クモ膜下出欠後の脳血管攣縮原因物質とその運命

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Whether a patient who has had unfortunate subarachnoid hemorrhage can lead a useful life or even survive is greatly influenced by cerebral vasospasm. We have conducted studies on vasoconstrictive substances developing after subarachnoid hemorrhage and also the possibilities of inactivating drugs as a treatment for vasospasm.Fresh blood and a supernate of the blood-CSF mixture incubated for 1 to 16 days were applied to the basilar artery of adult cats which were exposed by transcervical-transclival approach. After each application, the diameter of the artery was observed and the degree of constriction was measured using a surgical microscope.Constriction due to the application of fresh blood was about 30%, and recovery was observed shortly after. It seems that serotonin isolated from platelet participates greatly in the transient vasoconstriction induced by fresh blood, and that the early spasm clinically is caused by serotonin and mechanical stimulation.Supernate of blood-CSF mixture, incubated for 3 days, has weak activity compared to the powerful (50%) and long lasting activity of those incubated for 7 days. Furthermore, same mixture incubated for 15 days has little or no activity.This change in the vasoconstrictive activity is similar and coincides chronologically with the appearance of late spasm as reported in clinical studies by Suzuki in 1975^<4)>.Vasogenic substance in 7th day mixtures were investigated. Heat coagulation and ultrafiltration indicates that the vasogenic substance is a protein with a molecular weight exceeding 10,000. Sephadex G-100 gel chromatography and disc electrophoresis indicates that the substance is hemoglobin. Spectrophotography ensures that this Hb is oxyHb.On the other hand, in 15th day mixtures, oxyHb is converted to metHb. Experimentally, pure metHb has no vasoconstrictive activity.From the result of the present study, it is possible that bleeding from ruptured aneurysm stops spontaneously due to immediate coagulation and early spasm induced by serotonin and mechanical stimulation. Gradually oxyHb is excreted following the hemolysis. The oxyHb volume reaches its peak near or on the 7th day following the bleeding.During this progression, vasospasm is provoked when the oxyHb reaches a responsible volume. From the 7th day following the hemorrhage, oxyHb gradually changes into metHb. By the 15th day all oxyHb had been converted. Subsequently, the metHb is broken into hemin and globin and is absorbed into the blood.We have succeeded in oxidizing oxyHb into metHb with sodium nitrite, thus preventing experimental vasospasm.In the future we intend to continue work with sodium nitrite and other drugs to seek methods to prevent clinical vasospasm.
日本脳神経外科学会の論文

クモ膜下出欠後の脳血管攣縮原因物質とその運命

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