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はじめに
脳浮腫の発生ないしは促進に関与すると考えられている種々の要因のうち,hypercapniaに関しては,脳浮腫との関連で追求された研究がほとんどなく3),その意義は明らかではない。Fox5)は,脳のCO2濃度が高くなると,細胞膜の水素化した脂質の層が,水溶性イオンの正常の拡散を妨げ,さらにブドウ糖などの不可欠の物質の透過が困難になると,細胞内のグリコーゲン,脂質および蛋白質が分解し,結合イオンや分解産物を細胞液の中に放出する。これらの水溶性の物質が細胞内にとどまつていると,滲透圧の関係で細胞内に水をさそいこむ。さらに細胞膜中の分子に結合している水や細胞内物質の分解の結果生じた水が,細胞腫脹の原因となる,と推測し,hypercapniaの脳実質細胞の細胞膜への作用を強調している。
一方,hypercapniaが,フェノバルビタール21),サリチル酸,アセタゾールアミド,尿素7)8)およびRISA1)2),など種々の物質の血中より脳内へのとりこみを増加させることが報告されており,hypercapniaの脳血管の透過性におよぼす作用も推測されるが,これは脳浮腫との関連を論ずるとき,重要である。
The effects of hypercapnia on the ultrastructure and vascular permeability of Thorotrast in the cat cerebral cortex were studied with electron micro-scope. The cats inhaled a gas mixture containing 24% CO2 and 75% O2 for one or two hours, and were given 2. 5 cc/kg of Thorotrast into the femoral veins one hour prior to the sacrifice.
In many cases the ultrastructure of nerve cells and glial cells appeared normal. In some nerve cells vesicles were frequently observed in the endoplasmic reticulum. The intercellular space showed no evi-dence of enlargement. The most common abnor-mality was formation of microvilli and large vacuoles of the endothelial cells of the capillary. Increase of pinocytotic vesicles and high electron density of the endothelial cells were also noted. Vacuolation and splitting of the basement membrane were observed in some capillaries.
In normal brains, the lumina of the vessels con-tained abundant Thorotrast particles which, however, were not encountered within their walls. In the brain exposed to 25% CO2, Thorotrast particles were frequently seen in the large vacuoles of the endo-thelial cells. A few particles were also noted in the pinocytotic vesicles and cytoplasm of the endothelial cells as well as in the basement membrane, though almost no particles were observed between the endo-thelial cells. In some vessels the particles were noted in the perivascular astrocytes, distributing not in their vesicular system but in their cytoplasm.
It has been speculated that hypercapnia causes the distortion of the blood-brain barrier, damaging the endothelial cells and basement membrane as well as the membrane of the perivascular endfoot.
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