BIOCHEMICAL AND HISTOLOGICAL ALTERATIONS INDUCED BY FLUID PERCUSSION BRAIN INJURY IN THE RAT

In the present study we have characterized the time-course of the histopathological and biochemical alterations resulting from mechanical brain injury caused by lateral fluid percussion centered over the parietal cortex in the rat. The injury device used was an HPLC pump coupled to a solenoid valve which delivered a constant and short lasting (10 ms) impact pressure (1.6 atm). This traumatic procedure resulted in an accumulation of blood in the subarachnoid space and cortical edema art 4-24 h post-trauma. From 4 h after injury, cortical neurons exhibited a pathologic appearance and phagocytic cells invaded the brain parenchyma. At 3 and 7 days post-injury, complete neuronal loss was observed in the parietal cortex around the impact site. In the ipsilateral cortex, the time-course of histologically assessed neuronal loss and phagocytic/glial activation paralleled the time-course of the loss of omega1-2 (benzodiazepine) sites (a neuronal marker) and of the increase in p sites (peripheral-type benzodiazepine binding sites; a glial/macrophage marker). Neuronal loss and increase in the density of the glial/macrophage biochemical marker were also observed in the hippocampus but not in the contralateral cortex or in other subcortical structures, suggesting a selective vulnerability of the hippocampus to this traumatic procedure. There was a very good spatial correlation between the histological alterations and the changes in the density of the neuronal and glial/macrophage biochemical markers (as assessed by autoradiography). The volume of the lesion, integrated from the surface of the lesion measured at 10 coronal levels cut at a 1 mm interval and stained with haemalum and eosin, represented 32.9 +/- 1.7 mm3. There was a very small inter-experimental variation in this volume. These results demonstrate the feasibility of monitoring the extent of traumatic brain damage induced by fluid percussion by measuring the volume of the lesion.