DYNAMIC CHANGES IN CEREBRAL OXYGENATION IN CHEMICALLY-INDUCED SEIZURES IN RATS - STUDY BY NEAR-INFRARED SPECTROPHOTOMETRY
DYNAMIC CHANGES IN CEREBRAL OXYGENATION IN CHEMICALLY-INDUCED SEIZURES IN RATS - STUDY BY NEAR-INFRARED SPECTROPHOTOMETRY
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DOI：
10.1016/0006-8993(93)91240-s
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发表时间：
1993-02-19
期刊：
影响因子：
2.9
通讯作者：
TAMURA, M
中科院分区：
文献类型：
--
作者：
HOSHI, Y;TAMURA, M
使用近红外分光光度法，在化学诱导癫痫发作期间和之后原位测量大鼠大脑中细胞色素氧化酶中铜的氧化还原状态和血红蛋白氧合状态。在脑电图（EEG）显示去同步之前，给予戊四唑（PTZ）导致大脑中细胞色素氧化酶部分减少，然后血压升高并伴随脑血容量增加。当血压达到最大值时，脑电图上出现阵发性尖峰，细胞色素氧化酶被重新氧化达到初始氧化水平，在发作前细胞色素氧化酶出现快速、短暂的减少。在整个癫痫发作期间，血红蛋白的含氧量比给药前更高。在发作后期，细胞色素氧化酶再次部分减少，而血压仍然很高，血红蛋白的氧合程度比最初更高。在发作后期第二次施用 PTZ 诱导了与第一次施用后观察到的相同反应。通过降低癫痫发作期间吸入气体中的氧气浓度，细胞色素氧化酶比非癫痫大鼠减少更多，并且观察到尖峰活性，直到约 85% 的细胞色素氧化酶减少。发作前细胞色素氧化酶减少所反映的短暂性脑缺氧可能是脑血流量增加的触发因素，而不是自主神经反应延迟的结果。在发作后期观察到的细胞色素氧化酶的第二次减少可能是由于癫痫发作期间打开的持久动静脉分流所致。这些结果复兴了细胞缺氧导致癫痫性脑损伤的经典理论。
Using near-infrared spectrophotometry, the redox state of copper in cytochrome oxidase, and the hemoglobin oxygenation state were measured in the rat brain in situ during and after chemically induced seizures. Pentylentetrazol (PTZ) administration caused the partial reduction of cytochrome oxidase in the brain just before the electroencephalogram (EEG) showed desynchronization, and then blood pressure was elevated concomitantly with an increase in cerebral blood volume. When blood pressure reached a maximum, bursts of spikes appeared on the EEG and cytochrome oxidase was reoxidized to reach the initial oxidation level, giving a rapid, transient reduction of cytochrome oxidase in the preictal period. Hemoglobin was more oxygenated than before the administration throughout the seizure. In the late postictal phase, cytochrome oxidase was partially reduced again, while blood pressure remained high and hemoglobin was more oxygenated than initially. The second administration of PTZ in the late postictal phase induced the same responses as observed after the first administration. By decreasing oxygen concentrations in the inspired gas during the seizure, cytochromre oxidase was more reduced than in the non-epileptic rat, and spike activity was observed until about 85% of cytochrome oxidase was reduced. The transient cerebral hypoxia reflected by the reduction of cytochrome oxidase in the preictal period may be a trigger for an increase in cerebral blood flow rather than the result of a delayed autonomic response. The second reduction of cytochrome oxidase observed in the late postictal phase may be due to a lasting arterio-venous shunt that opens during seizures. These results revive the classical theory that cellular hypoxia is responsible for epileptic brain damage.