Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

OBJECTIVE: Experimental findings support clinical evidence that brain death impairs the viability of organs for transplantation, triggering hemodynamic, hormonal, and inflammatory responses. However, several of these events could be consequences of brain death-associated trauma. This study investigated microcirculatory alterations and systemic inflammatory markers in brain-dead rats and the influence of the associated trauma. METHOD: Brain death was induced using intracranial balloon inflation; sham-operated rats were trepanned only. After 30 or 180 min, the mesenteric microcirculation was observed using intravital microscopy. The expression of Pselectin and ICAM-1 on the endothelium was evaluated using immunohistochemistry. The serum cytokine, chemokine, and corticosterone levels were quantified using enzyme-linked immunosorbent assays. White blood cell counts were also determined. RESULTS: Brain death resulted in a decrease in the mesenteric perfusion to 30 percent, a 2.6-fold increase in the expression of ICAM-1 and leukocyte migration at the mesentery, a 70 percent reduction in the serum corticosterone level and pronounced leukopenia. Similar increases in the cytokine and chemokine levels were seen in the both the experimental and control animals. CONCLUSION: The data presented in this study suggest that brain death itself induces hypoperfusion in the mesenteric microcirculation that is associated with a pronounced reduction in the endogenous corticosterone level, thereby leading to increased local inflammation and organ dysfunction. These events are paradoxically associated with induced leukopenia after brain damage.

Effect of glycemic state in rats submitted to status epilepticus during development

O efeito do estado glicêmico sobre o desenvolvimento do status epilepticus (SE) foi estudado em animais de diferentes idades, submetidos ao modelo de epilepsia por pilocarpina. Grupos: I- Ratos com nove dias (P9): IA- Submetidos a 1SE; IB- Tratados com salina; IC- Hiperglicemia induzida; ID- Hiperglicemia induzida+SE; II- Ratos submetidos a 3 episódios consecutivos de SE em P7, P8 e P9; III- Ratos submetidos a 1SE em P17; IV- Ratos submetidos a 1SE em P21. Foram analisados no grupo I a morte celular hipocampal e a expressão do transportador de glicose GLUT3. Os resultados mostraram haver normoglicemia nos grupos IA, IB e II, hipoglicemia no grupo III e hiperglicemia no grupo IV, sendo a glicemia durante o SE, idade dependente. A hiperglicemia induzida durante o SE em P9 protegeu neurônios hipocampais e os grupos IC e ID apresentaram expressão aumentada de GLUT3, mostrando aumento no consumo de glicose pelo hipocampo.