首页> 美国卫生研究院文献>Physiological Reports >Stress hyperglycemia cardiac glucotoxicity and critically ill patient outcomes current clinical and pathophysiological evidence
【2h】

Stress hyperglycemia cardiac glucotoxicity and critically ill patient outcomes current clinical and pathophysiological evidence

机译:压力高血糖心脏葡萄糖毒性并且危重病人的患者结果发生了当前的临床和病理生理学证据

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Stress hyperglycemia is a transient increase in blood glucose during acute physiological stress in the absence of glucose homeostasis dysfunction. Its's presence has been described in critically ill patients who are subject to many physiological insults. In this regard, hyperglycemia and impaired glucose tolerance are also frequent in patients who are admitted to the intensive care unit for heart failure and cardiogenic shock. The hyperglycemia observed at the beginning of these cardiac disorders appears to be related to a variety of stress mechanisms. The release of major stress and steroid hormones, catecholamine overload, and glucagon all participate in generating a state of insulin resistance with increased hepatic glucose output and glycogen breakdown. In fact, the observed pathophysiological response, which appears to regulate a stress situation, is harmful because it induces mitochondrial impairment, oxidative stress‐related injury to cells, endothelial damage, and dysfunction of several cellular channels. Paradigms are now being challenged by growing evidence of a phenomenon called glucotoxicity, providing an explanation for the benefits of lowering glucose levels with insulin therapy in these patients. In the present review, the authors present the data published on cardiac glucotoxicity and discuss the benefits of lowering plasma glucose to improve heart function and to positively affect the course of critical illness.
机译:在没有葡萄糖稳态功能障碍的情况下,应激高血糖是急性生理胁迫期间血糖的瞬态增加。它的存在已经在批判性病患者中描述,受到许多生理侮辱的影响。在这方面,葡萄糖耐受性的高糖基因和受损的葡萄糖耐受性也频繁也频繁进入心力衰竭和心形成休克的重症监护病房。在这些心脏病紊乱开始时观察到的高血糖似乎与各种压力机制有关。主要压力和类固醇激素,儿茶酚胺过载和胰高血糖素的释放均参与产生胰岛素抵抗状态,肝葡萄糖产量和糖原崩溃增加。实际上,观察到的病理生理学反应似乎调节应激状况有害,因为它会诱导线粒体损伤,细胞,内皮损伤和几种细胞通道功能障碍的氧化应激损伤。目前,通过越来越多的证据表明含有葡氧毒性的现象,提供了对这些患者中胰岛素治疗的血糖水平的益处的益处来挑战。在本综述中,作者介绍了对心脏葡萄糖毒性发布的数据,并讨论降低血浆葡萄糖以改善心脏功能的益处,并积极影响危重疾病的过程。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号