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Related Experiment Videos

Nitric oxide system in needle-induced transmyocardial revascularization.

T Saito1, M P Pelletier, H Shennib

  • 1Department of Pathology, The Montreal General Hospital, McGill University, Quebec, Canada.

The Annals of Thoracic Surgery
|July 24, 2001
PubMed
Summary

Needle-induced transmyocardial revascularization (TMR) in ischemic cardiomyopathy models significantly increased vascular density. This procedure also elevated inducible nitric oxide synthase (iNOS) expression, suggesting a role for iNOS-derived nitric oxide in TMR's angiogenic response.

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Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Molecular Biology

Background:

  • Nitric oxide (NO) is crucial for endothelial cell proliferation and migration, key processes in angiogenesis.
  • Ischemic cardiomyopathy impairs heart function due to reduced blood flow.
  • Transmyocardial revascularization (TMR) is a surgical technique aimed at improving blood supply to ischemic heart muscle.

Purpose of the Study:

  • To investigate the cellular expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) after needle-induced TMR in an animal model of ischemic cardiomyopathy.
  • To assess the impact of TMR on vascular density and NO synthase expression in the infarcted myocardium.

Main Methods:

  • Myocardial infarction was induced in rats by ligating the left coronary artery.

Related Experiment Videos

  • Rats were divided into a control group (no TMR) and a TMR group, which underwent needle puncture to create transmural channels in the ischemic area.
  • Immunohistochemistry was used to evaluate the expression of iNOS, eNOS, and the endothelial cell marker factor VIII at 1, 2, 4, and 8 weeks post-procedure.
  • Vascular density and positive staining for iNOS and eNOS were quantified in the infarcted myocardium.

    • Main Results:

    • Transmyocardial revascularization (TMR) significantly increased vascular density in the infarcted myocardium (p < 0.001).
    • A significant increase in iNOS expression and staining intensity was observed in cardiomyocytes, vascular endothelium, and macrophages in the TMR group compared to controls (p < 0.05), primarily within the first 2 weeks post-TMR.
    • No significant differences in eNOS expression were found between the TMR and control groups.

    Conclusions:

    • Needle-induced TMR in an ischemic myocardium enhances vascular density.
    • The observed increase in iNOS expression following TMR suggests that nitric oxide derived from iNOS plays a role in the angiogenic response stimulated by this procedure.
    • Mechanical injury from TMR may trigger an inflammatory response that upregulates iNOS, contributing to neovascularization.