Experimental Studies On Cerebrovascular Damage After Fluid Percussion Brain Injury In Rats

Object:To investigate the changes of the cerebrovascular after fluid percussion brain injury in rats and to provide experimental evidence for posttraumatic cerebral ischemia.Methods:1,Sixty-four male Sprague Dawley rats were randomly divided into the normal control group, sham group and posttraumatic 3h, 6h, 12h, 24h, 48h, 72h groups of 8 rats each. Lateral fluid percussion brain injury model were reproduced in the present study to produce acute brain injury in rats. The morphologic changes of the cerebral microvasculature were inspected by transmission electron microscopy and optical microscopy, the shape of cerebral vessels was observed by the prepared ink irrigation.2,Sixty-four male Sprague Dawley rats were used, others same as above. Using immunohistochemical staining, changes of type IV collagen antigens, the main components of the microvascular basement membrane, and the expression of MMP-9 after lateral fluid percussion brain injury at various time points.3,Eighteen male Sprague Dawley rats were randomly divided into sham group and posttraumatic 3h, 72h groups of 6 rats each. Lateral fluid percussion brain injury model were reproduced in the present study to produce acute brain injury in rats. The morphologic changes of the middle cerebral artery were inspected by optical microscopy and transmission electron microscopy.Results:1,The changes of cerebral microvasculature including:â‘ On 3h and 6h,"non"or less microvessels area were observed in the injured cerebral cortex and around. On 24h-72h, a number of microvessels were more increased than that 3h and 6h.â‘¡HE staining show the obliteration and flexion and stricture and fragmentation and microthromb of microvasculature, aggregation of red cell, and edema which surrounding the microvasculature.â‘¢TEM observation indicated: On 3h, endothelium cells swelled slightly,internal elastic lamina was distorted slightly and perivascular swelling slightly. On 6h, the microvilli was formed, internal elastic lamina was distorted and ruptured. On 12h, the microvilli were more obvious than that 6h, internal elastic lamina swelled. On 24h, endothelium cells swelled evidently and the internal elastic membrane was rough and uneven in surface and disrupted. On 48h and 72h, endothelium cells swelled evidently and the nucleus was homogenous.â‘£Abundant acidophilia neurons were found around traumatic area and the ultrastructure of nervous were worsen.2,Collagen type IV and MMP-9 immunohistrochemitry: The basement membrane damages included degradation, defection and exfoliation. On 24h, the main components of the basement membrane type IV collagen, significantly decreased compared with that of the control group (P<0.05). On 72h, the positive unit of type IV collagen, significantly decreased compared with that of the control group (P<0.01). The results showed that MMP-9 on cerebral injured area was significantly increased at 3h and kepted at high level up to 72h.3,The changes of middle cerebral artery including: On 3h, the vessel wall was thickened and the vessel lumen was narrowed. On 72h, the range of narrowing the vessel lumen and the wall thickness were more obvious than that 3h. TEM observation indicated: middle cerebral artery in 3h group had no definite injury, endothelium cells swelled slightly,internal elastic lamina was plumped and smooth muscle cells distended slightly. On 72h, the ultrastructure of middle cerebral arteries show endothelium cells swelled evidently and the structure of the vessel wall was disordered, the internal elastic membrane was folded and disrupted,endothelial and smooth muscle cells degenerated and nucleus distorted.Conclusions:1,The microvasculature disappeared at traumatic area and a few microvasculature around it after LFPI. The cavum of microvasculature was narrowed and the microvilli was formed. Microthromb were found in part microvasculature. The microvasculature partly gradually recovered at posttraumatic period, but the micrangium endotheliocyte and numerous neurons were gradually damaged after LFPI. These suggest that early disturbances of cerebral microcirculation are the principle pathological base of cerebral ischemia after brain injury.2,The main components of the basement membrane type IV collagen, significantly decreased compared with that of the control group after LFPI. MMP-9 on cerebral traumatic area was significantly increased after LFPI. These suggest that MMP-9 probably take part in the primarily and secondary injury of microvascular internal elastic lamina in the rats with LFPI.3,The damage of middle cerebral artery caused by atrophy and desquamation in endothelial cells, corrugation of the internal elastic lamina, and blebbing and fibrosis in cytoplasm of smooth muscle cells were the key characteristic of LFPI. These suggest that more larger cerebral arteries were damaged when stress go through it.