Key result
In rats with monocrotaline-induced pulmonary hypertension, DDCI-01 at 9 mg/kg/day reduced mean pulmonary arterial pressure and medial wall thickness more effectively than tadalafil (P<0.05).
Why the study?
To evaluate the effects of DDCI-01, a novel long-acting phosphodiesterase-5 inhibitor, as an early intervention for monocrotaline-induced pulmonary hypertension in rats.
Does DDCI-01 improve hemodynamic and echocardiographic parameters in rats with monocrotaline-induced pulmonary hypertension compared to tadalafil or control?
Does DDCI-01 improve hemodynamic and echocardiographic parameters in rats with monocrotaline-induced pulmonary hypertension compared to tadalafil or control?
p-value: p=< 0.05
The novel long-acting PDE5 inhibitor DDCI-01 attenuated monocrotaline-induced pulmonary hypertension in rats, showing greater efficacy than tadalafil at higher doses.
Pulmonary arterial hypertension is a progressive, malignant heart disease, characterized by pulmonary arteriole remodeling and increased pulmonary vascular resistance, which eventually leads to right heart failure. This study sought to evaluate the effects of a novel long‐acting phospdiesterase‐5 inhibitor, namely DDCI‐01, as an early intervention for monocrotaline‐induced pulmonary hypertensive rats. To establish this model, 50 mg/kg of monocrotaline was intraperitoneally injected into rats. At Day 7 after monocrotaline injection, two doses of DDCI‐01 (3 or 9 mg/kg/day) or tadalafil (at 3 or 9 mg/kg/day) were intragastrically administered. The rats were anesthetized with pentobarbital for hemodynamic and echocardiographic measurements, at Day 21 after monocrotaline injection. Compared to the monocrotaline group, DDCI‐01 at 3 and 9 mg/kg/day (P) reduced the mean pulmonary arterial pressure (mPAP), right ventricular systolic pressure, right ventricular transverse diameter, pulmonary arterial medial wall thickness (WT%), and right ventricle hypertrophy. However, no significant difference in the indices mentioned as above was found between DDCI‐01 (3 mg/kg/day) and tadalafil (3 mg/kg/day). In addition, DDCI‐01 at 9 mg/kg/day resulted in lower mPAP and WT%, as well as higher cyclic guanosine monophosphate levels in the lung and plasma compared with the same dose of tadalafil (9 mg/kg/day) (all P < 0.05). These findings suggested that DDCI‐01 improved monocrotaline‐induced pulmonary hypertension in rats, and a dose of DDCI‐01 of 9 mg/kg/day might be more effective than the same dose of tadalafil in monocrotaline‐induced pulmonary hypertension in rats.
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Li et al. (2020) studied Monocrotaline-induced pulmonary hypertension. DDCI-01 vs. Monocrotaline group and tadalafil (3 or 9 mg/kg/day) was evaluated on Hemodynamic and echocardiographic measurements including mean pulmonary arterial pressure (mPAP) and pulmonary arterial medial wall thickness (WT%) (p=< 0.05). In rats with monocrotaline-induced pulmonary hypertension, DDCI-01 at 9 mg/kg/day reduced mean pulmonary arterial pressure and medial wall thickness more effectively than tadalafil (P<0.05).
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