Tracey K J
Division of Neurosurgery, New York Hospital-Cornell Medical Center, NY 10021.
Circ Shock. 1991 Oct;35(2):123-8.
The high mortality of septic shock syndrome has prompted extensive investigation into its pathogenesis. Tumor necrosis factor (TNF), a cytokine that is often over-produced during Gram-negative or Gram-positive infection, occupies a critical role in triggering this catastrophic illness. The net effects of TNF are dependent upon its concentration in certain vital tissues, and may be dissociated from the presence of the invading pathogens. Agents that inhibit TNF have been developed; these protect against shock and tissue injury and are currently being investigated in clinical trials of septic shock syndrome.
脓毒性休克综合征的高死亡率促使人们对其发病机制进行广泛研究。肿瘤坏死因子（TNF）是一种在革兰氏阴性或革兰氏阳性感染期间经常过度产生的细胞因子，在引发这种灾难性疾病中起关键作用。TNF的净效应取决于其在某些重要组织中的浓度，并且可能与入侵病原体的存在无关。已经开发出抑制TNF的药物；这些药物可预防休克和组织损伤，目前正在脓毒性休克综合征的临床试验中进行研究。
