Establishment Of A Controllable Spinal Cord Blast Injury Model And Research Of Drug Early Administration

With modernization of weapons and transition of strategies and tactics, the incidence of blast injuries in the battlefield kept increasing. Spine and spinal cord, owing to their central nervous system property, once injured, would at least affect the battle force, and in many severe cases would cause paralysis. Especially for those paralyzed, the work of nursing is very difficult and very expensive as well, and they're prone to develop various kinds of complications. As a result, battle injuries of spine and spinal cord have been the focus of relevant departments in every country.In the past, the research in central nervous system hot weapon injuries especially those of the spine and spinal cord focused mainly on bullet shot injuries. However, with the renewal of single soldier protective facilities, and increase of terrorist activities, the number of simple bullet shot injuries decreased, and the number of blast injuries increased markedly. To our knowledge, up to now there hasn't been a satisfactory spine and spinal cord blast injury animal model, and this made the researches on spinal cord blast injury mechanisms retarded and the rescue work in a relatively low level. The aim of the present study was to establish a experimental spinal cord blast injury animal model, which to the largest extent simulates the injuring effect of shock wave in the battlefield. We also observed the histopathological progression of spine and spinal cord injury tissues, and then investigated the effect of Methylprednisolone (MP) in control of secondary spinal cord injuries after spinal cord blast injuries. We hope this can provide some evidence for the clinical treatment of spinal cord blast injuries.The first part of the research was the establishment of a controllable spinal cord blast injury animal model. The RDX military explosive was chosen as the explosive material。The paper-made shell ensured the repeatability by ruling out the bias of shrapnel. The animal was sheltered, leaving only the thoracic spine at the level of inferior scapula angulus right inferior to the explosive source. The explosive was electrically ignited. The optimal distance from the explosive source was chosen after pre-measurement of explosive parameters and severity of injuries of the animal at different distances. The distance of 1, 2, 4 and 8 cm were assessed, and finally 4 cm was chosen to be the standardized distance to establish the spinal cord blast injury model.The animal in experiments with less than 4 cm distance from the explosive source died immediately. Autopsy showed large pieces of soft tissue avulsion at the wound, deep spinal plate fracture, pulmonary congestion and thoracic major blood vessel rupture. The distance of 4 cm form the explosive source didn't cause any animal death. The pathology showed acute spinal cord injury characteristics 6 hours after explosion, with obvious spinal cord edema and swollen neurons; irreversible degradations of neurons after 24 hours, with Nissl body disappearing, nucleus condensing and red staining, loosening or even breakdown of spinal cord shell laminar structure; and obvious necrosis areas in the spinal cord after 3 days. Functional examinations showed disappearance of both sensation and movement ability in the hind limbs.The second part of the research investigated the effects of MP therapy on spinal cord tissue and serum levels of Ca2+,MDA and SOD after acute spinal cord blast injuries. MP was administered at 8 hours after the injury, and specimens were collected at different points to test SOD, MDA and Ca2+ in the spinal cord tissue and SOD, MDA in the serum. The results indicated:1. Compared to the control group, the MDA and Ca2+ concentration in the local spinal cord tissues of injured group increased rapidly, and SOD concentration decreased within 6 hours. No obvious further increase was observed after 6 hours.2. Compared to the control group, the serum MDA level increased rapidly and SOD level decreased within 6 hours. In the following 24 hours, MDA level didn't increase markedly, while SOD level kept on slowly decreasing.3. MP obviously decreased the serum and tissue content of MDA and Ca2+, and increased SOD concentration, which to some extent inhibited the progression of secondary spinal cord injuries.