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我々は脳外傷により発生する諸種病態生理解明の一端に資せんとして,生化学面より脳外傷時に於ける大脳高エネルギー燐酸量につき検討し,実験的脳外傷時,大脳ATP量の減少が起こる事を先に報告した1)2)。(尚ATPを含む脳外傷時に於ける炭水化物代謝を中心とせる神経化学的研究についても著者らを含む当教室の研究が先に報告されている3)。)
前報はN-HCl, 100℃,7分間の水解で遊離してくる燐(Δ7P)即ちacid-soluble phosphate のPが,ATPの3つの燐酸基中2つだけ切れたものとして算出してATP-Pとみなした4)もので正常ラット大脳のそれは58.6mg%であつた。しかるに水解後のP値はlabile ATP-P以外にオルト燐酸及びクレアチン燐酸を含む総和と考えられLindbergとErnster5)によれば第1表の如くである。斯くしてPを論ずるにはATP-Pのみならず,他燐酸化合物をも検する必要が生じて来る事になる。
Experiments were done to investigate the change of creatine phosphate (CP) content of rats brain in head injury and to analyse the effect of ATP and AMP on CP content.
Deteribination of CP was carried out ac-cording to the method described by Enorr & Rosenberg. The experiments yielded the following results:
1) Normal value of CP content of rats cerebral tissue was 1.63μ2M/g, this value was smaller than other workers'. It seemed that this decrease was due to decapitation.
2) Head injury produced a fall in the CP of rats brain, 68.5% fell in 10 sec. and 17.2 % fell in day after injury.
3) Injection of ATP or AMP in abdominal cavity both produced increase in CP content, however there was difference between beha-vior of effect of ATP and of AMP, namely ATP showed greater effect while AMP sho-wed longer effect.
4) Immediately after head injury, injec-tion of ATP or AMP in abdominal cavity both produced increase in CP content.
From this series of experiment, then it may be concluded:
1) ATP or AMP injected can act on brain itself.
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