艾司洛尔在脓毒症诱导的心功能障碍中应用的研究进展

Research progress of esmolol in sepsis-induced myocardial dysfunction

适当的炎症反应有助于机体抵抗感染,但过度激活或持续时间过长的炎症反应可危及生命。新的脓毒症3.0对脓毒症定义突出了感染和器官功能障碍,其中脓毒症诱导的心功能障碍通常是脓毒症患者死亡的最后一步。脓毒症时大量儿茶酚胺可以介导包括高分解代谢状态、炎症反应、氧化应激、钙离子超载等在内的心肌细胞毒性作用,进而导致心肌细胞损伤、凋亡甚至坏死。脓毒性超肾上腺素能驱动导致持续性心动过速、心肌氧供需失衡、心脏舒张期明显缩短,造成心肌缺血损伤、组织灌注不足。β受体阻滞治疗可通过阻断高儿茶酚胺的细胞毒性作用、降低心率、改善心肌氧供、抑制炎症反应、抑制心肌细胞凋亡、改善β受体敏感性等作用治疗脓毒症心功能障碍。尤其以超短效选择性β1受体阻滞剂艾司洛尔在基础研究及临床中应用广泛,本研究综述艾司洛尔在脓毒症诱导的心功能障碍中作用的研究进展。

Proper inflammatory response helps the body resist infection, but excessive activation or prolonged inflammatory response is often dangerous to the body. The definition of sepsis in the new Sepsis 3.0 highlights the two characteristics of infection and organ dysfunction. Sepsis-induced myocardial dysfunction(SIMD) is usually the last step in the death of patients with sepsis. During sepsis, a large amount of catecholamines can mediate myocardial cytotoxicity including high catabolic state, inflammatory response, oxidative stress, calcium overload, etc., and then cause myocardial cell damage, apoptosis and even necrosis. Septic hyperadrenergic drive leads to persistent tachycardia, imbalance of myocardial oxygen supply and demand, significantly shortened diastolic phase, myocardial ischemic injury, and insufficient tissue perfusion. β-blocker therapy can treat septic cardiac dysfunction by blocking the cytotoxic effects of high catecholamines, reducing heart rate,improving myocardial oxygen supply, suppressing inflammatory responses, inhibiting myocardial cell apoptosis and improving beta-receptor sensitivity. Esmolol is an ultra-short-acting selective β1 receptor blocker widely used in basic research and clinical applications. This article reviewed the research progress of the role of esmolol in SIMD.