HEAD INJURY CLINICAL RESEARCH CENTER

脑内白色物质弥漫性轴索损伤（DAI） 大脑半球和脑干，以及脑肿胀的组合 和局部缺血，似乎是死亡的主要原因， 头部受伤后残疾。 根据对脑血的研究 使用133-氙IV技术和脑血流测量 02代谢（CMR 02）我们现在有证据表明， 过度通气增加了昏迷患者的CMR 02， 代谢性酸中毒是急性颅脑损伤的常见表现 患者，过度换气可能会产生更有利的 昏迷状态下大脑代谢过程的环境 病人 我们还确定了CBF的重要性， CMR 02在脑损伤急性期的后续治疗 结果。 我们的非影响模型的数据分析 恒河猴和狒狒的加速损伤 证明了头部对方向的敏感性 角加速度引起的损坏。 同时，我们发现 DAI和滑翔的病理生理机制 挫伤可能类似。 我们建立了一个轴突模型 豚鼠视神经损伤，初步证据表明 这种损伤具有与DAI产生的损伤相同的形态学 灵长类动物和人类的大脑中。 我们现在有证据 细胞内钙离子浓度显著增加 浓度后，在鱿鱼巨大的轴突， 似乎与复苏有关。 缺血性损伤 下托和前齿可能是由额外的乳酸引起的 来自相邻第三节脑脊液中葡萄糖的酸 脑室 使用31 P和1H NMR技术，我们有证据表明， 阈值缺血，如乳酸盐增加所示， 磷酸肌酸水平，发生在灌注压为10- 20 mm Hg. 最后，我们开始了一系列新的核磁共振实验， 从氟清除曲线定量测定rCBF 含有化合物。 初步结果非常令人鼓舞。 的 清除率曲线是双指数的，看起来非常像133- 氙清除率曲线。

Diffuse axonal injury (DAI) in the white matter of the cerebral hemispheres and brainstem, and combinations of brain swelling and ischemia, appear to be the principal cause of death and disability after head injury. Based on studies of cerebral blood flow using 133-Xenon IV techniques and measurements of cerebral 02 metabolism (CMR02) we now have evidence that hyperventilation increases CMR02 in comatose patients and, since metabolic acidosis is a common finding in acute head injury patients, hyperventilation may create a more favorable environment for cerebral metabolic processes in the comatose patient. We have also established the importance of CBF and CMR02 in the acute phase of head injury for subsequent outcomes. Analysis of data from our model of nonimpact acceleration injury in the rhesus monkey and baboon has provided evidence that the head has a profound directional sensitivity to damage induced by angular acceleration. Also, we have found that the pathophysiological mechanisms of DAI and gliding contusions may be similar. We have developed a model of axonal injury in the guinea pig optic nerve and initial evidence indicates that such injury has the same morphology as that produced by DAI in whole primate brains and in humans. We now have evidence that there are marked increases in intracellular calcium ion concentration after stretch injuries in the squid giant axon which appear to be related to recovery. Ischemic injury to the subiculum and anterior dentate may be caused by additional lactic acid derived from glucose in the CSF of the adjacent 3rd ventricle. Using 31P and 1H NMR techniques we have evidence that threshold ischemia, as indicated by increased lactate and phosphocreatine levels, occurs at perfusion pressures of 10-20mm Hg. Finally, we have begun a new set of NMR experiments to quantitatively measure rCBF from clearance curves of flourine containing compounds. Initial results are very encouraging. The clearance curves are biexponential and look very much like 133- Xenon clearance curves.