Debons A F, Krimsky I, From A, Siclari E
J Pathol. 1979 Oct;129(2):83-90. doi: 10.1002/path.1711290206.
Agents that lower serotonin levels or inhibit serotonin action prevent GTG-indurea and that such damage leads to abnormally increased capillary permeability. Since the VMH is rich in serotonin and since serotonin is a potent oedema-producing agent mice, these findings indicate that the production of necrosis by GTG is mediated by release of serotonin from the damaged pericapillary processes.
降低血清素水平或抑制血清素作用的药物可预防胍乙啶诱导的尿素生成,且这种损伤会导致毛细血管通透性异常增加。由于室旁核富含血清素,且血清素是一种能在小鼠体内产生水肿的强效物质,这些发现表明胍乙啶导致的坏死是由受损毛细血管周围突起释放血清素介导的。