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I.緒言
臨床的に脳浮腫という場合には,術中および手術直後に急速に生じる脳腫脹と,それよりやや遅れて発現する脳浮腫なるものを総称してさすことが多い。たしかに両者は脳容積の膨大という点では同様である。しかしその成因となるとまつたく異なつた作用機序より成り,前者のいわゆる急性期の脳腫脹は脳血管の麻痺のために脳血管が拡大し,血管床の増大をきたした状態をいう1)2)。
一方後者すなわちやや遅れて発現する脳浮腫は脳代謝機構の障害の結果,脳組織内に水分の異常に貯留した状態をいい,一般に脳浮腫という場合にはこれをさすことが多い3)4)。
Experimental brain edema was induced in cat by intraperitoneal injection of triethyl tin sulfate, epidu-ral compression and cold injury. Normal cat brains without such treatment were used as a control group. The brains were removed after exsanguina-tion, and quickly and carefully divided into gray and white matters in a cold room at 0-4℃, then the materials were examined of their water content and their lipid alteration was systematically studied.
The experiment showed a marked increase of water content in white matter of triethyl tin intox-icated and cold injured groups, which indicated the remarkable edema formation.
Total lipid was extracted by Folch et al.'s procedure using Santiago-Calvo et al.'s solvent of chloroform-methanol-cone. HC1 (200 : 100 : 1, v/v) and its content was determined by measuring the dry weight. In total lipid content, no significant change was observ-ed between normal and edema groups.
Total phospholipid was determined by measuring phosphorus content of lipid extract by Sekiguchi's method, which showed no significant change among all edema groups. With individual phospholipid, however, following significant changes between nor-mal and edema (triethyl tin intoxicated and cold injured) gray matters were demonstrated by quan-titative thin-layer chromatography ; a slight decrease in sphingomyelin, lecithin and phosphatidylethanol-amine in cold injured group, a remarkable diminu-tion of sphingomyelin, lecithin as well as a slight decrease in phosphatidylethanolamine in the intoxi-cated group, though no significant change in phosphatidylserine was found between normal and edema groups. These can be considered to be the result of an abnormal metabolism of individual phos-pholipid in these edematous gray matters.
Total cholesterol was determined by Zak-Henly's method, which showed a slight decrease in both gray and white matters of epidural compressed and cold injured groups while no significant changes were seen either in gray nor in white matter of triethyl tin intoxicated group. Cholesterol is the main lipid of myelin sheath. Therefore, the change of total cholesterol in traumatic edematous brains such as epidural compressed and cold injured groups may suggest the existence of demyelination in these brains.
Proteolipid protein was examined by a modified method of Lowry et al. for insoluble protein. The result was interesting in that it showed a marked increase in the gray matter but decrease in the white matter of both triethyl tin intoxicated and cold injured edematous brains. In addition, its di-minution in edematous white matter was shown to be roughly proportional to the increase of the water content. Proteolipid protein is generally considered to be a structural component of the membrane, mainly of myelin sheath. Therefore, its decrease in white matter of these two edema groups may sug-gest the change in myelin sheath structure, while its increase in gray matter may suggest the accelera-tion of proteolipid protein synthesis in these condi-tions.
Ganghoside content was determined by its N acetyl neuraminic acid according to Warren's thiobarbituric acid method. Ganglioside was elevated markedly in both gray and white matters of cold injured group but was reduced in those of the triethyl tin intoxi-cated group. It has been shown that cerebral gan-glioside is distributed in membrane fractions, such as microsome and synaptic membrane, which main-tain high membrane ATPase (Na-K activated ATPase) activity. However, it is yet to be elucidated how important a role such change of ganglioside may play in the formation of brain edema.
In conclusion it can be said that the present result of lipid analysis suggests the occurrence of some lesions of a membrane system such as myelin sheath in edematous brains.
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