Chronic L‐NAME Treatment in Rats Resulted in A Significant Increase in the Systemic and Right Ventricular Pressure, But the Pulmonary Arterial Pressure was not Altered.

The important role of NO in the modulation of vascular reactivity and pressure development is well established. We recently found that an acute and short‐term (1 to 2 weeks) treatment with L‐NAME resulted in a marked systemic hypertension, while the right ventricular (RV) and pulmonary pressure (PP) was not affected, suggesting a marked regional difference in NO vasomodulatory action. Continued L‐NAME treatment for 3 to 4 weeks resulted in a marked left ventricular hypertrophy (LVH), a decreased LV ejection fraction as well as an increase in the RV pressure, while the PP remains protected, suggesting a presence of pressure gradient between the RV and the pulmonary circulation. Using 2‐dimension, M‐mode and Doppler echocardiography we found that chronic NO inhibition resulted in a thickened RV wall, a turbulent RV flow pattern, a decreased RV ejection fraction, and a narrowed area in the RV outflow tract. Further histomorphological studies identified that impediment to RV outflow tract was due to massive hypertrophy of the crista supraventricularis. A similar clinical syndrome of subpulmonary stenosis induced RV outflow tract obstruction has been reported in certain patients with pulmonary disorder. Our findings suggest that this animal model of chronic L‐NAME treatment may be useful to investigate the development of hypertrophic obstructive cardiomyopathy and its clinical management.