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抗阻运动训练可减轻肺动脉高压模型的左心室功能障碍。

Resistance Exercise Training Mitigates Left Ventricular Dysfunctions in Pulmonary Artery Hypertension Model.

机构信息

Universidade Federal de Viçosa , Departamento de Educação Física , Viçosa , MG - Brasil.

Universidade Federal de Viçosa , Departamento de Biologia Geral , Viçosa , MG - Brasil.

出版信息

Arq Bras Cardiol. 2022 Oct;119(4):574-584. doi: 10.36660/abc.20210681.

DOI:10.36660/abc.20210681
PMID:36074480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9563884/
Abstract

BACKGROUND

The right ventricular hypertrophy and dilation observed in pulmonary artery hypertension (PAH) damages the left ventricle (LV) dynamics by flattening the interventricular septum.

OBJECTIVE

To investigate whether low- to moderate-intensity resistance exercise training (RT) is beneficial to LV and cardiomyocyte contractile functions in rats during the development of monocrotaline (MCT)-induced PAH.

METHODS

Male Wistar rats (Body weight: ~ 200 g) were used. To assess the time to potential heart failure onset (i.e., end point), rats were divided into sedentary hypertension until failure (SHF, n=6) and exercise hypertension until failure (EHF, n=6) groups. To test RT effects, rats were divided into sedentary control (SC, n = 7), sedentary hypertension (SH, n=7), and exercise hypertension (EH, n=7) groups. PAH was induced by two MCT injections (20 mg/kg, with 7 days interval). Exercise groups were submitted to an RT protocol (Ladder climbing; 55-65% of carrying maximal load), 5 times/week. Statistical significance was assumed at P < 0.05.

RESULTS

RT prolonged the end point (25 %), enhanced the physical effort tolerance ( 55%), and mitigated the LV and cardiomyocyte contractility dysfunctions promoted by MCT by preserving the ejection fraction and fractional shortening, the amplitude of shortening, and the velocities of contraction and relaxation in cardiomyocytes. RT also prevented increases in left ventricle fibrosis and type I collagen caused by MCT, and maintained the type III collagen and myocyte dimensions reduced by MCT.

CONCLUSION

Low- to moderate-intensity RT benefits LV and cardiomyocyte contractile functions in rats during the development of MCT-induced PAH.

摘要

背景

肺动脉高压(PAH)中观察到的右心室肥大和扩张通过使室间隔变平而损害左心室(LV)的动力学。

目的

研究低强度到中等强度的抵抗运动训练(RT)是否有益于 MCT 诱导的 PAH 大鼠发展过程中的 LV 和心肌细胞收缩功能。

方法

使用雄性 Wistar 大鼠(体重:~200 g)。为了评估潜在心力衰竭发作的时间(即终点),大鼠被分为久坐高血压直至衰竭(SHF,n=6)和运动高血压直至衰竭(EHF,n=6)组。为了测试 RT 效果,大鼠被分为久坐对照组(SC,n=7)、久坐高血压组(SH,n=7)和运动高血压组(EH,n=7)。PAH 由两次 MCT 注射(20 mg/kg,间隔 7 天)诱导。运动组进行 RT 方案(爬梯;携带最大负荷的 55-65%),每周 5 次。假设 P < 0.05 具有统计学意义。

结果

RT 延长了终点(25%),提高了体力耐受度(55%),并通过保留射血分数和缩短分数、缩短幅度以及心肌细胞收缩和舒张速度,减轻了 MCT 引起的 LV 和心肌细胞收缩功能障碍。RT 还预防了 MCT 引起的左心室纤维化和 I 型胶原增加,并维持了 MCT 降低的 III 型胶原和肌细胞尺寸。

结论

低强度到中等强度的 RT 有益于 MCT 诱导的 PAH 大鼠 LV 和心肌细胞收缩功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/4c68032ac261/0066-782X-abc-119-04-0574-gf03-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/96b70973e2df/0066-782X-abc-119-04-0574-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/3be412b8c759/0066-782X-abc-119-04-0574-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/c2df9bbc9d61/0066-782X-abc-119-04-0574-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/cddeb15a2031/0066-782X-abc-119-04-0574-gf01-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/81331b896c65/0066-782X-abc-119-04-0574-gf02-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/4c68032ac261/0066-782X-abc-119-04-0574-gf03-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/96b70973e2df/0066-782X-abc-119-04-0574-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/3be412b8c759/0066-782X-abc-119-04-0574-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/c2df9bbc9d61/0066-782X-abc-119-04-0574-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/cddeb15a2031/0066-782X-abc-119-04-0574-gf01-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/81331b896c65/0066-782X-abc-119-04-0574-gf02-en.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cd1/9563884/4c68032ac261/0066-782X-abc-119-04-0574-gf03-en.jpg

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