| Background: There is proved that the lethal and disable pathogenesis of huge epidural hematoma is not only the removal of brain content around, but also the ischemia and hypoxia of the tissue caused by compression provoking series of biochemical waterfalls (such as calcium overload, acidosis, free radicals increasing, etc).Therefore, the key to treat patients with epidural hematoma is rapid evacuation of hematoma and reduction of intracerebral pressure has no doubt. However, Shalamo found that in the dogs with epidural hematoma brain edema aggravated further on the contrary , intracerebral pressure (ICP) kept increasing once again after the hematoma decompression and all the animals died in the long run , which was much surprising. In addition, our 10 years' clinical practices and other neurosurgical centers showed that the patient'scondition once remarkably alleviating became deteriorating only 3~12 hours after operation, this is very obscure to us. The brain edema notably aggravating is obvious in the reexamined CT pictures. Many finding lacking reluctant basic research, such as more serious brain edema in the tissue around and aloof the hematoma; serious damages to endothelium and blood-brain barrier; lots of necrosis of Neuron are obvious in the dead body examination. In spite of surviving after the operation, Partial patients were either in long-term coma and died of the complications ,which led the mortality was up to 30%.According to the theory of ischemia/reperfusion injury, We infer: the widely-damaged brain tissue which has low perfusion because of the hematoma compression rapidly contract with quick decompression, and then the brain experiences ischemia/reperfusion injury.Objective: In order to test the hypothesis of ischemia/reperfusion injury , this project paid focus on the effects of rapid decompression on the regional cerebral blood flow(CBF), brain structure and [Ca2+]i.Methods: 50 New Zealand rabbits were at random divided into a control group(nl=5) , model testifying group (n2=5), and experimental groups (n3=40), which are once more divided into the CBF testing group and 7 group of brain hernitate , D10min, Ih, 6h, 24h, 48h, 72h. The changesof blood flow , [Ca2+]i and brain tissue water content were measured and their correlations were analyzed.Results1 The cell deeply dying, karyon shrinking , broadened space around the cell , some denaturalization and necrosis were observed after compression, the lesion and haemorrhage of Vascellum, edema with broadened space were observed 10min after evacuation. While the brain damage of 24hr post operation were characterized by the blood vessel closing up and necrosis of Neuron.2 The CBF of parital cortex was 65.98 ?1.79ml.loog-1.min-1 in normal condition, and it decreased notably as brain herniationo it had a short-timed fugacious hyper-reperfusion following depression and decreased gradually ,reached peak in 24 hours. Then it resume slowly and reach normal level in 72h.3 [Ca2+]i increased remarkably after being pressed ; it had a short-timed decreasing following depression and increased gradually ,reached peak in 24 hours.4 , The correlation between [Ca2+]i and brain water has magnificant value (v=38,r=0.493,P<0.01).ConclusionsThese findings indicate that the widely-damaged brain tissue which has low perfusion because of the hematoma compressionrapidly contract with quick decompression , which is the major mechanism of secondary brain insults with quick brain decompression and is worthy of being further studied...
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