DELAYED NEURONAL DEATH AND DELAYED NEURONAL RECOVERY IN THE HUMAN BRAIN FOLLOWING GLOBAL-ISCHEMIA
DELAYED NEURONAL DEATH AND DELAYED NEURONAL RECOVERY IN THE HUMAN BRAIN FOLLOWING GLOBAL-ISCHEMIA
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DOI：
10.1007/bf00304636
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发表时间：
1992-12-01
影响因子：
12.7
通讯作者：
SCHLOTE, W
中科院分区：
文献类型：
--
作者：
HORN, M;SCHLOTE, W
延迟海马死亡作为脑缺血后治疗的一个治疗窗口的理解，导致了大量的调查集中在沙鼠和大鼠的潜在细胞机制和药理学潜力。尽管如此。关于人脑中迟发性神经元死亡发生的研究是单一的，并且仅涉及少量患者。为了补充这些有限的数据，本研究纳入了26例有单次心脏骤停病史的成人患者。成功复苏后，个体存活时间范围为不到1小时至186天（xBAR = 11天）。海马CA1区，浦肯野细胞之间，或在额叶新皮层，分别所产生的缺血性损伤的严重程度，通过直接计数的坏死神经元进行定量。此外，海马标本进行神经元特异性烯醇化酶免疫染色。所获得的数据表明，在人类海马迟发性神经元死亡的发生，并在一个较小的形式，在小脑浦肯野细胞。这与新皮质中缺血性神经元坏死的直接表现形成对比。与之前在实验动物和人类中的发现不同，CA1细胞死亡的延迟可以定义为心脏骤停后持续约7天。此外，免疫组化结果表明，延迟神经元恢复在CA 1，这在时间过程中，海马神经元死亡的延迟表现相对应。对结果的解释必须考虑缺乏关于心脏骤停和复苏的确切个体持续时间的信息，以及缺少关于缺血前生理变量的数据。
The understanding of delayed hippocampal death as a therapeutic window for post-ischemic treatment of the brain has led to numerous investigations focusing upon underlying cellular mechanisms and pharmacological potentials in gerbils and rats. Nevertheless. studies on the occurrence of delayed neuronal death in the human brain have been singular and dealt with only small files of patients. To complement these limited data, in the present study 26 adult patients with a history of a single cardiac arrest were included. Following successful resuscitation, individual survival ranged from less than 1 h to 186 days (xBAR = 11 days). The severity of the resultant ischemic injury in hippocampus CA1, among Purkinje cells, or in frontal neocortex, respectively, was quantified by direct counting of necrotic neurons. Additionally, hippocampal specimens were immuno-stained for neuron-specific enolase. The data obtained demonstrate the occurrence of delayed neuronal death in human hippocampus and, in a minor form, in cerebellar Purkinje cells. This is in contrasts to the immediate manifestation of ischemic neuronal necrosis in the neocortex. Unlike previous findings in experimental animals and in humans, the delay of CA1 cell death could be defined as lasting about 7 days following cardiac arrest. Moreover, the immunohistochemical results indicate delayed neuronal recovery in CA1, which in the time course reciprocally corresponds to delayed manifestation of hippocampal neuronal death. Interpretation of the results must consider the lack of information about the exact individual duration of cardiac arrest and resuscitation, as well as missing data concerning pre-ischemic physiological variables.