CELLULAR MECHANISMS OF CEREBRAL VESSELS BREAKING IN DIFFERENT PATHOLOGICAL CONDITIONS.AN OPTICAL AND ELECTRON-OPTIC STUDY

摘要

The purpose of the present study is to reveal some histopathologic features of frankly break of the cerebral vessel wall and to suggest the cellular mechanisms involved in the pathogenesis of these breaches in various pathologic conditions. Small vascular segments collected during surgical procedures for thromboses, aneurysms and brain tumors from 11 patients were examined using light (LM) and partially electron microscopy (TEM and SEM). A single vascular fragment was processed by immunohystochemical technique for the detection of the proliferating cell nuclear antigen (PCNA). We have demonstrated significant differences between aspects of break, bleeding and repair in arterial versus vein wall. The combined analysis in LM, TEM and SEM of the broken vessels suggests that cortical vessels may suffer tears and/or breaks of the wall through the following mechanisms: a) focal degeneration of the wall by apoptotic cell death or necrosis; b) vasospasm (prolonged) of the brain vessels; c) transmural red blood cell diapedesis; d) loss of smooth muscle cell in bifurcation areas comprising atherosclerotic obstructive lesions; e) proliferation and transmural migration of the pathologic neointima cells (a mechanism not yet reported in the literature). In addition, at ultrastructural level we describe for the first time at intracranial level the presence of mononuclear cells with specialized cytoplasm and glycogen deposits and also the modulation of the smooth muscle cells in cases having pseudomicroaneurysms. All the examined vascular segments were denudated of endothelium and had the tunica media degenerated, fact that implies a particular condition of the smooth muscle as a determinant condition in the break- occurrence, both in the veins and the cortical arteries and make controversial the apoptotic and/or necrotic death of cells in the cerebral vessels walls, the labeling index for PCNA being negative on significant areas of the vascular wall.