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体温过低诱导的复极后不应期是冬眠和活跃状态的黄鼠(Citellus undulatus)心房肌对生物电活动紊乱具有耐受性的原因。

Hypothermia-Induced Postrepolarization Refractoriness Is the Reason of the Atrial Myocardium Tolerance to the Bioelectrical Activity Disorders in the Hibernating and Active Ground Squirrel Citellus undulatus.

作者信息

Kuzmin V S, Abramov A A, Egorov Yu V, Rosenshtraukh L V

机构信息

Institute of Experimental Cardiology, Russian Research and Production Cardiological Complex, Ministry of Health, 121552, Moscow, Russia.

出版信息

Dokl Biol Sci. 2019 May;486(1):63-68. doi: 10.1134/S0012496619030050. Epub 2019 Jul 17.

Abstract

The electrophysiological mechanism of the atrial myocardium resistance to the cold-induced arrhythmias was studied in the hibernating ground squirrel Citellus undulatus. The atrial action potentials (APs) and refractoriness were recorded with microelectrodes in isolated multicellular preparations of the atrial myocardium taken from the hibernating and summer active ground squirrels (HS and SAS, respectively) at 37, 27, and 17°С to estimate the AP and refractoriness durations. In both HS and SAS, hypothermia increased the duration of the AP and refractoriness period (APD and RD, respectively), and in both animal groups RD was longer than APD under hypothermia but not at 37°С. This last observation can be a result of the postrepolarization refractoriness (PRR), which seems to contribute substantially to the atrial myocardium tolerance of the hibernating animals to the hypothermia-induced arrhythmias because it prevents afterdepolarizations.

摘要

在冬眠的黄鼠(Citellus undulatus)中研究了心房肌对冷诱导心律失常的电生理机制。在37℃、27℃和17℃下,用微电极记录从冬眠和夏季活跃的黄鼠(分别为HS和SAS)分离的多细胞心房肌制备物中的心房动作电位(AP)和不应期,以估计AP和不应期的持续时间。在HS和SAS中,体温过低均增加了AP和不应期(分别为APD和RD)的持续时间,并且在两个动物组中,低温下RD均长于APD,但在37℃时并非如此。这一最后的观察结果可能是复极化后不应期(PRR)的结果,PRR似乎对冬眠动物心房肌对低温诱导心律失常的耐受性有很大贡献,因为它可防止后去极化。

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