病态的
心脏病学
心室重构
医学
内科学
肺动脉高压
阻力训练
心力衰竭
作者
Luciano Bernardes Leite,Leôncio Lopes Soares,Luiz Otávio Guimarães Ervilha,Sebastião Felipe Ferreira Costa,Sara Caco dos Lúcio Generoso,Marcos Xavier,Thainá Iasbik-Lima,Leandro Licursi de Oliveira,Ceres Mattos Della Lúcia,Sara Elis Bianchi,Valquíria Linck Bassani,Flávio Gilberto Herter,Patrick Türck,Alex Sander da Rosa Araújo,Pedro Forte,Emily Correna Carlo Reis,Mariana Machado‐Neves,Antônio José Natali
出处
期刊:Nutrients
[Multidisciplinary Digital Publishing Institute]
日期:2025-03-26
卷期号:17 (7): 1145-1145
摘要
To investigate whether the regular administration of blueberry extract and low-intensity resistance exercise training (RT), either alone or in combination, during the development of monocrotaline (MCT)-induced severe pulmonary arterial hypertension (PAH) in rats protect the left ventricle (LV) from redox dysregulation and pathological remodeling. Groups of seven male Wistar rats were formed for the experiment: sedentary control; sedentary hypertensive; sedentary hypertensive blueberry; exercise hypertensive; and exercise hypertensive blueberry. PAH was experimentally induced through a single intraperitoneal administration of MCT at a dose of 60 mg/kg. One day after injection, the blueberry groups started receiving a daily dose of blueberry extract (100 mg/kg) by gavage, while the exercise groups initiated a three-week program of RT (ladder climbing; 15 climbs carrying 60% of maximum load; one session/day; 5 times/week). Echocardiographic evaluations were conducted 23 days after injection, and the rats were euthanized the next day to harvest LV tissue. Separately, blueberry extract and RT mitigated augments in pulmonary artery resistance, LV tissue redox dysregulation (i.e., increased PC levels) and detrimental remodeling (i.e., reduced inflammation), and reductions in ejection fraction (EF) and fractional shortening (FS) caused by PAH. The combination of treatments prevented reductions in EF and FS, along with the development of a D-shaped LV. blueberry extract and moderate-intensity resistance training administered during the development of MCT-induced severe PAH in rats prevented LV redox dysregulation and pathological remodeling, thereby preserving its function.
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