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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
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.
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.
- 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.