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慢性运动部分恢复自发性高血压大鼠左心室心肌细胞动作电位时程的跨壁异质性。

Chronic exercise partially restores the transmural heterogeneity of action potential duration in left ventricular myocytes of spontaneous hypertensive rats.

机构信息

Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.

出版信息

Clin Exp Pharmacol Physiol. 2012 Feb;39(2):155-7. doi: 10.1111/j.1440-1681.2011.05669.x.

Abstract

Hypertension leads to electrophysiological changes in the heart. Chronic exercise induced by a treadmill-running programme (TRP) is considered a potential non-pharmacological treatment for hypertension and may have implications in heart remodelling. However, it is not known whether the TRP is able to improve the electrophysiological properties of the heart in spontaneously hypertensive rats (SHR). In the present study, we investigated whether TRP affects the electrical properties of left ventricular (LV) myocytes isolated from different layers of the LV wall of SHR. Male SHR were divided into exercised (chronic treadmill running for 8 weeks; CEX-SHR) and sedentary (SED-SHR) groups. Age-matched normotensive Wistar male rats served as controls. Action potentials (AP) and transient outward potassium current (I(to) ) were recorded in subepicardial (EPI) and subendocardial (ENDO) LV myocytes. In normotensive controls, AP duration (APD) was longer in ENDO cells than in EPI cells. This sort of transmural heterogeneity in the LV was not observed in sedentary SHR and was partially restored in SHR subject to chronic exercise. This partial recovery was associated with an increase in I(to) density in EPI cells but not in ENDO cells. The electrophysiological changes observed in the CEX-SHR group were not accompanied by either amelioration of systolic blood pressure or a reduction in heart hypertrophy. These findings imply that a TRP is able to improve the electrophysiological parameters of isolated cardiac myocytes in SHR. This sort of adaptation contributes to the overall improvement of heart physiology in this model.

摘要

高血压会导致心脏的电生理变化。跑步机运动方案(TRP)引起的慢性运动被认为是高血压的一种潜在非药物治疗方法,可能对心脏重构有影响。然而,目前尚不清楚 TRP 是否能够改善自发性高血压大鼠(SHR)心脏的电生理特性。在本研究中,我们研究了 TRP 是否会影响 SHR 左心室(LV)不同壁层分离的心肌细胞的电生理特性。雄性 SHR 分为运动(慢性跑步机运动 8 周;CEX-SHR)和不运动(SED-SHR)组。年龄匹配的正常血压 Wistar 雄性大鼠作为对照组。记录心外膜(EPI)和心内膜(ENDO)LV 心肌细胞的动作电位(AP)和瞬间外向钾电流(I(to))。在正常血压对照组中,ENDO 细胞的 AP 持续时间(APD)长于 EPI 细胞。这种 LV 的跨壁异质性在不运动的 SHR 中未观察到,在接受慢性运动的 SHR 中部分恢复。这种部分恢复与 EPI 细胞中 I(to)密度的增加有关,但与 ENDO 细胞无关。在 CEX-SHR 组观察到的电生理变化既没有伴随收缩压的改善,也没有伴随心脏肥大的减少。这些发现表明,TRP 能够改善 SHR 分离心肌细胞的电生理参数。这种适应有助于改善该模型的心脏生理学的整体状况。

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