脳動脈攣縮の電子顕微鏡的研究

抄録

Despite of recent progress in neurosurgical techniques and managements, cerebral arterial spasm has been a difficult problem, which has great influence on prognosis for life as well as for function of patients with the ruptured aneurysm. Mechanisms of vasospasm after subarachnoid hemorrhage (SAH) have been intensively studied and elucidated to a certain extent in experimental models, however, once cerebral vasospasm has occurred in patients after subarachnoid hemorrhage, restoration of vascular caliber is extremely difficult. Moreover, it has been recently found that prolonged constriction of the vascular lumen in so-called vasospasm was partly due to organic changes of the arterial wall, such as myonecrosis and intimal thickenings. Since only a part of patients with prolonged vasospasm develops ischemic symptoms of the brain, intimal changes such as endothelial degeneration and desquamation with possible mural thrombosis might play an additional part to narrowness of the vascular lumen for manifestation of cerebral ischemia.
From this point of view, the author studied the luminal surface of cerebral arteries of experimental vasospasm as well as human autopsy materials using a scanning electron microscope.
1) Experimental studies:
Prolonged spasm was induced in dogs by introducing fresh blood into the cisterna magna or by puncturing the intracranial internal carotid artery with a fine needle.
On the luminal surface of the arteries four days after SAH, there were segmental longitudinal folds covered with undisrupted flat endothelial lining. The segmental presence of longitudinal folds in the specimen perfusion-fixed under pressure was interpreted that constriction of the arterial wall in vasospasm was not equally intense throughout the whole spastic portion, although narrowing of the arteries appeared diffuse on the angiomas, and that segments in severer spasm were not completely extended out at the time of fixation under pressure. The folds of the luminal surface were no more present in the specimens 10 days after SAH.
Apparent degeneration and/or desquamation of the endothelial cells in the spastic segments were not recognized.
2) Studies with h uman materials:
Four fatal cases of severe subarach noid hemorrhage were studied. The arterial segments at the base of the brain were dissected at autopsy and examined on SEM.
There were patches of area which was covered with fibrin network in three cases. In the remaining case the mural thrombus with fibrin and red blood cells were noted in a segment prepared for a light microscope. There was no endothelial lining beneath or around a fibrin net on the luminal surfaces. As a control study, proximal middle cerebral arteries were obtained at either medico-legal or pathological autopsy from 17cases died from other than intracranial diseases.
There was frequent patchy desquamati on of the endothelial lining, showing flat and smooth surface, however, fibrin nets as well as fibrous structures alike were never encountered in a control study.
It was assumed that in a severe prolonged spasm the endothelial cells underwent degeneration by prolonged compression, and that subsequent mural deposit of fibrin net could take place if increased coagulability of some kind and/or stasis of blood stream favoured it.
3) Expe rimental studies could not supply any evidence supporting the assumption derived from findings obtained in human materials. The failure was undoubtedly due to great difficulty to reproduce prolonged spasm in dogs so severe as seen in clinical cases manifesting ischemic symptoms.
It would be important for further experiments to establish experimental models, in which long-lasting severe spasm could be induced and yet no threatening to life of animals would exist.