Aspirin Attenuates Pulmonary Arterial Hypertension in Rats by Reducing Plasma 5-Hydroxytryptamine Levels |
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Authors: | Lan Shen Jieyan Shen Jun Pu Ben He |
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Institution: | (1) Cardiovascular Department, Renji Hospital, Shanghai Jiaotong University School of Medicine, Dong Fang Road 1630, Shanghai, 200127, China; |
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Abstract: | Pulmonary arterial hypertension (PAH) is characterized by increasing pulmonary pressure, right ventricular failure, and death.
The typical pathological changes include medial hypertrophy, intimal fibrosis and in situ thrombosis. Serotonin (5-HT) and
other factors contribute to the development of pathologic lesions. Aspirin (ASA), a platelet aggregation inhibitor, inhibits
5-HT release from platelets. The aim of this study was to determine the efficacy of ASA in preventing or attenuating PAH.
Sprague–Dawley rats injected with monocrotaline (MCT) developed severe PAH within 31 days. One hundred forty rats were randomized
to receive either vehicle or ASA (0.5, 1, 2, or 4 mg/kg/day). The pre-ASA group was treated with ASA (1 mg/kg/day) for 30 days
before the MCT injection. Thirty-one days after the injection (day 61 for the pre-ASA group), pulmonary arterial pressure
(PAP), right ventricular hypertrophy and pulmonary arteriole thickness were measured. Plasma 5-HT was measured by high-performance
liquid chromatography. Aspirin suppressed PAH and increased the survival rate compared with the control group (84 vs. 60%,
P < 0.05). Aspirin treatment also reduced right ventricular hypertrophy and pulmonary arteriole proliferation in ASA-treated
PAH model. In addition, plasma 5-HT was decreased in our ASA-treated PAH model. The degree of 5-HT reduction was associated
with systolic PAP, right ventricular hypertrophy and wall thickness of pulmonary arterioles in rats. These results showed
that ASA treatment effectively attenuated MCT-induced pulmonary hypertension, right ventricular hypertrophy, and occlusion
of the pulmonary arteries. The effects of ASA was associated with a reduction of 5-HT. |
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