ISAAC AZEVEDO SILVA

(Fonte: Lattes)
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  • article 9 Citação(ões) na Scopus
    Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats
    (2015) SIMAS, Rafael; FERREIRA, Sueli G.; MENEGAT, Laura; ZANONI, Fernando L.; CORREIA, Cristiano J.; SILVA, Isaac A.; SANNOMIYA, Paulina; MOREIRA, Luiz F.P.
    OBJECTIVES: Brain death is typically followed by autonomic changes that lead to hemodynamic instability, which is likely associated with microcirculatory dysfunction and inflammation. We evaluated the role of the microcirculation in the hemodynamic and inflammatory events that occur after brain death and the effects of autonomic storm inhibition via thoracic epidural blockade on mesenteric microcirculatory changes and inflammatory responses. METHODS: Male Wistar rats were anesthetized and mechanically ventilated. Brain death was induced via intracranial balloon inflation. Bupivacaine (brain death-thoracic epidural blockade group) or saline (brain death group) infusion via an epidural catheter was initiated immediately before brain death induction. Sham-operated animals were used as controls (SH group). The mesenteric microcirculation was analyzed via intravital microscopy, and the expression of adhesion molecules was evaluated via immunohistochemistry 180 min after brain death induction. RESULTS: A significant difference in mean arterial pressure behavior was observed between the brain death-thoracic epidural blockade group and the other groups, indicating that the former group experienced autonomic storm inhibition. However, the proportion of perfused small vessels in the brain death-thoracic epidural blockade group was similar to or lower than that in the brain death and SH groups, respectively. The expression of intercellular adhesion molecule 1 was similar between the brain death-thoracic epidural blockade and brain death groups but was significantly lower in the SH group than in the other two groups. The number of migrating leukocytes in the perivascular tissue followed the same trend for all groups. CONCLUSIONS: Although thoracic epidural blockade effectively inhibited the autonomic storm, it did not affect mesenteric hypoperfusion or inflammation induced by brain death.
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    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
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    PULMONARY MICROCIRCULATION INTRAVITAL MICROSCOPIC STUDY: THE IMPACT OF BRAIN DEATH INDUCTION IN RATS.
    (2015) SIMAS, Rafael; ZANONI, Fernando L.; SILVA, Raphael C.; MENEGAT, Laura; SILVA, Isaac A.; SANNOMIYA, Paulina; MOREIRA, Luiz F.
  • article 6 Citação(ões) na Scopus
    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 Pinho
    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.
  • article 4 Citação(ões) na Scopus
    Inhibition of Autonomic Storm by Epidural Anesthesia Does Not Influence Cardiac Inflammatory Response After Brain Death in Rats
    (2012) SILVA, I. A.; CORREIA, C. J.; SIMAS, R.; CORREIA, C. D. J.; CRUZ, J. W. M. C.; FERREIRA, S. G.; ZANONI, F. L.; MENEGAT, L.; SANNOMIYA, P.; MOREIRA, L. F. P.
    Background. After brain death (BD) donors usually experience cardiac dysfunction, which is responsible for a considerable number of unused organs. Causes of this cardiac dysfunction are not fully understood. Some authors argue that autonomic storm with severe hemodynamic instability leads to inflammatory activation and myocardial dysfunction. Objectives. To investigate the hypothesis that thoracic epidural anesthesia blocks autonomic storm and improves graft condition by reducing the inflammatory response. Methods. Twenty-eight male Wistar rats (250-350 g) allocated to four groups received saline or bupivacaine via an epidural catheter at various times in relation to brain-death induction. Brain death was induced by a sudden increase in intracranial pressure by rapid inflation of a ballon catheter in the extradural space. Blood gases, electrolytes, and lactate analyses were performed at time zero, and 3 and 6 hours. Blood leukocytes were counted at 0 and 6 hours. After 6 hours of BD, we performed euthanasia to measure vascular adhesion molecule (VCAM)-1, intracellular adhesion molecule (ICAM)-1, interleukin (IL)-1 beta, tumor necrosis factor (TNF)-alpha, Bcl-2 and caspase-3 on cardiac tissue. Results. Thoracic epidural anesthesia was effective to block the autonomic storm with a significant difference in mean arterial pressure between the untreated (saline) and the bupivacaine group before BD (P < .05). However, no significant difference was observed for the expressions of VCAM-1, ICAM-1, TNF-alpha, IL-1 beta, Bcl-2, and caspase-3 (P > .05). Conclusion. Autonomic storm did not seem to be responsible for the inflammatory changes associated with BD; thoracic epidural anesthesia did not modify the expression of inflammatory mediators although it effectively blocked the autonomic storm.
  • article 23 Citação(ões) na Scopus
    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.
  • article 1 Citação(ões) na Scopus
    Inhibition of Autonomic Storm by Epidural Anesthesia Does Not Influence Cardiac Inflammatory Response After Brain Death in Rats (September, pg 2213, 2012)
    (2012) SILVA, I. A.; CORREIA, C. J.; SIMAS, R.; CRUZ, J. W. M. C.; FERREIRA, S. G.; ZANONI, F. L.; MENEGAT, L.; SANNOMIYA, P.; MOREIRA, L. F. P.
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    INHIBITION OF AUTONOMIC STORM DOES NOT IMPROVE MICROCIRCULATORY IMPAIRMENT AND INFLAMMATORY RESPONSE IN BRAIN DEAD RATS
    (2013) SIMAS, Rafael; SILVA, Isaac Azevedo; MENEGAT, Laura; FERREIRA, Sueli Gomes; CORREIA, Cristianode Jesus; SANNOMIYA, Paulina; MOREIRA, Luiz Felipe