Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock, the most common form of vasodilatory shock, is a subset of sepsis in which circulatory and cellular/metabolic abnormalities are severe enough to increase mortality. Inflammatory shock constitutes the hallmark of sepsis, but also a final common pathway of any form of severe long-term tissue hypoperfusion. The pathogenesis of inflammatory shock seems to be due to circulating substances released by pathogens (e.g., bacterial endotoxins) and host immuno-inflammatory responses (e.g., changes in the production of histamine, bradykinin, serotonin, nitric oxide [NO], reactive nitrogen and oxygen species, and arachidonic acid [AA]-derived eicosanoids mainly through NO synthase, cyclooxygenase, and cytochrome P450 [CYP] pathways, and proinflammatory cytokine formation). Therefore, refractory hypotension to vasoconstrictors with end-organ hypoperfusion is a life threatening feature of inflammatory shock. This review summarizes the current knowledge regarding the role of eicosanoids derived from CYP pathway of AA in animal models of inflammatory shock syndromes with an emphasis on septic shock in addition to potential therapeutic strategies targeting specific CYP isoforms responsible for proinflammatory/anti-inflammatory mediator production.

中文翻译：

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类花生酸来源于花生四烯酸和炎性休克的细胞色素P450途径。

败血症是由宿主对感染的反应失调引起的威胁生命的器官功能障碍。败血性休克是血管舒张性休克的最常见形式，是脓毒症的一个子集，其中循环系统和细胞/代谢异常严重至足以增加死亡率。炎性休克是败血症的标志，也是任何形式的长期严重组织低灌注的最终共同途径。炎性休克的发病机制似乎是由于病原体释放的循环物质（例如细菌内毒素）和宿主的免疫炎症反应（例如组胺，缓激肽，5-羟色胺，一氧化氮[NO]，反应性氮和氧物种和花生四烯酸[AA]衍生的类花生酸主要通过NO合酶，环加氧酶和细胞色素P450 [CYP]途径产生，和促炎性细胞因子的形成）。因此，难治性低血压伴终末器官灌注不足的血管收缩药是威胁生命的炎症性休克特征。这篇综述总结了关于从AA的CYP途径衍生的类花生酸在炎性休克综合症动物模型中的作用的当前知识，除了针对负责促炎性/抗炎性介质产生的特定CYP亚型的潜在治疗策略外，还着重于败血性休克。