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血管扩张性休克的定义和病理生理学。

Definitions and pathophysiology of vasoplegic shock.

机构信息

University of Cambridge, Cambridge, UK.

Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK.

出版信息

Crit Care. 2018 Jul 6;22(1):174. doi: 10.1186/s13054-018-2102-1.

Abstract

Vasoplegia is the syndrome of pathological low systemic vascular resistance, the dominant clinical feature of which is reduced blood pressure in the presence of a normal or raised cardiac output. The vasoplegic syndrome is encountered in many clinical scenarios, including septic shock, post-cardiac bypass and after surgery, burns and trauma, but despite this, uniform clinical definitions are lacking, which renders translational research in this area challenging. We discuss the role of vasoplegia in these contexts and the criteria that are used to describe it are discussed. Intrinsic processes which may drive vasoplegia, such as nitric oxide, prostanoids, endothelin-1, hydrogen sulphide and reactive oxygen species production, are reviewed and potential for therapeutic intervention explored. Extrinsic drivers, including those mediated by glucocorticoid, catecholamine and vasopressin responsiveness of the blood vessels, are also discussed. The optimum balance between maintaining adequate systemic vascular resistance against the potentially deleterious effects of treatment with catecholamines is as yet unclear, but development of novel vasoactive agents may facilitate greater understanding of the role of the differing pathways in the development of vasoplegia. In turn, this may provide insights into the best way to care for patients with this common, multifactorial condition.

摘要

血管麻痹综合征是一种病理性低全身血管阻力的综合征,其主要临床特征是在正常或升高的心输出量的情况下出现血压降低。该血管麻痹综合征在许多临床情况下都会出现,包括感染性休克、心脏搭桥手术后和手术后、烧伤和创伤,但尽管如此,缺乏统一的临床定义,这使得该领域的转化研究具有挑战性。我们讨论了血管麻痹综合征在这些情况下的作用,并讨论了用于描述它的标准。我们还回顾了可能导致血管麻痹的内在过程,如一氧化氮、前列腺素、内皮素-1、硫化氢和活性氧物质的产生,并探讨了潜在的治疗干预措施。还讨论了包括糖皮质激素、儿茶酚胺和血管加压素对血管反应性介导的外在驱动因素。在维持足够的全身血管阻力与儿茶酚胺治疗的潜在有害影响之间取得最佳平衡尚不清楚,但新型血管活性药物的开发可能有助于更好地了解血管麻痹发展过程中不同途径的作用。反过来,这可能为治疗这种常见的多因素疾病提供最佳方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/757f/6035427/b82250e14ed5/13054_2018_2102_Fig1_HTML.jpg

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