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过劳性恶性心律失常可能导致过劳死。

Karoshi May Be a Consequence of Overwork-Related Malignant Arrhythmia.

机构信息

School of Forensic Medicine, Southern Medical University, Guangzhou, Guangdong, China (mainland).

Department of Orthopedics, Yiling Hospital of Yichang, Yichang, Hubei, China (mainland).

出版信息

Med Sci Monit. 2019 Jan 12;25:357-364. doi: 10.12659/MSM.911685.

Abstract

BACKGROUND Karoshi, which is sudden death associated with overwork, has become a serious problem in China. Many studies have examined the relationship between cardiovascular risks and karoshi, but there is little evidence that explains the exact mechanism by which overwork induces sudden death. In these cases, there are few obvious positive findings from forensic autopsies except for histories of overwork prior to death. Therefore, we assume that abnormalities, such as cardiac arrhythmia, rather than organic changes are the cause of karoshi. MATERIAL AND METHODS In the present study, the forced swim test (FST) was used to establish models of overwork. The myocardial tissues of SD rats taking FST (1 h per day, for 30 consecutive days) were collected. The arrhythmia-related molecule CX43 as well as its upstream regulation molecule Cav-1 and cSrc were tested by Western blot (WB) and immunohistochemistry (IHC). HE staining and Masson's staining were performed in the myocardium tissue section. RESULTS We observed downregulation of caveolin-1 (Cav1) followed by cSrc activation, resulting in the decrease of connexin43 (Cx43) levels in overwork models. Myocardial interstitial fibrosis, which is associated with electrophysiological aberrances that result in arrhythmia, was also found in the overwork models. CONCLUSIONS These data provide a mechanistic explanation for the speculated link between karoshi and cardiac arrhythmias.

摘要

背景

过劳死,即与过度工作相关的猝死,已成为中国的一个严重问题。许多研究已经探讨了心血管风险与过劳死之间的关系,但几乎没有证据能够解释过度工作导致猝死的确切机制。在这些情况下,除了死亡前有过度工作的病史外,法医尸检很少有明显的阳性发现。因此,我们假设心律失常等异常,而不是器质性变化,是导致过劳死的原因。

材料和方法

在本研究中,使用强迫游泳试验(FST)来建立过度工作模型。收集接受 FST(每天 1 小时,连续 30 天)的 SD 大鼠的心肌组织。通过 Western blot(WB)和免疫组织化学(IHC)检测心律失常相关分子 CX43 及其上游调节分子 Cav-1 和 cSrc。对心肌组织切片进行 HE 染色和 Masson 染色。

结果

我们观察到 Cav1 下调,随后 cSrc 激活,导致过度工作模型中连接蛋白 43(Cx43)水平降低。还发现过度工作模型中有心肌间质纤维化,这与导致心律失常的电生理异常有关。

结论

这些数据为推测的过劳死与心律失常之间的联系提供了机制解释。

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