PAULINA SANNOMIYA

(Fonte: Lattes)
Índice h a partir de 2011
10
Lattes
ResearcherID
Projetos de Pesquisa
Unidades Organizacionais
BMF, ICB - Docente
LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação, Hospital das Clínicas, Faculdade de Medicina

Filtros

Limpar filtros

Configurações

Autor e Coautores FMUSP-HC Normalizados: RAFAEL SIMAS ×

Resultados de Busca

Agora exibindo 1 - 10 de 22
  • conferenceObject
    BRAIN DEATH PARADOXICALLY INDUCES LEUCOPENIA AND REDUCTION IN THE NUMBER OF BONE MARROW CELLS
    (2013) MENEGAT, Laura; BORELLI, Primavera; SIMAS, Rafael; CALIMAN, Julia Maria; SILVA, Luiz Fernando Ferraz; MOREIRA, Luiz Felipe; SANNOMIYA, Paulina
  • conferenceObject
    LYMPHOCYTE SUBSETS, EXPRESSION OF ADHESION MOLECULES AND APOPTOSIS IN BONE MARROW CELLS OF BRAIN-DEAD RATS
    (2015) MENEGAT, Laura; SIMAS, Rafael; ZANONI, Fernando; BORELLI, Primavera; JACYSYN, Jacqueline; MOREIRA, Luiz Felipe; SANNOMIYA, Paulina
  • article 11 Citação(ões) na Scopus
    Intrathecal injection of human umbilical cord blood stem cells attenuates spinal cord ischaemic compromise in rats
    (2014) JUDAS, Gustavo Ieno; FERREIRA, Sueli Gomes; SIMAS, Rafael; SANNOMIYA, Paulina; BENICIO, Anderson; SILVA, Luiz Fernando Ferraz da; MOREIRA, Luiz Felipe Pinho
    OBECTIVES: Spinal cord ischaemia with resulting paraplegia remains a devastating and unpredictable complication after thoraco-abdominal aortic surgery. With the advent of stem cell therapy and its potential to induce nervous tissue regeneration processes, the interest in the use of these cells as a treatment for neurological disorders has increased. Human stem cells, derived from the umbilical cord, are one of the strong candidates used in cell therapy for spinal cord injury because of weak immunogenicity and ready availability. We sought to evaluate the use of human umbilical cord blood stem cells (HUCBSCs) to attenuate the neurological effects of spinal cord ischaemia induced by high thoracic aorta occlusion. METHODS: Forty Wistar rats were randomized to receive intrathecal injection of 10 mu l phosphate buffered saline (PBS) solution containing 1 x 10(4) HUCBSCs, 30 min before (Tpre group: n = 10) and 30 min after (Tpos group: n = 10) descending thoracic aorta occlusion by intraluminal balloon during 12 min. Control groups received only PBS solution (Cpre group: n = 10; and Cpos group: n = 10). During a 28-day observational period, motor function was assessed by a functional grading scale (Basso, Beattie and Bresnahan). Segments of thoracolumbar spinal cord specimens were analysed for histological and immunohistochemical assessment for detection and quantification of human haematopoietic cells (CD45(+)) and apoptosis (transferase-mediated deoxyuridine triphosphate-biotin nick-end labelling). RESULTS: Overall mortality was 12 animals (30%). Therefore, the observational sample was composed of 28 animals. All groups showed similar incidence of paraplegia and mortality. The mean motor function scores showed no difference during time between the animals of each group, excepting for the Tpos group, which improved from 8.14 (+/- 8.6) to 14.28 (+/- 9.8) (P < 0.01). A treatment-by-time interaction was detected among animals that received HUCBSCs 30 min after ischaemia, with BBB scores higher from Days 14 to 28 compared with the first observational day with statistical difference (P = 0.01). Number of viable neurons was higher in the Tpos group (P = 0.14) and the incidence of apoptosis was lower in the same animals (P = 0.048), but showed no difference with its respective control. We confirmed the presence of CD45(+) cells 4 weeks after intrathecal injection in both therapeutic groups but mainly in the Tpos group. CONCLUSIONS: Intrathecal transplantation of HUCBSCs is feasible, and it improved spinal cord function, when they were delivered 30 min after spinal cord ischaemia, in a model of endovascular descending thoracic aorta occlusion in rats. Human umbilical cord blood is one of the potentially useful sources of stem cells for therapy of spinal cord ischaemia.
  • 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 1 Citação(ões) na Scopus
    Effects of the association of diabetes and pulmonary emphysema on cardiac structure and function in rats
    (2015) PETTA, Antonio Di; SIMAS, Rafael; FERREIRA, Clebson L.; CAPELOZZI, Vera L.; SALEMI, Vera M. C.; MOREIRA, Luiz F. P.; SANNOMIYA, Paulina
    Chronic obstructive pulmonary disease is often associated with chronic comorbid conditions of cardiovascular disease, diabetes mellitus and hypertension. This study aimed to investigate the effects of the association of diabetes and pulmonary emphysema on cardiac structure and function in rats. Wistar rats were divided into control non-diabetic instilled with saline (CS) or elastase (CE), diabetic instilled with saline (DS) or elastase (DE), DE treated with insulin (DEI) groups and echocardiographic measurements, morphometric analyses of the heart and lungs, and survival analysis conducted 50 days after instillation. Diabetes mellitus was induced [alloxan, 42 mg/kg, intravenously (iv)] 10 days before the induction of emphysema (elastase, 0.25 IU/100 g). Rats were treated with NPH insulin (4 IU before elastase plus 2 IU/day, 50 days). Both CE and DE exhibited similar increases in mean alveolar diameter, which are positively correlated with increases in right ventricular (RV) wall thickness (P = 0.0022), cavity area (P = 0.0001) and cardiomyocyte thickness (P = 0.0001). Diabetic saline group demonstrated a reduction in left ventricular (LV) wall, interventricular (IV) septum, cardiomyocyte thickness and an increase in cavity area, associated with a reduction in LV fractional shortening (P < 0.05), and an increase in LViv relaxation time (P < 0.05). Survival rate decreased from 80% in DS group to 40% in DE group. In conclusion, alloxan diabetes did not affect RV hypertrophy secondary to chronic emphysema, even in the presence of insulin. Diabetes per se induced left ventricular dysfunction, which was less evident in the presence of RV hypertrophy. Survival rate was substantially reduced as a consequence, at least in part, of the coexistence of RV hypertrophy and diabetic cardiomyopathy.
  • 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 9 Citação(ões) na Scopus
    Acute administration of oestradiol or progesterone in a spinal cord ischaemia-reperfusion model in rats
    (2018) CAVALCANTE, Leonardo Pessoa; FERREIRA, Sueli Gomes; PEREIRA, Daniel Romano; MORAES, Sergio Rodrigues de; SIMAS, Rafael; SANNOMIYA, Paulina; BREITHAUPT-FALOPPA, Ana Cristina; MOREIRA, Luiz Felipe Pinho
    OBJECTIVES: Despite research into protective pharmacological adjuncts, paraplegia persists as a dreaded complication after thoracic and thoracoabdominal aortic interventions. Reports on gender-related neurological outcomes after ischaemic and traumatic brain injuries have led to increased interest in hormonal neuroprotective effects and have generated other studies seeking to prove the neuroprotective effects of the therapeutic administration of 17 beta-oestradiol and of progesterone. We hypothesised that acute administration of oestradiol or progesterone would prevent or attenuate spinal cord ischaemic injury induced by occlusion of the descending thoracic aorta. METHODS: Male rats were divided into groups receiving 280 A mu g/kg of 17 beta-oestradiol or 4 mg/kg of progesterone or vehicle 30 min before transitory endovascular occlusion of the proximal descending thoracic aorta for 12 min. Hindlimb motor function was assessed by a functional grading scale (that of Basso, Beattie and Bresnahan) for 14 days after reperfusion. On the 14th day, a segment of the thoracolumbar spinal cord was harvested and prepared for histological and immunohistochemical analyses. RESULTS: There was significant impairment of the motor function of the hindlimb in the 3 study groups, with partial improvement noticed over time, but no difference was detected between the groups. On Day 1 of assessment, the 17 beta-oestradiol group had a functional score of 9.8 (0.0-16.5); the progesterone group, a score of 0.0 (0-17.1) and the control group, a score of 6.5 (0-16.9); on the 14th day, the 17 beta-oestradiol group had a functional score of 18.0 (4.4-19.4); the progesterone group had a score of 7.5 (0-18.5) and the control group had a score of 17.0 (0-19.9). Analysis of the grey matter showed that the number of viable neurons per section was not different between the study groups on the 14th day. Immunostaining of the spinal cord grey matter was also similar among the 3 groups. CONCLUSIONS: Acute administration of oestradiol or of progesterone 30 min before transitory occlusion of the proximal descending thoracic aorta of male rats could not prevent or attenuate spinal cord ischaemic injury based on an analysis of functional and histological outcomes.
  • conferenceObject
    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 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.