Objective: Evidence that vasodilator nitric oxide mediates normal pulmonary vascular tone has led to the hypothesis that endothelial injury induced by congenital heart disease with increased pulmonary blood flow disrupts these regulatory mechanisms and its associated altered vascular reactivity. Therefore, we hypothesized that increased pulmonary blood flow results in altered expression of endothelial nitric oxide synthase (eNOS). Methods: We created an arteriovenous shunt in female Wistar (5-week-old) and measured the change of pulmonary blood flow and pressure immediately after and 1 month after the shunt operation. The protein levels of eNOS in the lung tissues of rats were assessed. Results: The shunt immediately resulted in a significant increase in pulmonary blood flow (16.5±2.7%), pulmonary artery pressure (2.3±0.7mmHg), and blood O2 saturation (16.1±11.8%) in the pulmonary artery. After 4 weeks, there was a significant increase in pulmonary blood flow (30.7±1.6%), pulmonary artery pressures (4.3±1.1mmHg), and blood O2 content (43.3±17.5%). Western blot analysis demonstrated that eNOS protein was increased in the shunt lung 72h after surgery and recovered to the control level 1 week later. Conclusion: This simple shunt model can induce early upregulation of eNOS expression with increased pulmonary blood flow and pulmonary artery pressure in rats.
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