脳損傷における糖質代謝に関する組織化学的観察

Histochemical Observation on Carbohydrate Metabolism in Brain Injury

I．はじめに

　最近の組織化学の進歩はめざましいものがあり，脳の代謝とか，機能の解明にも幾多の貢献がなされてきた。さて，脳がその機能を正常に維持するためのエネルギーの大部分は糖質より得ていることは周知の事実である。すなわち，グルコース，あるいはグリコーゲンは嫌気的状態のもとでEmbden-Meyerhof pathwayによつてピルビン酸（または乳酸）となり，さらに好気的にKrebsのTCA cycleを経て，CO₂とH₂Oに分解され，そのさいに得られた高エネルギー燐酸化合物が各種の神経作用に利用されている^{17）19）29）}。

　一方Warburg-Dickensのhexose-monophosphateshuntも明らかに存在する^9）16）。その意義はかならずしも明らかではないが，TPNH産生系として，核酸などの重要な物質の合成に必要であるとされている^2）18）。

Histochemical observations were made for gly-cogen, nucleic acid and several enzymes related to carbohydrate metabolism in unilateral anoxic-ische-mic brain injury of rat, produced as described by Levine, S. and in human peritumoral brain injury.

Generally the severe neuronal lesions showed re-duction or loss of glycogen, nucleic acid and every enzyme activity, but within a certain threshold of damage intensity abnormal deposition of glycogen granules was demonstrated in glial cells (predomi-nantly reactive astrocytes). These glial cells showed marked increase in phosphorylase and glucose-6-phosphate dehydrogenase activities with plenty of nucleic acid.

Under the same condition glycogen accumulation was never seen in neurons, in spite of the increase in phosphorylase and glucose-6-phosphate dehydro-genase activities and the increase staining with gal-locyanin.

Fructose-1, 6-diphosphate aldoase and succinate dehydrogenase were characterized generally by re-duction in their activities in lesions.

From the present results it is suggested that the characteristic change of glucose-6-phosphate de-hydrogenase activity can be used as one of the in-dexes for vulnerability of neurons by anoxia or ischemia and that the hexose-monophosphate shunt in carbohydrate metabolism plays the most impor-tant part in resistance against and repair from pathological conditions.