CRISTIANO DE JESUS CORREIA

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Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação, Hospital das Clínicas, Faculdade de Medicina

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Autor e Coautores FMUSP-HC Normalizados: PAULINA SANNOMIYA ×

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Agora exibindo 1 - 10 de 25
  • conferenceObject
    Sexual Dimorphism in Lung Inflammatory Process After Brain Death Induction in Rats
    (2014) MOREIRA, L. P.; FERREIRA, S. G.; KUDO, G. K.; CORREIRA, C. J.; TAVARES-DE-LIMA, W.; BREITHAUPT-FALOPPA, A. C.; SANNOMIYA, P.
  • 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.
  • article 7 Citação(ões) na Scopus
    Effects of ethyl pyruvate on leukocyte-endothelial interactions in the mesenteric microcirculation during early sepsis treatment
    (2015) GUARDA, Ismael Francisco Mota Siqueira; CORREIA, Cristiano Jesus; BREITHAUPT-FALOPPA, Ana Cristina; FERREIRA, Sueli Gomes; MORENO, Ana Carolina Ramos; MARTINEZ, Marina Baquerizo; ROCHA-E-SILVA, Mauricio; SANNOMIYA, Paulina
    OBJECTIVES: Experimental studies on sepsis have demonstrated that ethyl pyruvate is endowed with antioxidant and anti-inflammatory properties. This study aimed to investigate the effects of ethyl pyruvate on leukocyteendothelial interactions in the mesenteric microcirculation in a live Escherichia coli-induced sepsis model in rats. METHODS: Male Wistar rats were administered an intravenous suspension of E. coli bacteria or were subjected to a sham procedure. Three hours after bacterial infusion, the rats were randomized into the following groups: a control group without treatment, a group treated with lactated Ringer's solution (4 mL/kg, i.v.), and a group treated with lactated Ringer's solution (4 mL/kg, i.v.) plus ethyl pyruvate (50 mg/kg). At 24 h after bacterial infusion, leukocyte-endothelial interactions were investigated using intravital microscopy, and the expression of P-selectin and intercellular adhesion molecule-1 was evaluated via immunohistochemistry. White blood cell and platelet counts were also determined at baseline and 3 h and 24 h after E. coli inoculation. RESULTS: The non-treated and lactated Ringer's solution-treated groups exhibited increases in the numbers of rolling leukocytes (similar to 2.5-fold increase), adherent cells (similar to 3.0-fold), and migrated cells (similar to 3.5-fold) compared with the sham group. In contrast, treatment with Ringer's ethyl pyruvate solution reduced the numbers of rolling, adherent and migrated leukocytes to the levels observed in the sham group. Additionally, the expression of P-selectin and intercellular adhesion molecule-1 was significantly increased on mesenteric microvessels in the non-treated group compared with the sham group (p<0.001). The expression of both adhesion molecules was reduced in the other groups, with ethyl pyruvate being more effective than lactated Ringer's solution. Infusion of bacteria caused significant leukopenia (3 h), followed by leukocytosis with granulocytosis (24 h). There was also an intense and progressive reduction in the number of platelets. However, no differences were observed after treatment with the different solutions. CONCLUSIONS: The presented data suggest that ethyl pyruvate efficiently reduces the inflammatory response in the mesenteric microcirculation in an experimental model of sepsis induced by live E. coli and is associated, at least in part, with down-regulation of P-selectin and intercellular adhesion molecule-1.
  • article 10 Citação(ões) na Scopus
    Pentoxifylline attenuates leukocyte-endothelial interactions in a two-hit model of shock and sepsis
    (2015) NAKAGAWA, Naomi Kondo; CRUZ JR., Ruy J.; AIKAWA, Priscila; CORREIA, Cristiano J.; CRUZ, Jose Walber Miranda Costa; MAUAD, Thais; ZHANG, Haibo; ROCHA-E-SILVA, Mauricio; SANNOMIYA, Paulina
    Background: This study investigated the effects of pentoxifylline (PTX) combined with resuscitation fluids on microcirculatory dysfunctions in a two-hit model of shock and sepsis. Materials and methods: Male Wistar rats (250 g) were submitted to hemorrhagic shock and reperfusion followed by sepsis induced by cecal ligation and puncture. For the initial treatment of shock, rats were randomly divided into: sham, no injury, no treatment; hypertonic saline solution (HS) (7.5%, 4 mL/kg); lactated Ringer's solution (LR, 3 x shed blood volume); HS + PTX (4 mL/Kg + 25 mg/kg PTX); and LR + PTX (3 x shed blood volume = 25 mg/kg PTX). After 48 h of being exposed to the double injury, leukocyte eendothelial interactions were assessed by intravital microscopy of the mesentery. Endothelial expression of P-selectin and intercellular adhesion molecule-1 (ICAM-1) was evaluated by immunohistochemistry, as well as lung neutrophil infiltration by histology. Results: Lactated Ringer's solution induced marked increases (P < 0.001) in the number of rolling leukocytes per 10 min (two-fold), adherent leukocytes per 100 mu m venule length (sixfold), migrated leukocytes per 5000 mu m(2) (eight-fold), P-selectin and ICAM-1 expression (four-fold), and lung neutrophil infiltration (three-fold) compared with sham. In contrast, PTX attenuated leukocyte-endothelial interactions, P-selectin and ICAM-1 expression at the mesentery when associated with either LR (P < 0.001) or HS (P < 0.05). Neutrophil migration into the lungs was similarly reduced by PTX (P < 0.05). Conclusions: Data presented showed thatpentoxifylline attenuates microcirculatory disturbances at the mesenteric bed with significant minimization of lung inflammation after a double-injury model of hemorrhagicshock and reperfusion followed by sepsis.
  • conferenceObject
    EFFECTS OF 17BETA-ESTRADIOL ON A SUDDEN ONSET BRAIN DEATH MODEL IN MALE RATS
    (2017) VIEIRA, Roberta Figueiredo; BREITHAUPT-FALOPPA, Ana Cristina; MATSUBARA, Bruno Carvalho; RODRIGUES, Geovana; SANCHES, Marcelo Petrof; FERREIRA, Sueli Gomes; CORREIA, Cristiano De Jesus; MOREIRA, Luiz Felipe; SANNOMIYA, Paulina
  • 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
  • article 8 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.
  • conferenceObject
    17 beta-ESTRADIOL AS A NEW THERAPY TO PRESERVE MICROCIRCULATORY PERFUSION IN SMALL BOWEL DONOR
    (2019) VIEIRA, Roberta; BREITHAUPT-FALOPPA, Ana Cristina; MATSUBARA, Bruno Carvalho; FERREIRA, Sueli Gomes; DEJESUSCORREIA, Cristiano; MOREIRA, Luiz Felipe; SANNOMIYA, Paulina
  • article 11 Citação(ões) na Scopus
    17 beta-Estradiol protects against lung injuries after brain death in male rats
    (2018) VIEIRA, Roberta Figueiredo; BREITHAUPT-FALOPPA, Ana Cristina; MATSUBARA, Bruno Carvalho; RODRIGUES, Geovana; SANCHES, Marcelo Petrof; ARMSTRONG- JR., Roberto; FERREIRA, Sueli Gomes; CORREIA, Cristiano de Jesus; MOREIRA, Luiz Felipe P.; SANNOMIYA, Paulina
    BACKGROUND: Brain death elicits microvascular dysfunction and inflammation, and thereby compromises lung viability for transplantation. As 17 beta-estradiol was shown to be anti-inflammatory and vascular protective, we investigated its effects on lung injury after brain death in male rats. METHODS: Wistar rats were assigned to: sham-operation by trepanation only (SH, n = 7); brain death (BD, n = 7); administration of 17-estradiol (280 tg/kg, iv) at 60 minutes after brain death (BD-E2, n = 7). Experiments were performed 180 minutes thereafter. Histopathological changes in the lung were evaluated by histomorphometry. Gene expression of inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), and endothelin-1 was measured by real-time polymerise chain reaction. Protein expression of NO synthases, endothelin-1, platelet endothelial cell adhesion molecule-1 (PECAM-1), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), BCL-2, and caspase 3 was assessed by immunohistochemistry. Cytokines were quantified by enzyme linked immunosorbent assay. RESULTS: Treatment with 17P-estradiol after brain death decreased lung edema and hemorrhage (p < 0.0001), and serum levels of cytokine-induced neutrophil chemoattractant-1 (CINC-1; p = 0.0020). iNOS (p < 0.0001) and VCAM-1 (p < 0.0001) also diminished at protein levels, while eNOS accumulated (p = 0.0002). However, gene expression of iNOS, eNOS, and endothelin-1 was comparable among groups, as was protein expression of endothelin-1, ICAM-1, BCL-2, and caspase 3. CONCLUSIONS: 17P-Estradiol effectively reduces lung injury in brain-dead rats mainly due to its ability to regulate NO synthases. Thus, the drug may improve lung viability for transplantation. J Heart Lung Transplant 2018;37:1381-1387 (C) 2018 International Society for Heart and Lung Transplantation. All rights reserved.