Trarable ischemic neuronal damage

蒙古兔短暂性脑缺血对海马产生选择性神经元损伤。沙鼠在贫血后立即给予普妥巴比妥、地氮西泮或尼佐tenone。治疗组CA1区神经元密度显著增加。然而，当给药时间延迟超过15分钟时，没有发现明显的影响。选择性缺血易损的机制尚不完全清楚。采用小脑缺血实验，比较其与海马的病理变化。%的小脑浦肯野细胞在压迫性缺血10 min后出现了缺血性细胞损伤。然而，这种变化比海马体的变化要快得多。潜在的机制似乎有所不同。局灶性脑缺血在临床上更为常见。为了研究局灶性缺血时神经元的可逆性，我们对大鼠进行了永久性的单侧大脑中动脉闭塞。在缺血区，可以注意到梗死的快速进展，而在海马体中所见的缓慢进程未被识别。另一方面，在大脑的远端区域，如丘脑和黑质，观察到缓慢而深刻的形态变化。目前正在研究大鼠短暂局灶性脑缺血，以检查短暂局灶性脑缺血后可逆神经元改变的可能性。

Brier transient forbrain ischemia in to Mongolian gearbil produces a selective neuronal damage in the hippocampus. Immeciately follwing ishemia, prentobarbvtal,diazapem, or nizotenone were given in gerbils. The neuronal density in the CA1 sector showed a significant inforease in the treated goups. when froug administration was delayed fro longer than 15 minutes, however, no definite eccets were found. The mechanism of selective vulnerability of ischemia is not fully understood. An experiment of cerbellar ischemia was done in order to compare thr pathological change with that og thr hippocampus. %cerebella purkinje cells showed ishiemic cell damage following 10 min of comression ischemia. The alteration was, however, much faster than taht in the hippocampus. The underlying mechanism seems to be different. Focal cetebral ischiemia is more frequently sdeen in clinical case. To tsudy the reversibility of neurons in focal ischema, rats were subjected to permanent unilatearal middle cerebral artery occtusion. In ischemic region, rapid prograssion in infaction was noticed and slow process as is seen in the hippocampus was not recognized. On the other hand, in the distant areas of the brain, such as the thalamus, and substntia nigra, a slow buyt proufnd morphological changes were obsearved. Transizent focal cerebral ischemia in the rat is now being studeid in order to examine the possibility of reversible neuronal change following brief focal ischemia.