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.

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.

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 Pselectin 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

PRUPOSE: Bacterial translocation has been shown to occur in critically ill patients after extensive trauma, shock, sepsis, or thermal injury. The present study investigates mesenteric microcirculatory dysfunctions, the bacterial translocation phenomenon, and hemodynamic/metabolic disturbances in a rat model of intestinal obstruction and ischemia. METHODS: Anesthetized (pentobarbital 50 mg/kg, i.p.) male Wistar rats (250-350 g) were submitted to intestinal obstruction or laparotomy without intestinal obstruction (Sham) and were evaluated 24 hours later. Bacterial translocation was assessed by bacterial culture of the mesenteric lymph nodes (MLN), liver, spleen, and blood. Leukocyte-endothelial interactions in the mesenteric microcirculation were assessed by intravital microscopy, and P-selectin and intercellular adhesion molecule (ICAM)-1 expressions were quantified by immunohistochemistry. Hematocrit, blood gases, lactate, glucose, white blood cells, serum urea, creatinine, bilirubin, and hepatic enzymes were measured. RESULTS: About 86% of intestinal obstruction rats presented positive cultures for E. coli in samples of the mesenteric lymph nodes, liver, and spleen, and 57% had positive hemocultures. In comparison to the Sham rats, intestinal obstruction induced neutrophilia and increased the number of rolling (~2-fold), adherent (~5-fold), and migrated leukocytes (~11-fold); this increase was accompanied by an increased expression of P-selectin (~2-fold) and intercellular adhesion molecule-1 (~2-fold) in the mesenteric microcirculation. Intestinal obstruction rats exhibited decreased PaCO2, alkalosis, hyperlactatemia, and hyperglycemia, and increased blood potassium, hepatic enzyme activity, serum urea, creatinine, and bilirubin. A high mortality rate was observed after intestinal obstruction (83% at 72 h vs. 0% in Sham rats). CONCLUSION: Intestinal obstruction and ischemia in rats is a relevant model for the in vivo study of mesenteric microcirculatory dysfunction and the occurrence of bacterial translocation. This model parallels the events implicated in multiple organ dysfunction (MOD) and death.

Este estudo avaliou o efeito de métodos de desinfecção [desinfecção química (imersão em solução clorada 100 ppm) ou desinfecção por microondas (690 W por 6 min)] na adaptação interna de bases de próteses totais e na rugosidade superficial da resina. Para o teste de adaptação, 18 bases superiores foram duplicadas a partir de um modelo-mestre metálico e submetidas aos seguintes tratamentos: 1) controle (sem desinfecção), 2) desinfecção química ou 3) desinfecção por microondas. Os procedimentos de desinfecção foram realizados duas vezes (T1, T2) com intervalo de 7 dias. A adaptação interna foi medida no baseline (T0), após T1 e T2 por pesagem de um filme de silicona de adição que reproduzia o espaço entre base de resina e modelo-mestre. Para a rugosidade superficial, 60 espécimes retangulares (5x10x40 mm) receberam polimento mecânico ou químico e foram submetidos aos tratamentos de desinfecção. A rugosidade superficial (Ra) foi registrada após o polimento (T0) e após T1 e T2. Os dados foram analisados por ANOVA GLM para medições repetidas e teste de Bonferroni com nível de significância de 5%. As bases submetidas à desinfecção por microondas tiveram aumento gradual de desadaptação, enquanto que as bases imersas em solução clorada não diferiram do grupo controle. A rugosidade superficial aumentou nos grupos de polimento mecânico e desinfecção por microondas e diminuiu nos grupos de polimento químico.

This study evaluated the effect of disinfection methods [chemical disinfection (immersion in 100 ppm chloride solution) or microwave disinfection (690 W for 6 min)] on the internal adaptation of denture bases and resin surface roughness. For the adaptation test, 18 maxillary denture bases were obtained from stone casts duplicated from a metallic master model and submitted to the following treatments: 1) control (no disinfection), 2) chemical disinfection or 3) microwave disinfection. Disinfection procedures were performed twice (T1, T2) with a 7-day interval between them. Internal adaptation was measured at baseline (T0) and after T1 and T2 by weighing a vinyl polysiloxane film reproducing the gap between the resin base and the master model. For surface roughness measurement, 60 rectangular (5x10x40 mm) resin specimens were either mechanically or chemically polished and then submitted to the disinfection treatments. Surface roughness (Ra) was recorded after polishing (T0) and after T1 and T2. Data were analyzed by ANOVA GLM for repeated measures and Bonferroni correction at 5% significance level. Bases submitted to microwave disinfection had gradual increase of misfit, while bases immersed in chloride solution did not differ from the control group. Surface roughness increased in the mechanical polishing groups with microwave disinfection and decreased in the chemical polishing groups.

OBJETIVO: Este trabalho avaliou o efeito do polimento químico sobre a adaptação interna de bases de próteses totais confeccionadas em resina acrílica ativada termicamente Veracril® polimerizada por técnica convencional (C) ou por microondas (M). MATERIAIS E MÉTODOS: Foram testados seis grupos (n=6/grupo): 1) C + sem polimento (CO); 2) C + polimento químico (CQ); 3) C + banho de água a 75ºC (CW); 4) M + sem polimento (MO); 5) M + polimento químico (MQ); e 6) M + banho de água a 75ºC (MW). A adaptação interna foi avaliada por pesagem em balança analítica de precisão de uma película de silicona de adição interposta entre base de resina e modelo-mestre metálico. A adaptação foi medida imediatamente após o polimento e após 30 dias de armazenamento em água a 37ºC. Os dados foram analisados por ANOVA e teste de Tukey, e por teste t de Student pareado, ao nível de significância de 0,05. RESULTADOS: Não houve diferença significativa na adaptação imediata em função do tipo de polimerização, do polimento ou da interação polimerização/polimento. Após 30 dias, as médias de adaptação (g) foram: CO=2,46 0,32 a; CQ=3,40 ± 0,23 d; CW=3,14 ± 0,22 c; MO=3,23 ± 0,37 c, d; MQ=3,41 ± 0,47 d; MW=2,81 ± 0,33 b (médias seguidas por letras diferentes diferem entre si, alfa=0,05). Todos os grupos apresentaram aumento significativo de desadaptação ao longo do tempo, com exceção do grupo CO. CONCLUSÃO: Os resultados sugerem que as bases de resina Veracril® submetidas a polimento químico apresentaram diminuição de adaptação interna em 30 dias, embora a adaptação imediata não tenha sido afetada.

OBJECTIVE: This study evaluated the effect of chemical polishing on the internal adaptation of complete denture bases fabricated with Veracril® resin and polymerized by either the conventional (C) or microwave (M) techniques. MATERIAL AND METHODS: Six groups (n=6/group) were tested: 1) C + no polishing (CO); 2) C + chemical polishing (CQ); 3) C + immersion in hot water at 75ºC (CW); 4) M + no polishing (MO); 5) M + chemical polishing (MQ); and 6) M + immersion in hot water at 75ºC (MW). Internal adaptation immediately after the polishing treatment and after 30 days of storage in water at 37ºC was evaluated by weighing a vinyl polysiloxane film reproducing the gap between resin base and metallic master model, using a precision scale. Data were analyzed by ANOVA and Tukey test and paired Student's t test, at a significance level of 0.05. RESULTS: No significant difference in immediate adaptation was found as a function of technique, polishing treatment, or interaction of technique/polishing. After 30 days, adaptation means (g) were: CO=2.46±0.32 a; CQ=3.40±0.23 d; CW=3.14±0.22 c; MO=3.23±0.37 c, d; MQ=3.41±0.47 d; MW=2.81±0.33 b (means followed by different letters are statistically different at alpha=0.05). All groups but group CO had significant increase of misfit over the tested period. CONCLUSION: The present results suggest that Veracril® resin denture bases submitted to chemical polishing had decrease of internal adaptation in 30 days, although immediate adaptation was not affected.