Abstract
Many histopathological studies on the pathogenesis of the cerebrovascular lesions have been made from the aspects of the angiopathy in intracerebral vessels, particularly at basal ganglia, but no systemic histopathological researches in pial vessels located in the peripheral area of the cerebrovascular trees have been documented.
In this communication, the author has made an observation of the angiosclerotic changes of pial vessels induced in cerebrovascular diseases and made the investigation of thevarious degrees of the cerebrovascular disorder which might proceed to the cerebral apoplectic attacks.
In the first part of the present study, the angiosclerotic changes of small and middle sized pial arteries (50.300 micron in diameter), arterioles (under 50 micron in diameter) and veins and also vessels at basal ganglia were observed light microscopically in 37 cerebral hemorrhage and 14 cerebral infarction autopsy cases. Moreover, 10 autopsy cases with hypertension and 14 cases without hypertension, in which no evident macroscopical cerebral lesions had been noticed (except 5 year-old girl case with traumatic epidural hematoma in non-hypertension group), were observed in the same manner as the control groups.
The results obtained from the light microscopical investigations of those autopsy cases were as follows: In the almost cases of cerebral hemorrhages and cerebral infarctions, remarkable perivascular fibrosis of pial arteries by the increase of collagen fibers was found which was not related to the medial and endothelial sclerotic changes. The same perivascular fibrosis was found also in hypertension group as well as in the cases with the possible occurrence of cerebral circulatory derangement without hypertension.
In the second part, the author paid special attention to the perivascular fibrosis of pial arteries and made the experimental pathological investigations using spontaneously hypertensive rats (SHR) for the purpose of clarifying the pathogenesis and the significance of the perivascular fibrosis. Fifteen SHR rats with confirmation of the persisting systolic hypertension over 180 mmHg and ten normotensive Wistar-Kyoto rats as the controls were used. Some of those SHR were fedvascular wall of SHR was substantiated by the visualization of the electron tracing peroxidase and the perivascular fibrosis of pial arteries in SHR was observed accompanied by the perivascular edema. Conclusively, the author is inclined to believe that in the cerebrovascular diseases extensive recurrent cerebrovascular disorder may proceed to the cerebral apoplectic attacks. This may be correlated with the perivascular fibrosis of pial arteries and the pathologic importance of this finding was fully augmented in this communication with 1% saline solution for six to eight weeks. The changes of their intracerebral and pial vessels were observed mainly electron microscopically. Moreover, vascular permeability clearance study was performed using horseradish peroxidase as the electron microscopic tracer.
The results obtained from the electron microscopical investigations of SHR and Wistar-Kyoto rats were as follows: In comparison with the control group, the increased permeability in the vascular wall of SHR was substantiated by the visualization of the electron tracing peroxidase and the perivascular fibrosis of pial arteries in SHR was observed accompanied by the perivascular edema.
Conclusively, the author is inclined to believe that in the cerebrovascular diseases extensive recurrent cerebrovascular disorder may proceed to the cerebral apoplectic attacks. This may be correlated with the perivascular fibrosis of pial arteries and the pathologic importance of this finding was fully augmented in this communication.
