Three Experimental Models for Evaluation of Three Different Mechanisms in Blast TBI

摘要: Traumatic Brain Injuries (TBI) induced by blast waves from detonations provides huge diagnostic problems. It may be assumed that several mechanisms contribute to the injury. Thus, primary overpressure, acceleration movements, focal impacts as well heating could In a number of experiments we have evaluated injuries these mechanisms. Our experimental models include tube in which an anesthetized rat can exposed controlled PETN explosives result pressure wave with magnitude between 130 and 600 kPa. this model, animal is fixed metal net avoid head forces. The simple Friedlander type, duration less than 0.5 ms. Animals are side on suffer lethal bleedings lungs if peak exceeds 300 recent mounted animals rigid metallic body protection covers all parts except for head, rests bar prevents movements. With survive second model penetration 2 mm thick needle, represent impact fragments. third subjected high-speed sagittal rotation angular acceleration. This relevant rapid movements occur after explosions. Immunohistochemical labeling amyloid precursor protein revealed signs diffuse axonal injury (DAI) models. Signs punctuate inflammation were observed Exposure did not induce DAI or detectable cell death, but functional changes. Affymetrix Gene arrays showed changes expression large gene families including neurotransmittors hippocampus both injuries. limited shifts hippocampus. most interesting findings down regulation genes involved neurogenesis synaptic transmission. These indicate rotational critical factor other acute TBI. further exploration TBI will search long-term effects. Detailed studies anxiety related pathways brainstem important part continued studies.