Study of Neuroimmunological Disorders Discovered at Acute Stress

Proceedings of the 9th International Multidisciplinary Conference «Stress and Behavior» Saint-Petersburg, Russia, 16–19 May 2005.For hemmorage stroke, the cause of death in >80 % of patients is the development of somatic complications (Davydovski, 1961; Vereschagin, 1973), especially pneumonia, infections of urinary tract, pathogenesis of conjunctiva and cornia of the eye. According to Vilensky, the main cause of infectious complications are disorders of the central regulation of organs and systems. In this study we did not assess disorders of immune system, focusing predominantly on the acute disorder of brain circulation (ADBC). Subjects were adult white mice and rats.Methods: For evaluation of immune disorders during experimental hemorrage stroke (EHS), experiments were performed on 105 non-lineal white mice (18–22 g) undergoing EHS. The 1st group (light acute disorder of brain circulation) the provocation of HS was performed by mandrel metal with deviation extruding from injection needle, previously prepared and perfected with rubber fixator. Brain injuries were induced in stereotaxic apparatus by 5–6 turns of mandrel for «conelike» cut of tissue and damage of vessels in the or near capsular interna (CI). Animals of the 2nd group (middle intensity EHS) additionally underwent lesions of the central part of semicut tissue cone and upper placed locus. White mice of the 3rd group (high intensity of ADBC) additionally received 0.05–0.08 mm3 of blood in the mentioned regions. We also studied the initial immune humoral response and cell hypersensitivity of slow type (RHSST, reflecting functional activity of T-lymphocytes).Results and discussion: Modeling of acute stress and EHS in mice was accompanied by marked immune disorders, as assessed by altered weight of thymus and spleen, and disturbed antybodies production and development of RHSST. Modeling of acute form of EHS did not allow us to study immune markers in dynamics because of quick death of animals within 1–3 days. Light and mild ADBC were characterized by lower thymus weight, subsiding of production of hemolisin, and increased spleen weight and RHSST. The increase of agglutinizing bodies was especially robust in the 1st group of animals. These findings indicate that infectious process during EHS develops not only in lung, kidneys, but also in the CNS. Second part of the study was performed on 20 white rats. EHS was provoked as described earlier (n = 14). Animals were killed on 1st, 3rd, and 10th day by thiopental. Morphological control of subneocortical injury was performed on teonin-coloured (according to Nissel) frontal cuts of brain. 10 rats out of 14 under microscopical examination of brain, in addition to generally known and typical changes for acute ADBC, also showed clear inflammation of brain tissue close and far from the centre of EHS. Signs of productive ependimatitis and local vaculitis consisting of microglia cell and lymphocytes resemble inflammatory changes in brain during viral infections. In control group (n = 6) such changes were seen only in 1 rat out of 6, suggesting that activation of latent infection without EHS develops much more seldom.Conclusions: Our experimental model may be used to model EHS of different degree of intensity on small laboratory animals such as mice. During the EHS, immunopathology-like immunodeficiency of different levels was observed. During the development of post-stroke condition, the development of nonspecific morphological changes and activation of latent infection in the form of encephalitis were hystologically detected