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首页> 外文期刊>Current opinion in anaesthesiology >Inhibition of potassium channels in critical illness.
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Inhibition of potassium channels in critical illness.

机译：严重疾病中钾离子通道的抑制作用。

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PURPOSE OF REVIEW: The development of refractory arterial hypotension represents a significant problem in the treatment of critically ill patients, especially during sepsis. Increased activation of ATP-sensitive potassium channels in vascular smooth muscle cells is critically implicated in the pathophysiology of sepsis-induced vasodilation and vascular hyporesponsiveness to catecholamines. Pharmacological blockade of ATP-sensitive potassium channels has been proposed as a goal-directed therapeutic approach to stabilize hemodynamics in septic patients. RECENT FINDINGS: In different animal models of sepsis, ATP-sensitive potassium channel inhibition with intravenously infused sulfonylureas effectively reversed sepsis-induced systemic vasodilation and hypotension. Two recent clinical trials, however, failed to demonstrate beneficial effects of enterally administered glibenclamide on norepinephrine requirements and blood pressure in septic shock patients. Relevant problems related to ATP-sensitive potassium channel blockade with sulfonylureas in human septic shock include the route of administration (enteral versus intravenous) and the dose itself (benefit-risk relationship). In addition, significant adverse events may result from unspecific inhibition of nonvascular ATP-sensitive potassium channels. SUMMARY: Inhibition of ATP-sensitive potassium channels remains an attractive option to treat excessive vasodilation in the presence of systemic inflammation. Before this knowledge can be translated into clinical practice, however, future research is needed to define the role of ATP-sensitive potassium channels in critical illness and their specific inhibition in different tissues in more detail.
机译：审查的目的：难治性动脉低血压的发展代表着重症患者的治疗中的重大问题，尤其是在败血症期间。血管平滑肌细胞中ATP敏感性钾通道激活的增加与脓毒症诱导的血管舒张和儿茶酚胺的血管低反应性的病理生理密切相关。 ATP敏感性钾通道的药理学阻断已被提议作为一种稳定脓毒症患者血流动力学的目标治疗方法。最近的发现：在败血症的不同动物模型中，静脉内注入磺酰脲类药物对ATP敏感的钾通道抑制作用有效地逆转了败血症引起的全身性血管舒张和低血压。但是，最近的两项临床试验未能证明肠溶性格列本脲对败血性休克患者的去甲肾上腺素需求量和血压的有益作用。与人类败血性休克中的磺酰脲类药物对ATP敏感的钾离子通道阻滞有关的相关问题包括给药途径（肠内或静脉内）和剂量本身（受益风险关系）。此外，非血管性ATP敏感性钾通道的非特异性抑制可能导致严重的不良事件。简介：抑制ATP敏感性钾通道仍然是在存在全身性炎症时治疗过度血管舒张的有吸引力的选择。但是，在将这些知识转化为临床实践之前，需要进行进一步的研究以更详细地定义ATP敏感钾通道在危重疾病中的作用以及它们在不同组织中的特异性抑制作用。

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