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抄録 脳腫瘍内および腫瘍周囲脳組織のグルコース代謝の変化を定量的オートラジオグラフ法を用いて検討した。脳腫瘍モデルはethylnitrosoureaで誘発したラット神経膠腫を用い,ケタラール麻酔下に14C—deoxyglucoseを静注し,45分後に脳切片のautoradiographを作成し,Sokoloffらの演算式により局所グルコース利用率を求めた。その結果,直径2mm以下のmicrotumorにおいては,14C-deoxyglucoseの腫瘍内へのとりこみは周囲脳皮質よりも低く,腫瘍内グルコース利川率は平均30μmol/100g/minであつた。直径2mm以上のmacrotumorにおいては腫瘍内グルコース利用率は高い部分(49μmol/100g/min)と低い部分(38/umol/1OOg/min)に分かれたが,いずれも正常皮質(63/umol/100g/min)と正常白質(corpuscallosum;26μmol示100g/min)の中間の値を示した。microtumorに接する脳組織では局所グルコース利用率の変化は認められず,macrotumorに接する脳組織では皮質において有意な局所グルコース利用率の低下を認めた。にれらの結果は,本法が腫瘍のviabilityや悪性度を示す良いparameterとなりうる可能性を示唆し,また浮腫脳組織のグルコース代謝を示す良いindicatorとなることを示唆している。
Local cerebral glucose utilization (LCGU) of anesthetized rats bearing ethylnitrosourea (ENU)-induced gliomas was studied with 14C-deoxyglucose autoradiography.
Single subcutaneous injection of ethylnitroso-urea (50mg/kg) was made to the newborn rats, and animals were used for experiment at 150 to 300 days after birth. Under ketamine anesthesia, 14C-deoxyglucose was injected through a venous catheter, and timed arterial sampling was made. Brains were removed at 45 min after injection, and prepared for macro-autoradiography. LCGU values were measured by the equation developed by Sokoloff et al.
In the microtumors (<2 mm in diameter), mean LCGU value was 30 pmo1/100 g/min, which was significantly (p <0.01) lower than mean value of normal cortex (63 itino1/100 g/min). In the macro-tumors (>2 ram in diameter), LCGU values in the tumor were separated to high part (mean; 49 pmol/100 g/min) and low part (mean; 38 itmol/ 100 g/min), which were still lower than mean cortical value and higher than mean white matter value (corpus callosum;26μmol/100 g/min). No LCGU changes were noted in the brain tissue adjacent to the microtumors. Whereas, macrotumor significantly reduced LCGU in the adjacent cortex.
The present data may indicate that glucose metabolism of the ENU induced glioma and edematous periturnoral brain tissue is lower than that of normal cortex.
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