腫瘍性脳浮腫に対するdexamethasoneの効果—局所脳血流量および局所脳グルコース利用率の変化

EFFECT OF DEXAMETHASONE ON RAT BRAIN WITH IMPLANTED TUMOR:CHANGES OF REGIONAL CEREBRAL BLOOD FLOW AND GLUCOSE UTILIZATION

　抄録　A．A．　ascites tumorをラット脳内に移植有ることにより，実験脳腫瘍モデルを作成した。これを用い，¹⁴C-iodoantipyrineおよび¹⁴C-deoxyglucose quantitative autoradiography法により，それぞれ局所脳血流量およびグルコース利用率をdexamethasone治療群・非治療群について測定し，担腫瘍脳におけるこの両者の変化および腫瘍性脳浮腫に対するdexamethasoneの効果を検討した。無治療群では腫瘍隣接脳において，対照群に比し局所血流量およびグルコース利用率がそれぞれ75％，60％減少していた。腫瘍と同側の広範な領域の皮質でも両者は中等度に低下していたが，対側半球では有意の変化は認められなかった。Dexamethasone治療群では，無治療群で認められた局所血流量の低下がすべての部位で有意に改善していた。また治療群では，血中グルコース値が高値となるため局所グルコース利用率を定量できないが，optical densityで比較有ると腫瘍隣接脳でグルコース利用率の低下が改善していることが示唆された。以上の結果，腫瘍隣接脳は浮腫のため可逆的な乏血状態に陥っており，dexamethasoneはこれを回復させる効果をもつことが確忍できた。

An experimental brain tumor was produced by implanting a piece of A. A. ascites tumor into the parietal brain of rat. Local cerebral blood flow (LCBF) and glucose utilization (LCGU) were de-termined in this model with ¹⁴C-iodoantipyrine and ¹⁴C-deoxyglucose quantitative autoradiographic methods, respectively, to investigate the change of blood flow and glucose metabolism and the effect of dexamethasone in the brain with tumor.

LCBF and LCGU in the peritumoral brain tissue were reduced 75% and 60%, respectively, compared with the values of the control. In the ipsilateral frontal and occipital cortical areas far from the tumor, 50% and 45% reduction of LCBF, respecti-vely, was observed. More than 30% reduction of LCGU was seen in the same areas. In the caudate and corpus callosum ipsilateral to the tumor, LCBF was diminished 25% and 40%, respectively. LCGU was not significantly changed in these areas. No significant changes of LCBF and LCGU were observed in the contralateral hemisphere.

In the dexamethasone-treated animal, the reduc-tion of LCBF was less in all areas where it was reduced in the untreated animal. In the peri-tumoral brain tissue, LCBF was significantly higher compared to that of the untreated group, and 80% of the normal level. In the ipsilateral frontal and occipital cortical areas, caudate and corpus cal-losum, LCBF was about the same as that of the control group. In the animal treated with dexamethasone, quantitative analysis of LCGU could not be made because of high glucose levels in plasma. However, by comparing the local optical density of the autoradiogram, less reduction of LCGU in the peritumoral brain was suggested in the dexamethasone-treated animal.

These results indicate that the peritumoral brain tissue is in the reversible ischemic and hypometa-bolic state, and that dexamethasone has a powerful capability to restore it towards the normal state. And these findings may also explain the mechanism of the dexamethasone effect on tumor bearing brain, and the pathophysiological process in the resolution of the neurological signs by dexametha-sone in patients with brain tumor.