Wahab Fazal, Atika Bibi, Oliveira-Pelegrin Gabriela Ravanelli, Rocha Maria José Alves
Department of Morphology, Physiology and Basic Pathology, FORP, University of Sao Paulo Campus de Ribeirao Preto, Avenida do Cafe s/n, Monte Alegre, CEP 14040-904 Ribeirao Preto, São Paulo, Brazil.
Endocr Metab Immune Disord Drug Targets. 2013 Dec;13(4):335-47. doi: 10.2174/1871530313666131211120723.
Sepsis is a fatal systemic inflammatory disease. It is caused by an immune system inflammatory response to the entry of microorganisms or their products into the blood circulatory system. The pathophysiological mechanisms of sepsis are still poorly understood. The presence of microorganisms in the systemic circulation causes activation of the immune system, which in turn leads to a robust release of inflammatory cytokines. These inflammatory cytokines result in alterations across all important physiological systems, including the neuroendocrine system. Neuroendocrine responses differ between the acute and the late phase of sepsis. In the acute phase there are robust alterations in the secretion of neuroendocrine hormones in response to body demand. In the late phase, the plasma concentrations of some hormones remain low, despite heavy systemic demand, whereas several others increase despite of diminished needs. In this review, we give a brief overview on sepsis-induced major alterations in neuroendocrine secretions, and summarize current knowledge about mechanisms and targets for their treatment.
脓毒症是一种致命的全身性炎症性疾病。它是由免疫系统对微生物或其产物进入血液循环系统的炎症反应所引起的。脓毒症的病理生理机制仍未被充分了解。全身循环中微生物的存在会导致免疫系统激活，进而引发炎症细胞因子的大量释放。这些炎症细胞因子会导致所有重要生理系统发生改变，包括神经内分泌系统。脓毒症急性期和晚期的神经内分泌反应有所不同。在急性期，神经内分泌激素的分泌会因身体需求而发生显著改变。在晚期，尽管全身需求强烈，但某些激素的血浆浓度仍保持较低水平，而其他几种激素尽管需求减少却有所增加。在本综述中，我们简要概述了脓毒症引起的神经内分泌分泌的主要变化，并总结了目前关于其治疗机制和靶点的知识。
