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 P-selectin 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%, a 2.6-fold increase in the expression of ICAM-1 and leukocyte migration at the mesentery, a 70% 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.

PURPOSE:To evaluate histopathological alterations triggered by brain death and associated trauma on different solid organs in rats. METHODS: Male Wistar rats (n=37) were anesthetized with isoflurane, intubated and mechanically ventilated. A trepanation was performed and a balloon catheter inserted into intracraninal cavity and rapidly inflated with saline to induce brain death. After induction, rats were monitored for 30, 180, and 360 min for hemodynamic parameters and exsanguinated from abdominal aorta. Heart, lung, liver, and kidney were removed and fixed in paraffin to evaluation of histological alterations (H&E). Sham-operated rats were trepanned only and used as control group. RESULTS: Brain dead rats showed a hemodynamic instability with hypertensive episode in the first minute after the induction followed by hypotension for approximately 1 h. Histological analyses showed that brain death induces vascular congestion in heart (p<0.05), and lung (p<0.05); lung alveolar edema (p=0.001), kidney tubular edema (p<0.05); and leukocyte infiltration in liver (p<0.05). CONCLUSIONS: Brain death induces hemodynamic instability associated with vascular changes in solid organs and compromises most severely the lungs. However, brain death associated trauma triggers important pathophysiological alterations in these organs. Key words: Brain Death. Craniocerebral Trauma. Pathology. Rats. RESUMO OBJETIVO:Avaliar as alterações histopatológicas desencadeadas pela morte encefálica e pelo trauma associado em diferentes órgãos sólidos em ratos. MÉTODOS: Ratos Wistar machos (n=37) foram anestesiados com isoflurano, entubados e mecanicamente ventilados. Foi realizada trepanação e um cateter foi inserido na cavidade intracraniana e insuflado rapidamente para induzir morte encefálica. Após a indução, os ratos foram monitorados por 30, 180 e 360 min para parâmetros hemodinâmicos e exsanguinados pela aorta abdominal. Coração, pulmão, fígado e rim foram removidos e fixados em parafina para avaliação de alterações histológicas (H&E). Ratos falso-operados foram apenas trepanados e usados como grupo controle. RESULTADOS: Ratos com morte encefálica apresentaram instabilidade hemodinâmica com episódio hipertensivo no primeiro minuto após a indução seguido de hipotensão por aproximadamente 1 hora. Análises histológicas demonstraram que a morte encefálica induz congestão vascular no coração (p<0,05) e pulmão (p<0,05); edema alveolar (p=0,001); edema tubular (p<0,05); e infiltrado leucocitário no fígado (p<0,05). CONCLUSÕES: A morte encefálica induz instabilidade hemodinâmica associada com mudanças vasculares em órgãos sólidos e compromete mais severamente os pulmões. Contudo, o trauma associado à morte encefálica desencadeia importantes alterações fisiopatológicas naqueles órgãos. Descritores: Morte Encefálica. Traumatismos Craniocerebrais. Patologia. Ratos.Simas R et al.

Brain perfusion for adequate cerebral protection has changed over the years. The limitations of the time during total circulatory arrest with deep hypothermia, the inefficient cerebral metabolism during retrograde perfusion and special care to prevent cerebral embolism during antegrade perfusion have resulted in the development of different methods of cerebral protection during the evolution of aortic arch operations. Antegrade cerebral perfusion associated with moderate hypothermia is today, considered the best option for cerebral protection. 236DIAS, RR ET AL -Cerebral protection: sites of arterial cannulation and brain perfusion routes Braz J Cardiovasc Surg 2007; 22(2): 235-240

The new surgical strategy to treat patients with acute type A aortic dissection, the hybrid procedure with an uncovered aortic stent, allows surgeons to treat the aortic arch and the proximal descending aorta, besides the ascending segment, without extension of cerebral or systemic ischemia.

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