni University, Faculty of Pharmacy, Istanbul, Turkey. guldemiko@gmail.com.

European Review for Medical and Pharmacological Sciences
|January 9, 2016
PubMed
Abstract

Insights

Nebivolol treatment improves heart function after myocardial infarction (MI) by modulating nitric oxide synthase (NOS) pathways. This study reveals nebivolol reduces oxidative damage and normalizes NOS expression, crucial for preventing pathological cardiac remodeling.

Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Molecular Biology

Background:

  • Pathological left ventricular (LV) remodeling post-myocardial infarction (MI) is a significant cause of mortality.
  • Nebivolol has demonstrated beneficial nitric oxide (NO)-mediated effects in preclinical MI models.
  • Understanding the specific nitric oxide synthase (NOS) related mechanisms underlying nebivolol's efficacy is crucial.

Purpose of the Study:

  • To investigate the NOS-related mechanisms by which nebivolol exerts beneficial effects following MI in a rat model.
  • To evaluate the impact of nebivolol on both acute and sub-acute phases of cardiac remodeling post-MI.

Main Methods:

  • Rats underwent sham operation or MI induction via LAD ligation.
  • Treatment groups included immediate intravenous nebivolol loading and daily oral administration.
  • Histological, hemodynamic, and biological assessments were performed at acute (2-day) and sub-acute (28-day) time points.

Main Results:

  • Nebivolol treatment preserved LV physiological functions (LVEDP, Δ±dp/dt) and anatomical parameters (LEV, HW, LVW/HW).
  • Nebivolol limited oxidative and nitrosative damage, indicated by decreased MDA and ONOO-, and increased SOD levels.
  • Significant alterations in inducible NOS (iNOS) and neuronal NOS (nNOS) labeling were observed in nebivolol-treated groups compared to controls.

Conclusions:

  • Nebivolol diminishes iNOS expression and restores eNOS activation in the acute phase post-MI.
  • Nebivolol prevents the deterioration of nNOS expression in myocardial cells during the sub-acute phase.
  • These NOS-mediated mechanisms contribute to nebivolol's cardioprotective effects against pathological remodeling after MI.

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