Vasoplegia treatments: the past, the present, and the future.
Vasoplegia treatments: the past, the present, and the future.
复制标题
血管血管治疗：过去，现在和未来。
DOI：
10.1186/s13054-018-1967-3
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发表时间：
2018-02-27
期刊：
影响因子：
--
通讯作者：
Kimmoun A
中科院分区：
文献类型：
--
作者：
Levy B;Fritz C;Tahon E;Jacquot A;Auchet T;Kimmoun A
血管麻痹是所有晚期休克状态中普遍存在的现象，包括感染性休克、心源性休克、失血性休克和过敏性休克。其病理生理机制复杂，涉及血管平滑肌细胞G蛋白偶联受体脱敏(肾上腺素受体、加压素1受体、血管紧张素1型受体)、第二信使通路改变、危重疾病相关的皮质类固醇激素缺乏和一氧化氮生成增加等多种机制。这篇综述基于对文献的批判性评价，讨论了目前的主要治疗方法和未来的治疗方法。我们对这些机制的深入了解正在逐步改变我们对血管麻痹的治疗方法，从标准化治疗转变为个性化的多模式治疗，并开出几种血管加压剂的处方。虽然去甲肾上腺素已被确认为治疗血管麻痹的一线药物，但最新的幸存败血症运动指南也认为，血管对血管加压素低反应的最佳治疗方法可能是多种血管加压素的组合，包括去甲肾上腺素和早期处方的加压素。这种新的方法似乎是合理的，因为需要限制肾上腺素受体脱敏以及交感神经过度激活，因为它随后会对血流动力学和炎症产生有害影响。最后，基于新的病理生理学数据，两种潜在的药物--选择性加压素和血管紧张素II--目前正在评估中。
Vasoplegia is a ubiquitous phenomenon in all advanced shock states, including septic, cardiogenic, hemorrhagic, and anaphylactic shock. Its pathophysiology is complex, involving various mechanisms in vascular smooth muscle cells such as G protein-coupled receptor desensitization (adrenoceptors, vasopressin 1 receptors, angiotensin type 1 receptors), alteration of second messenger pathways, critical illness-related corticosteroid insufficiency, and increased production of nitric oxide. This review, based on a critical appraisal of the literature, discusses the main current treatments and future approaches. Our improved understanding of these mechanisms is progressively changing our therapeutic approach to vasoplegia from a standardized to a personalized multimodal treatment with the prescription of several vasopressors. While norepinephrine is confirmed as first line therapy for the treatment of vasoplegia, the latest Surviving Sepsis Campaign guidelines also consider that the best therapeutic management of vascular hyporesponsiveness to vasopressors could be a combination of multiple vasopressors, including norepinephrine and early prescription of vasopressin. This new approach is seemingly justified by the need to limit adrenoceptor desensitization as well as sympathetic overactivation given its subsequent deleterious impacts on hemodynamics and inflammation. Finally, based on new pathophysiological data, two potential drugs, selepressin and angiotensin II, are currently being evaluated.
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