西地那非对肺动脉高压大鼠心房钠尿肽水平的影响

Mukhallad A Aljanabi, Nasr Alrabadi, Sahar H Mahmoud, Razan Haddad, Karem H Alzoubi
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摘要

背景:肺动脉高压(PH)会导致肺血管结构改变、右心室肥大和心力衰竭。目的:研究西地那非缓解单克瑞林(MCT)诱导的大鼠肺动脉高压的能力,并估计其对心房利钠肽(ANP)水平的作用和影响:A组(对照组;n=7)。B组(MCT治疗组;n=7)皮下注射单剂量MCT 60 mg/kg。C组(逆转组;人数=7)皮下注射单剂量MCT 60毫克/千克,持续三周,然后每天服用西地那非50毫克/千克,持续三周。D组(预防组;n=7)同时接受单剂量 60 毫克/千克的 MCT 皮下注射和每天 50 毫克/千克的西地那非治疗,持续三周:结果:与逆转组和 MCT 治疗组相比,预防组动物的 ANP 水平显著下降。与逆转组相比,预防组动物的富尔顿指数比值明显下降。逆转组的一氧化氮水平也明显高于对照组:结论:预防性西地那非治疗可显著降低 ANP 水平,并减轻 MCT 诱导的大鼠心肌肥厚。
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Sildenafil Effect on Atrial Natriuretic Peptide Level in Pulmonary Hypertensive Rats.

Background: Pulmonary Hypertension (PH) leads to changes in pulmonary vascular architecture, hypertrophy of the right ventricle, and heart failure. Sildenafil is a drug that can modulate PH by inducing smooth muscle relaxation and vasodilation.

Aims: To investigate the ability of sildenafil to alleviate the monocritaline (MCT)-induced PH in rats and to estimate the role and its effect on the atrial natriuretic peptide (ANP) levels.

Methods: 28 adult male rats were divided randomly into four groups: Group A (control group; n=7). Group B (MCT-treated group; n=7) was given a single dose of MCT 60 mg/kg subcutaneously. Group C (The reversal group; n=7) received a single dose of MCT 60 mg/kg subcutaneously for three weeks and then sildenafil at 50 mg/kg/day, given daily for another three weeks. Group D (The prevention group; n=7) simultaneously received a single dose of MCT 60 mg/kg subcutaneously and sildenafil daily at 50 mg/kg for three weeks.

Results: The animals in the prevention group showed a significant decrease in ANP levels compared to the reversal and MCT-treated groups. This decrease was associated with a significant reduction in the Fulton index ratio in the prevention group compared to the reversal group. The nitric oxide levels were also significantly higher in the reversal group than in the control group.

Conclusion: Preventive sildenafil treatment was associated with a significant decrease in ANP levels and reduced MCT-induced cardiac hypertrophy in rats.

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