Suppr超能文献

致心律失常性脂质代谢产物对糖尿病和非糖尿病大鼠心脏L型钙电流的影响。

Effects of arrhythmogenic lipid metabolites on the L-type calcium current of diabetic vs. non-diabetic rat hearts.

作者信息

Ziolo M T, Sondgeroth K L, Harshbarger C H, Smith J M, Wahler G M

机构信息

Department of Physiology, Midwestern University, Downers Grove, IL 60515, USA.

出版信息

Mol Cell Biochem. 2001 Apr;220(1-2):169-75. doi: 10.1023/a:1010992900387.

Abstract

Accumulation of lipid metabolites, such as palmitoylcarnitine and lysophosphatidylcholine, is thought to be a major contributor to the development of cardiac arrhythmias during myocardial ischemia. This arrhythmogenicity is likely due to the effects of these metabolites on various ion channels. Diabetic hearts have been shown to accumulate much higher concentrations of these lipid metabolites during ischemia, which may be an important factor in the enhanced incidence of arrhythmias in diabetic hearts. However, it is not known whether these metabolites have similar effects on the ion channels of diabetic hearts as in non-diabetic hearts. Previous studies on myocytes from non-diabetic hearts have reported either enhancement or inhibition of L-type calcium current (I(Ca)) by these lipid metabolites. Thus, it is not clear whether the effects of palmitoylcarnitine and/or lysophosphatidlycholine on I(Ca) contribute to the enhanced arrhythmogenicity of diabetic hearts or protect against arrhythmias. We determined the effect of exogenous palmitoylcarnitine and lysophosphatidylcholine on the (I(Ca)) in ventricular myocytes from streptozotocin-diabetic and non-diabetic rat hearts under identical conditions. We found that palmitoylcarnitine and lysophosphatidylcholine exhibited a dose-dependent inhibition of I(Ca), which was virtually identical in diabetic and non-diabetic cardiac myocytes. Thus, we conclude that these arrhythmogenic lipid metabolites have similar actions on calcium channels in diabetic and non-diabetic hearts. Therefore, the greater susceptibility of diabetic hearts to arrhythmias during myocardial ischemia is not due to an altered sensitivity of the L-type calcium channels to lipid metabolites, but may be explained, in large part, by the greater accumulation of these metabolites during ischemia.

摘要

脂质代谢产物如棕榈酰肉碱和溶血磷脂酰胆碱的积累被认为是心肌缺血期间心律失常发生的主要原因。这种致心律失常性可能是由于这些代谢产物对各种离子通道的影响。研究表明,糖尿病心脏在缺血期间会积累更高浓度的这些脂质代谢产物,这可能是糖尿病心脏心律失常发生率增加的一个重要因素。然而,尚不清楚这些代谢产物对糖尿病心脏离子通道的影响是否与非糖尿病心脏相似。先前对非糖尿病心脏心肌细胞的研究报告称,这些脂质代谢产物可增强或抑制L型钙电流(I(Ca))。因此,尚不清楚棕榈酰肉碱和/或溶血磷脂酰胆碱对I(Ca)的影响是导致糖尿病心脏致心律失常性增强还是预防心律失常。我们在相同条件下测定了外源性棕榈酰肉碱和溶血磷脂酰胆碱对链脲佐菌素诱导的糖尿病大鼠和非糖尿病大鼠心室肌细胞中I(Ca)的影响。我们发现棕榈酰肉碱和溶血磷脂酰胆碱对I(Ca)表现出剂量依赖性抑制,这在糖尿病和非糖尿病心肌细胞中几乎相同。因此,我们得出结论,这些致心律失常的脂质代谢产物对糖尿病和非糖尿病心脏的钙通道具有相似的作用。因此,糖尿病心脏在心肌缺血期间对心律失常的易感性增加并非由于L型钙通道对脂质代谢产物的敏感性改变,而在很大程度上可能是由于这些代谢产物在缺血期间积累更多所致。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验