23. クモ膜下出血時にみられるイオン環境の経時的変化

-特にクモ膜下血腫中のカリウムイオン濃度の変化について-

抄録

Electrolytes which are known to have vasomotor effects have not been well evaluated as to their possible role in the induction of vasospasm.
Present study was undertaken to clarify some contributions of electrolytes, especially potassium ion which are liberated in the process of hemolysis of the blood clot.
The basilar arteries of adult rats were used. Under pentobarbital anesthesia the basilar arteries were exposed by transclival approach under the operating microscope. Subarachnoid hemorrhage was induced by puncture on a small branch artery with a: fine needle. In each of 10 minutes, two hours, and 24 hours after subarachnoid bleeding, the fresh arterial strips were removed and the specimens were immediately frozen in liquid nitrogen, cryosectioned at -120°C and freeze-dried at -85°C. Electron probe X-ray microanalysis of drycryosection was performed to determine the elemental compositions of extravasated erythrocyte and periarterial space. The K concentration was increased in the extracellular space to 8 times above the baseline in 24 hours after subarachnoid bleeding. The K concentration of extravasated erythrocyte was decreased in 24 hours.
Time course of potassium ion liberation from extravasated erythrocytes was also reported. The hypertensive intracerebral hematomas were collected during surgery. By the flamephotometer, K concentrations of supernatants of the hematomas were measured chronologically. On the other hand, peak of potassium ion level in the intracerebral hematoma is reached around the third or the fourth post hemorrhagic day, and the level is gradually reduced to normal approximately in three weeks.
Potassium has been known to have potent vasomotor effects but the importance of this ion has not been well appreciated. It is obvious from our present study that ionic environment is of cardinal importance in development of vasospasm and especially potassium should be reevaluated in its possible role for cerebral vasospasm caused by subarachnoid hemorrhage.