| Experimental investigation on craniocerebral fire-arm wounds was started at late 19th century, and related animal models were not gratifying to proceed research on the mechanisms of secondary brain lesion after wounding, because excessive kinetic energy of firearms often resulted in immediate death of postinjury, or insufficient kinetic energy was not consistent with ballistics. Following development and application of high-tech weapon, the cure in craniocerebral fire-arm wounds had appeared much more troublesomely. In the latest 20 years, the experimental investigation on craniocerebral fire-arm wounds was one of the primary topics at all times in internal and overseas. Discussions involved mechanisms of secondary brain lesion and cerebral edema after craniocerebral fire-arm wounds were not profound in literatures. Therefore, a rational and feasible animal model of craniocerebral fire-arm wounds appeared urgent, and to further observe with new experimental technique and instrument in immediate trajectory morphology, pathophysiology, biochemistry, and the cellular and molecular changes during cerebral edema progressing after fire-arm injuries. Such experiments were involved in innovations as: (1)Directly and dynamically observed a phenomenon of the intracellular Ca2+ overload after craniocerebral fire-arm wounds by specific fluorescent probe and laser scanning confocal microscope (2)observed a rule of the expression of AQP4 in braintissues close to trajectory at the earlier period after wounding by immunohistochemistry staining.The laboratory musketshot was made in Germany, with a collimator and the test missile a -5.56mm 2.57-g steel sphere. Directly shot at canine frontal parts from right to left. 14 local canines from Xi'an city were divided into control group (n=5) and trial group (n=9) at random. Experimental procedure of control group was the same of trial group except being shot. All animals were anesthetized and endotracheally intubated, and veno-passage was set up and connected to multipurpose polygraph and ICP monitor. After eyelashes reflect recovered, canines were shot from 25 m away. Then the injured canines were given artificial respiration 25 breaths per minute continually.All canines were kept alive till corresponding time spots except 1 dead at 5 min after wounding, and four of 9 lived longer than 6 h. Five of 9 wounded canines exhibited TBI and three of 9 exhibited PCI (subjective assessment). All wounded canines exhibited bradycardia and reduced BP and still-elevated ICP immediately after wounding. Meanwhile all wounded canines exhibited apnoea immediately after wounding except 1. Average time of apnoea in PCI was longer than that in TBI. In our test, average missile velocity and energy were 350.0 m s-1 and 160.0 J. So this animal model was reasonable and feasible.Each 1 unwounded canine was killed at 0.5,1, 6, 12, and 24 hour after experiment. And 2 wounded canines (vital signs is transient )at 0.5 and 1 hour, 1 wounded canine at 6, 12, 24 and 72 hour after wounding. Subcortical encephalon tissues were sampled nearby 0.5 cm bullet entrance and 5.0 cm trajectory. Sampls were disposed routinely for subsequent tests.Experimental findings under optic microscope exhibited the normal cerebral structure around primary wound track disappeared, consisted of massive necro-tissue and perivascular 'ring'haemorrhages. Contusion region exhibited hemorrhage, neuronal degeneration, glial cell swelling and hyperplasia. Some samples of concussion region and medulla oblongata exhibited gore in microvessel. Under electric microscope, the destruction of ultrastructure was more and more serious. It was related with the degree of apneic. Auther thought apnoea after wounding was caused by kineti energy transmited to the respiratory center, and it caused the principal and momentary neuron injury in the medulla oblongata.Active cell suspensions of brain tissue were prepared at every stage time after wounding, and marked by special Ca2+ fluorescence probe(Fluo-3/AM). Observed... |
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