脳浮腫における呼吸機構について

THE RESPIRATORY SYSTEM IN CEREBRAL EDEMA

Ｉ．はじめに

　脳浮腫は脳外科医が遭遇する重大な問題であり，それについての研究は形態学的^{3）14）15）18）21）24）27）32）39）40）40）45）47）51）54）56）57）61）62）}，組織化学的^{10）55）58）60）}，生理学的^{23）31）52）}ならびに生化学的^{6）20）25）34）36）37）38）46）}と，非常に多くみられる。しかしその病態生理はまだよくわかつていないというのが現状である。

　最近脳浮腫では，脳組織への水分増加とイオン類のアンバランスが問題となり，そのため生化学的領域で，細胞レベルにおけるエネルギー産生機序の障害が，イオン輸送の障害と結びつけて考えられるようになつてきた^{6）25）36）46）}。

Despite the clinical importance and intensitive studies by numerous investigators, the pathogenesis of cerebral edema is not adequately understood.

The present paper is concentrated on the oxida-tive phosphorylation or electron transport system to get profounder informations biochemically at the basis of cellular energy metabolism.

The depressed respiratory control, decreased P : O ratio and accelerated state 4 respiration of edema-tous brain mitochondria, brought the author to the spectrophotometric analysis of total content of each component of the electron transport system and their steady state reduction levels.

In cerebral edema, the total quantity of the cytochromes and nicotinamide adenine dinucleotide was within normal limits except a slight decrease in the cytochrome c, while the steady state reduction levels of the cytochromes were revealed to be decreased.

From the standpoint of partial electron transport of mitochondria themselves, the mitochondrial dis-order or damage in cerebral edema was suggested by the decreased rotenone or antimycin A sensitive NADH cytochrome c reductase, the depressed elec- tron transport from glutamate to NADH dehydro-genase, and the increased rotenone or antimycin A insensitive MADH cytochrome c reductase.

On the other hand, the succinate linked electron transport was not involved in cerebral edema in spite of affected NADH linked respiration. The content of the cytochrome b5 in cerebral microsomes was measured as a representative of the enzyme activity in the endoplasmic reticulum without any significant changes in cerebral edema.