Key result
Sildenafil treatment significantly reduced right ventricular systolic pressure in rats with monocrotaline-induced pulmonary hypertension compared to untreated controls, with no significant difference between early and late initiation.
Why the study?
Does sildenafil reduce right ventricular systolic pressure and improve echocardiographic parameters in rats with monocrotaline-induced pulmonary hypertension?
Does sildenafil reduce right ventricular systolic pressure and improve echocardiographic parameters in rats with monocrotaline-induced pulmonary hypertension?
Absolute Event Rate: 30% vs 61%
p-value: p=<0.001
Sildenafil prevents the increase in right ventricular systolic pressure and preserves diastolic function in a rat model of pulmonary hypertension, regardless of whether treatment is initiated early or late in the disease course.
Supports preclinical sildenafil evaluation in pulmonary hypertension models; leaves open translation to human disease and optimal timing.
This study aimed to investigate the potential effects of sildenafil on pulmonary hypertension (PH) in the monocrotaline (MCT)-induced PH rat. Twenty-four, 12-week-old, male Sprague-Dawley rats were injected with MCT or saline solution. After injection of MCT, rats received oral sildenafil immediately (early-phase treatment group: E group), 4 weeks after injection (late-phase treatment group: L group) or no treatment (MCT group) until 6 weeks after injection. Serial echocardiography and right ventricular systolic pressure (RVSP) measurements via a cardiac catheter were performed. RVSP was reduced in the E and L groups compared with the MCT group. Echocardiography indicated that sildenafil therapy prevents an increase in RVSP and preserves diastolic function, and this effect is not dependent on timing of initiation of therapy.
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Yoshiyuki et al. (2016) studied Monocrotaline-induced pulmonary arterial hypertension (n=24). Sildenafil vs. Placebo (no treatment) was evaluated on Right ventricular systolic pressure (RVSP) (p=<0.001). Sildenafil treatment significantly reduced right ventricular systolic pressure in rats with monocrotaline-induced pulmonary hypertension compared to untreated controls, with no significant difference between early and late initiation.
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