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抄録 S-adenosyl-L—methionine・sulfate・tosylate (SAMe)は,細胞膜を構成するリン脂質の主成分であるphosphatidyl cholineの合成促進作用,赤血球の変形能の亢進作用等を持つ。一方,脳損傷に伴って脳内リン脂質の減少することが知られている。従って,これらの作用を持つSAMeは脳虚血の急性期の治療薬として応用されることが期待できる。Wistar kyoto rats (WKY)を用いた(1)心摘出による完全虚血,および自然発症高血圧ラット(SHRSP)を用いた(2)両側総頸動脈閉塞による再開通モデルを使用して,SAMeを投与し,その効果について脳代謝諸量(ATP,lactate,c-AMP),脳含水量を測定して検討した。(1)完全虚血モデルでは,対照群に比してATP,c-AMP値の低下を有意に抑制したが,lactate値には影響を及ぼさなかった。(2)再開通モデルでは,lactateの蓄積を有意に減少させたが, ATP,c-AMP値には影響を及ぼさなかった。また,脳含水量に対しては効果を認めなかった。以上の結果より,SAMeは脳虚血時および虚血の回復過程において,虚血脳の脳代謝を改善することを示した。
Effects of S-adenosyl-L-methionine (SAMe) on experimental cerebral ischemia were investigated using two different ischemic models. Cerebral energy metabolites (ATP, lactate, c-AMP) andbrain water content were measured.
It is reported that SAMe accelerates synthesis of phosphatydyl choline and increases erythrocyte membrane fluidity.
Complete ischemia was produced by heart exci-sion using wistar kyoto rats. SAMe (100 mg/kg, I. P.) was administered twice at one hour and im-mediately before inducing ischemia. The brain of rats were irradiated by microwave to stop the enzyme activity exactly 60 seconds after inducing ischemia and brain energy metabolites were mea-sured.
Recirculation model was produced by one hour recirculation following two hours ischemia induced by clipping of bilateral common carotid arteries using stroke-prone spontaneously hypertensive rats. SAMe (100 mg/kg, I. V.) was administered twice one hour after clipping and ten miniutes after recirculation. The brain metabolites andwater content were measured one hour after recirculation.
In the complete ischemia, ATP and c-AMP le-vels were statistically high in the SAMe treated group compared to the untreated group (vehicle). But there was no statistical difference in lactate between the treated group and the untreated group.
In the recirculation model, lactate elevation was suppressed in the SAMe treated group compared to the vehicle group with statistical difference, but there was no difference in ATP and c-AMP. Also, there was no difference in water content between the treated and the untreated group.
SAMe protected energy failure in ischemia and accelerated recovery from ischemia. It is indicated that this agent is beneficial for treatment of ce-rebral ischemia in the acute stage.
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