| Objection: The most common pathogenesises of the cerebrovascular malformations are CVMs and cerebral saccular aneurysms. The cerebral saccular aneurysms, CSAs are persistent localized dilatation of the vessel wall, which exist in abnormal weak structure. CSAs is the most cause of subarachnoid hemorrhage, SAH, which happen acutely, progress promptly, danger life, and cause critial neurologic deficits. The arteriovenous malformations, AVMs, is the most disease in the cerebrovascular malformations. The cerebral AVMs is a congenital vascular lesion caused by abnormally developed in the embryomic life. The most clinic symptom presents with hemorrhage, seizure or neurologic deficits. There is no clear in the original and developing mechanism of CVMs. The historical research of CSAs and AVMs can help us to elucidate the original and developing mechanism. Now, the historical morphologic research of AVMs and CSAs has been perfected in the light microscopy, the ultrastructural features have been little published. The examination of AVMs and CMs used transmission electron microscopy by Jonh H wong compared them the ultrastructral pathological features, they found endothelium denudation. Meyermann and Yasagil made the systematic research of the ultrastructure of CSAs. They concluded some classical features in CSAs. But as far as we know, the comparative research of AVMs and CSAs has not been made. So in the test, through transmission electron microscopy, we investigate the ultrastructural features of AVMs and CSAs, we try to elucidate the differences between AVMs and CSAs, discuss the original and developing mechanism, and try to provide some evidences for the molecular biological research of AVMs and CSAs.Material and Method: We divided into three groups: AVMs group, CSAs group and normal control group. There were 10 patients in CSAs group (sex: men 4, women 6;age:14?6y, mean 45.6y).8 ones in AVMs group( sex: men 6, women 2 ;age:17?7y, mean 28.8y), 4 ones in normal control group .All specimens were resected from patients undergoing cerebrovascular surgery underthe same condition. The control specimens were obstained from the patients suffered from the craniocerebral trauma. The surgical specimens were prepared for ultrastructural investigation, used the standard protocol. After the sac of CSAs, the nidus of AVMs and the normal vessel of the adjacent tissue of the injured brain were recected, all the specimens were immediately immersed and fixed in 2.5% glutaraldehyde in 30 s, preserved in 4C. In 24h to 72h, the specimens were rinsed sequentially in O.lmol/L phosphate buffer. Sequential dehydration of the specimens was performed by serial increasing concentrations of ethanol( EtoH).They were embedding in epoxy resin and propulene oxid. After stained in 1% toluidine blue and 2%osmium tetroxide, the specimens were made the serial ultrathin sectioning and were observed the specific ultrastructure features in the electron microscopy.Results: The control specimens demonstrated the normal ultrastructural features:all layers existed indegratedly, having an intact endothelial cell layer, internal elastic lamina layer and smooth muscle cells layer.Ecs were flat with ovoid nuclei,all inter-Ec junctions were uniformly tight-junction, and smooth muscles cells have the typical fusifoid features. The feeding vessels of the AVMs specimens demonstrated the ultrastrucrural features like the normal groups, also having an intact EC layer, internal elastic lamina layer and smooth muscle cells layer. But at the nidus of AVMs, Ecs were also flat with ovoid nuclei. But in subenthelial layer, the internal elastic lumina disppeared, or were sparse. The collagen buddies were disrupted, the smooth muscle cells appeared undeveloped malformations. Only few aneurysms examined in the test had been EC layer, most of them collaped.The remnant Ecs existed in ball-like degeneration. There were few elastic materials in the internal elastic layer. In the various depth of the internal elastic layer, there were bundles of collagen fibrils. The gaps... |
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