Willmore L J, Triggs W J
Department of Neurology, University of Texas Medical School, Houston 77030.
Int J Dev Neurosci. 1991;9(2):175-80. doi: 10.1016/0736-5748(91)90009-b.
Head trauma with cerebral contusion causes extravasation of red blood cells, followed by hemolysis and deposition of iron-containing blood products within the neuropil. Liberation of heme compounds is associated with deposition of hemosiderin, and with gliosis, neuronal loss and occasionally the development of seizures. In this experiment we injected components of red blood cell contents into rat amygdala, and then measured the rate of appearance of products of lipid peroxidation. Injection of microliter volumes of hemin and hemoglobin, with hematoprotoporphyrin and rodent plasma injection and contralateral uninjected tissue as controls, showed that the presence of the iron moiety within the protoporphyrin ring was required to initiate and propagate peroxidation. Free radical reactions initiated by iron or heme deposited within the neuropil may be a fundamental reaction associated with brain injury responses, and possibly with posttraumatic epileptogenesis.
伴有脑挫伤的头部创伤会导致红细胞外渗，随后发生溶血以及含铁血液产物在神经纤维网内沉积。血红素化合物的释放与含铁血黄素的沉积、神经胶质增生、神经元丢失以及偶尔的癫痫发作有关。在本实验中，我们将红细胞内容物的成分注入大鼠杏仁核，然后测量脂质过氧化产物的出现速率。注射微升体积的血红素和血红蛋白，并以血卟啉原和啮齿动物血浆注射以及对侧未注射组织作为对照，结果表明原卟啉环内铁部分的存在是引发和传播过氧化作用所必需的。由沉积在神经纤维网内的铁或血红素引发的自由基反应可能是与脑损伤反应相关的基本反应，并且可能与创伤后癫痫发生有关。
