ISAAC AZEVEDO SILVA
Projetos de Pesquisa
Unidades Organizacionais
3 resultados
Resultados de Busca
Agora exibindo 1 - 3 de 3
conferenceObject Brain death impairs microcirculation with or without autonomic storm: an intravital microscopy study with thoracic epidural anesthesia in rats(2013) SILVA, Isaac Azevedo; SIMAS, Rafael; MENEGAT, Laura; CORREIA, Cristiano de Jesus; FERREIRA, Sueli Gomes; SANNOMIYA, Paulina; MOREIRA, Luiz Felipe Pinho- Influence of brain death and associated trauma on solid organ histological characteristics(2012) SIMAS, Rafael; KOGISO, Diogo Haruo; CORREIA, Cristiano de Jesus; SILVA, Luiz Fernando Ferraz da; SILVA, Isaac Azevedo; CRUZ, Jose Walber Miranda Costa; SANNOMIYA, Paulina; MOREIRA, Luiz Felipe PinhoPURPOSE: 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.
- Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study(2012) SIMAS, Rafael; SANNOMIYA, Paulina; CRUZ, Jose Walber M. C.; CORREIA, Cristiano de Jesus; ZANONI, Fernando Luiz; KASE, Mauricio; MENEGAT, Laura; SILVA, Isaac Azevedo; MOREIRA, Luiz Felipe P.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.