HEAD INJURY CLINICAL RESEARCH CENTER

头部损伤临床研究中心

• 批准号: 3099313
• 负责人: THOMAS A GENNARELLI
• 金额: $ 20.13万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 1976
• 资助国家: 美国
• 起止时间: 1976-08-01 至 1991-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3099313
• 关键词: brain injury; head /neck injury

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.

脑白质弥漫性轴索损伤 大脑半球和脑干，以及脑肿胀的组合 和缺血，似乎是死亡的主要原因 头部损伤后的残疾。基于对脑血的研究 应用~(133)Xe~(4+)技术测量脑血流 新陈代谢(CMR02)我们现在有证据表明 过度换气会增加昏迷患者的CMR02，因为 代谢性酸中毒是急性颅脑损伤的常见表现 对患者来说，过度换气可能会创造更有利的 昏迷状态下脑代谢过程的环境 有耐心的。我们还确定了CBF和 CMR02在颅脑损伤急性期为后续 结果。对我们的非碰撞模型的数据进行分析 恒河猴和狒狒的加速损伤提供了 有证据表明头部对 角加速度引起的损伤。另外，我们还发现 DAI和滑行的病理生理机制 挫伤可能是相似的。我们开发了一个轴突模型 豚鼠视神经损伤和初步证据表明 这种损伤与戴所造成的损伤具有相同的形态 在整个灵长类动物的大脑和人类中。我们现在有证据 细胞内钙离子显著增加 拉伸损伤后鱿鱼巨大轴突中的浓度 似乎与康复有关。脑缺血损伤 下丘和前齿状核可能是由额外的乳酸引起的 邻近第3天的脑脊液中葡萄糖衍生的酸 脑室。使用31P和1H核磁共振技术，我们有证据 门槛缺血，表现为乳酸和 磷酸肌酸水平，出现在灌流压力为10-20 mm时 HG。最后，我们已经开始了一系列新的核磁共振实验 从氟的清除曲线定量测定rCBF 含有化合物的。初步结果非常令人鼓舞。这个 间隙曲线是双指数的，看起来很像133- 氙气清除曲线。