The Histopathologic Observation For Intracranial Saccular Aneurysms

Objective The aim of the present study is to investigate the fundamental mechanism on the origin, growth and rupture of saccular aneurysms by the basic pathological methods.Methods Aneurysm group: Twenty cases of intracranial aneurysms were taken from the patients who underwent surgical clipping in the Second Hospital of Shandong University recently; Control group: Ten cases of normal intracranial arteries were from the patients who suffered from traumatic intracranial hematomas and contusion and laceration of the brain with no cardiovascular disease and cerebrovascular disease. In the aneurysm group H&E staining was used for microscopic analysis and ultrastructural study was performed by the transmission electron microscope; SMC in human ISA and normal intracranial artery was observed by anti-α-actin immunohistochemistry stain. In situ terminal transferase-mediated dUTP nick end-labeling (TUNEL) was used to detect the apoptosis of SMC in these two groups; We compared the elastic fibers, collagenic fibers, reticular fibers by special staining in the two groups by special staining.Results(1) H&E stainingIn aneurysm group, the normal three-layer structure had lost in all intracranial saccular aneurysm walls, the fundamental histopathological changes were inury, denaturalization and repair. Most aneurysms specimens showed structure changes, including injury of endothelial cell, disrupture or disappearance of the internal elasticlayer, scarce of contractile fiber cells. The number of smooth muscle cell become less , the left SMC swelled and become denaturalization , the middle layer was filled with fibre tissue; the outer layer turned thinner, most was fibre tissue, no outer elastic layer. In all layers of aneurysm were coated with more or less inflammation cells, the regional necrosis and different stage of atherosclerosis could be detected in relative large aneurysms ,but were rare in relatively small ones.(2) Electron microscopeThe normal artery structure in aneurysm wall had been destroyed, the three layers were hard to distinguish, Cytolysis was serious, cell organ reduced. Most endothelial cells fell off, elastic fibre autolyze; the number of SMC decreased, some SMC nucleus contracted completely or depressed, typical apoptosis body were seen in later stage, muscle silk autolyzed and disappeared mostly; in outer layer saw much collagenic fiber, arranged unorderly; inflammation cells were seen in the aneurysm wall(hypertrophy cell et al.).(3) Anti-α-actin immunohistochemistry stainingSMC of anti-α-actin positive cell were seen in the middle layer of normal intracranial artery, and arranged orderly. The anti-α-actin positive cell in the middle layer of ISA decreased obviously, and arranged in turbulence. Significant difference of SMC expression intensity was found between the ISA group (gray value:108.53±6.36) and the normal intracranial artery group (gray value:177.23±12.78), p<0.01.(4) Apoptosis of SMCThere was significant increase in the apoptosis of SMC in ISA compared with normal intracranial artery (12.8% vs 0.9%, p<0.01). Increased apoptosis of SMC may explain the decreased number of SMC commonly(5) Special stain of ECMControl group: cerebral artery wall was very thin and less elastic fibre, only one layer elastic tissue- internal elastic layers, absence of outer elastic layer, located in the wall between middle membrane and internal membrane, had a good continuity and typical wavilness; reticular fibre located in the middle layer of cerebral artery, formedthin net, mixed with smooth muscle , distributed densely, arrange uniformly. In every layer of aneurysm wall were seen collagenic fiber, but mostly located in the middle membrane, arranged uniformly.Aneurysm group: The aneurysm wall was mostly or only made of collagenic fiber, but arranged loosely, unorderly, the colouration shoaled compared with the control group. The reticular fibre decreased or lacked especially in the outer of middle membrane, the fibre shortened , internal elastic layer ruptured or bedded, no typical wavilness. ConclusionsRupture or disspearence of internal elastic layer, soakage of inflammation cell, different stage of atherosclerosis, apoptosis of SMC and changes of ECM, and so on are the pathological and morphological base of the occurrence and development of ISA.Increased apoptosis of SMC may explain the decreased density of SMC commonly seen in the media of ISA, which influences the formation of ECM., reduces the elasticity and anti-dilatation of the artery and lead to form the aneurysm and even rupture under the concussion of blood stream.ECM of the ISA lose the normal morphological structure, which influences the regulation for SMC and the normal function of the artery wall and plays an important role in the happening and development of ISA.Factors related with the pathological happening of ISA are not isolated, but interacted, which accelerate the happening and development of ISA.The fundamental histopathological changes of intracranial aneurysms are inury, denaturalization and repair. Long standing chronic injuries destroy the original structure, the aneurysmal wall continuously proliferate to repair and reconstruct its structure which will make the sac to grow and rupture.Therefore, intracranial saccular aneurysms are acquired lesions which have multiple complicated etiological factors.