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Copyright of Brazilian Journal of Biology is the property of Instituto Internacional de Ecologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Resumo Justificativa e objetivos Dexmedetomidina demonstrou efeitos protetores contra a lesão pulmonar in vitro. Neste estudo, investigamos se o pré‐condicionamento com dexmedetomidina protege contra a lesão pulmonar em ratos com choque hemorrágico. Métodos Ratos machos, Sprague‐Dawley , foram aleatoriamente divididos em quatro grupos (n = 8): grupo controle, grupo com choque hemorrágico, grupo com 5 μg.kg−1 de dexmedetomidina (DEX1) e grupo com 10 μg.kg−1 de dexmedetomidina (DEX2). Solução salina ou dexmedetomidina foi administrada durante 20 minutos. Trinta minutos após a injeção, a hemorragia foi iniciada nos grupos choque hemorrágico, DEX1 e DEX2. Quatro horas após a ressuscitação, a proteína e o conteúdo celular no lavado broncoalveolar e a histopatologia pulmonar foram medidos. Malondialdeído, superóxido dismutase, Bcl‐2, Bax e caspase‐3 também foram testados no tecido pulmonar. Resultados Na comparação com o grupo choque hemorrágico, o pré‐tratamento com 5 ug.kg−1 de dexmedetomidina reduziu a apoptose (2,25 ± 0,24 vs. 4,12 ± 0,42%, p < 0,05), escore histológico (1,06 ± 0,12 vs. 1,68 ± 0,15, p < 0,05) e proteína (1,92 ± 0,38 vs. 3,95 ± 0,42 mg.mL−1, p < 0,05) e leucócitos (0,42 ± 0,11 vs. 0,92 ± 0,13 × 109/L, p < 0,05) no lavado broncoalveolar; o que está correlacionado com o aumento da atividade da superóxido dismutase (8,35 ± 0,68 vs. 4,73 ± 0,44 U.mg−1 de proteína, p < 0,05) e diminuição do malondialdeído (2,18 ± 0,19 vs. 3,28 ± 0,27 nmoL.mg−1 de proteína, p < 0,05). O pré‐condicionamento com dexmedetomidina também aumentou o nível de Bcl‐2 (0,55 ± 0,04 vs. 0,34 ± 0,05, p < 0,05) e diminuiu o nível de Bax (0,46 ± 0,03 vs. 0,68 ± 0,04, p < 0,05), caspase‐3 (0,49 ± 0,03 vs. 0,69 ± 0,04, p < 0,05). No entanto, não houve diferença entre os grupos DEX1 e DEX2 para essas proteínas (p > 0,05). Conclusão O pré‐condicionamento com dexmedetomidina tem um efeito protetor contra a lesão pulmonar causada por choque hemorrágico em ratos. Os potenciais mecanismos envolvidos são a inibição da morte celular e a melhora da antioxidação. Porém, não mostrou um efeito dose‐dependente. Abstract Background and objectives Dexmedetomidine has demonstrated protective effects against lung injury in vitro. Here, we investigated whether dexmedetomidine preconditioning protected against lung injury in hemorrhagic shock rats. Methods Male Sprague‐Dawley rats were randomly divided into four groups (n = 8): control group, hemorrhagic shock group, 5 ug.kg−1 dexmedetomidine (DEX1) group, and 10 ug.kg−1 dexmedetomidine (DEX2) group. Saline or dexmedetomidine were administered over 20 min. 30 min after injection, hemorrhage was initiated in the hemorrhagic shock, DEX1 and DEX2 group. Four hours after resuscitation, protein and cellular content in bronchoalveolar lavage fluid, and the lung histopathology were measured. The malondialdehyde, superoxide dismutase, Bcl‐2, Bax and caspase‐3 were also tested in the lung tissue. Results Compare with hemorrhagic shock group, 5 ug.kg−1 dexmedetomidine pretreatment reduced the apoptosis (2.25 ± 0.24 vs. 4.12 ± 0.42%, p < 0.05), histological score (1.06 ± 0.12 vs. 1.68 ± 0.15, p < 0.05) and protein (1.92 ± 0.38 vs. 3.95 ± 0.42 mg.mL−1, p < 0.05) and WBC (0.42 ± 0.11 vs. 0.92 ± 0.13 × 109/L, p < 0.05) in bronchoalveolar lavage fluid. Which is correlated with increased superoxide dismutase activity (8.35 ± 0.68 vs. 4.73 ± 0.44 U.mg−1 protein, p < 0.05) and decreased malondialdehyde (2.18 ± 0.19 vs. 3.28 ± 0.27 nmoL.mg−1 protein, p < 0.05). Dexmedetomidine preconditioning also increased the Bcl‐2 level (0.55 ± 0.04 vs. 0.34 ± 0.05, p < 0.05) and decreased the level of Bax (0.46 ± 0.03 vs. 0.68 ± 0.04, p < 0.05), caspase‐3 (0.49 ± 0.03 vs. 0.69 ± 0.04, p < 0.05). However, we did not observe any difference between the DEX1 and DEX2 groups for these (p > 0.05). Conclusion Dexmedetomidine preconditioning has a protective effect against lung injury caused by hemorrhagic shock in rats. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation. But did not show a dose‐dependent effect. [ABSTRACT FROM AUTHOR]

Copyright of Brazilian Journal of Biology is the property of Instituto Internacional de Ecologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Arquivo Brasileiro de Medicina Veterinaria e Zootecnia is the property of Universidade Federal de Minas Gerais, Escola de Veterinaria and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Arquivo Brasileiro de Medicina Veterinaria e Zootecnia is the property of Universidade Federal de Minas Gerais, Escola de Veterinaria and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Resumo Justificativa O objetivo deste estudo foi investigar os efeitos do brometo de rocurônio administrado intracerebroventricularmente sobre o sistema nervoso central, determinar a dose do limiar convulsivo de rocurônio em ratos e investigar os efeitos de rocurônio no sistema nervoso central em diluições de 1/5, 1/10 e 1/100 da dose do limiar convulsivo determinada. Métodos Uma cânula permanente foi colocada no ventrículo lateral do cérebro dos animais. O estudo foi projetado em duas fases. Na primeira, a dose do limiar convulsivo do brometo de rocurônio foi determinada. Na segunda, o Grupo R 1/5 (n = 6), o Grupo 1/10 (n = 6) e Grupo 1/100 (n = 6) foram formados com doses de 1/5, 1/10 e 1/100, respectivamente, da dose do limiar convulsivo de brometo de rocurônio obtida. Resultados Descobrimos que o valor do limiar convulsivo de brometo de rocurônio é 0,056 ± 0,009 μmoL. O limiar convulsivo, como uma função do peso corporal dos ratos, foi calculado como 0,286 μmoL/kg −1 . Uma dose de 1/5 da dose do limiar convulsivo causou principalmente abertura postural dos membros e tremores em todo o corpo, enquanto uma dose de 1/10 da dose do limiar convulsivo causou agitação e tremores. Uma dose de 1/100 da dose do limiar convulsivo foi associada à diminuição da atividade locomotora. Conclusões Este estudo mostrou que o brometo de rocurônio tem efeitos deletérios relacionados com a dose sobre o sistema nervoso central e pode produzir efeitos excitatórios dependentes da dose e convulsões. Background The aim of this study was to investigate the effects of intracerebroventricularly administered rocuronium bromide on the central nervous system, determine the seizure threshold dose of rocuronium bromide in rats, and investigate the effects of rocuronium on the central nervous system at 1/5, 1/10, and 1/100 dilutions of the determined seizure threshold dose. Methods A permanent cannula was placed in the lateral cerebral ventricle of the animals. The study was designed in two phases. In the first phase, the seizure threshold dose of rocuronium bromide was determined. In the second phase, Group R 1/5 ( n = 6), Group 1/10 ( n = 6), and Group 1/100 ( n = 6) were formed using doses of 1/5, 1/10, and 1/100, respectively, of the obtained rocuronium bromide seizure threshold dose. Results The rocuronium bromide seizure threshold value was found to be 0.056 ± 0.009 μmoL. The seizure threshold, as a function of the body weight of rats, was calculated as 0.286 μmoL/kg −1 . A dose of 1/5 of the seizure threshold dose primarily caused splayed limbs, posturing, and tremors of the entire body, whereas the dose of 1/10 of the seizure threshold dose caused agitation and shivering. A dose of 1/100 of the seizure threshold dose was associated with decreased locomotor activity. Conclusions This study showed that rocuronium bromide has dose‐related deleterious effects on the central nervous system and can produce dose‐dependent excitatory effects and seizures. [ABSTRACT FROM AUTHOR]

Copyright of Pesquisa Veterinaria Brasileira is the property of Colegio Brasileiro de Patologia Animal - CBPA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Resumo Justificativa e objetivos Alterações funcionais e estruturais sérias do trato gastrointestinal são observadas na insuficiência de irrigação sanguínea, levando a alterações da motilidade gastrointestinal. A ativação dos receptores opioides proporciona um efeito cardioprotetor contra a lesão de isquemia/reperfusão ( I /R). O objetivo do presente estudo foi determinar se remifentanil pode ou não reduzir a lesão de I /R do intestino delgado. Métodos Ratos machos albinos, da linhagem Wistar, foram submetidos à isquemia mesentérica (30 minutos) seguida de reperfusão (3 horas). Quatro grupos foram designados: sham controle; remifentanil isolado; controle I /R; remifentanil + I /R. Os animais do grupo remifentanil + I /R foram submetidos à infusão de remifentanil (2 μg kg −1 min −1 ) por 60 min, metade dos quais iniciou antes da indução da isquemia. Coletando os tecidos do íleo, a avaliação dos danos foi baseada nas respostas contráteis ao carbacol, nos níveis de peroxidação lipídica e infiltração de neutrófilos e na observação das características histopatológicas no tecido intestinal. Resultados Após a reperfusão, uma diminuição significativa da resposta contrátil induzida por carbacol, um notável aumento tanto da peroxidação lipídica quanto da infiltração de neutrófilos e uma lesão significativa da mucosa foram observados. A média da resposta contrátil no grupo remifentanil + I /R foi significativamente diferente daquela do grupo I /R. A peroxidação lipídica e a infiltração de neutrófilos também foram significativamente suprimidas pelo tratamento. As amostras de tecido do grupo I /R apresentaram grau 4 na avaliação histopatológica. No grupo remifentanil + I /R, por outro lado, a lesão da mucosa foi moderada, apresentando estadiamento de grau 1. Conclusões O pré‐tratamento com remifentanil pode atenuar a lesão intestinal de I /R em um grau notável, possivelmente pela redução da peroxidação lipídica e da infiltração leucocitária. Background and objectives Serious functional and structural alterations of gastrointestinal tract are observed in failure of blood supply, leading to gastrointestinal dismotility. Activation of opioid receptors provides cardioprotective effect against ischemia–reperfusion ( I /R) injury. The aim of the present study was to determine whether or not remifentanil could reduce I /R injury of small intestine. Methods Male Wistar Albino rats were subjected to mesenteric ischemia (30 min) followed by reperfusion (3 h). Four groups were designed: sham control; remifentanil alone; I /R control; and remifentanil + I /R. Animals in remifentanil + I /R group were subjected to infusion of remifentanil (2 ug kg −1 min −1 ) for 60 min, half of which started before inducing ischemia. Collecting the ileum tissues, evaluation of damage was based on contractile responses to carbachol, levels of lipid peroxidation and neutrophil infiltration, and observation of histopathological features in intestinal tissue. Results Following reperfusion, a significant decrease in carbachol‐induced contractile response, a remarkable increase in both lipid peroxidation and neutrophil infiltration, and a significant injury in mucosa were observed. An average contractile response of remifentanil + I /R group was significantly different from that of the I /R group. Lipid peroxidation and neutrophil infiltration were also significantly suppressed by the treatment. The tissue samples of the I /R group were grade 4 in histopathological evaluation. In remifentanil + I /R group, on the other hand, the mucosal damage was moderate, staging as grade 1. Conclusions The pretreatment with remifentanil can attenuate the intestinal I /R injury at a remarkable degree possibly by lowering lipid peroxidation and leukocyte infiltration. [ABSTRACT FROM AUTHOR]

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Resumo Justificativa e objetivos Neste estudo pesquisamos os efeitos anestésicos e sobre a mucosa da aplicação retal de dexmedetomidina em ratos. Métodos Ratos machos albinos Wistar, com 250‐300 g, foram divididos em quatro grupos: Grupo S (n = 8) foi um grupo sham que serviu de parâmetro para os valores basais normais; Grupo C (n = 8) consistiu em ratos que receberam a aplicação retal apenas de soro fisiológico; Grupo IPDex (n = 8) consistiu em ratos que receberam aplicação intraperitoneal de dexmedetomidina (100 μg kg −1 ) e Grupo RecDex (n = 8) consistiu em ratos que receberam a aplicação retal de dexmedetomidina (100 μg kg −1 ). Para a administração dos fármacos por via retal, usamos cânulas intravenosas de calibre 22, com os estiletes removidos. A administração consistiu em avançar a cânula 1 cm no reto e o volume de administração retal foi de 1 mL para todos os ratos. Os tempos (min) de latência e de anestesia foram registrados. Duas horas após a administração por via retal, 75 mg kg −1 de cetamina foram administrados a todos os grupos para anestesia intraperitoneal, seguido por remoção dos retos dos ratos a uma distância 3 cm distal por meio de procedimento cirúrgico abdominoperineal. Os retos foram histopatologicamente examinados e classificados. Resultados A anestesia foi feita em todos os ratos do grupo RecDex após a administração de dexmedetomidina. O tempo de início da anestesia no Grupo RecDex foi significativamente mais longo e com uma duração mais curta do que no Grupo IPDEx (p < 0,05). No Grupo RecDex, a administração de dexmedetomidina induziu perdas leves a moderadas da arquitetura da mucosa do cólon e reto duas horas após a inoculação retal. Conclusão Embora a administração de 100 μg kg −1 de dexmedetomidina por via retal em ratos tenha resultado em uma duração significativamente maior da anestesia, em comparação com a administração retal de soro fisiológico, nossas avaliações histopatológicas mostraram que a administração retal de 100 μg kg −1 de dexmedetomidina ocasionou danos leves a moderados à estrutura da mucosa retal. Background and objectives In this study, we investigated the anesthetic and mucosal effects of the rectal application of dexmedetomidine to rats. Methods Male Wistar albino rats weighing 250‐300 g were divided into four groups: Group S (n = 8) was a sham group that served as a baseline for the normal basal values; Group C (n = 8) consisted of rats that received the rectal application of saline alone; Group IPDex (n = 8) included rats that received the intraperitoneal application of dexmedetomidine (100 μg kg −1 ); and Group RecDex (n = 8) included rats that received the rectal application of dexmedetomidine (100 μg kg −1 ). For the rectal drug administration, we used 22 G intravenous cannulas with the stylets removed. We administered the drugs by advancing the cannula 1 cm into the rectum, and the rectal administration volume was 1 mL for all the rats. The latency and anesthesia time (min) were measured. Two hours after rectal administration, 75 mg kg −1 ketamine was administered for intraperitoneal anesthesia in all the groups, followed by the removal of the rats’ rectums to a distal distance of 3 cm via an abdominoperineal surgical procedure. We histopathologically examined and scored the rectums. Results Anesthesia was achieved in all the rats in the Group RecDex following the administration of dexmedetomidine. The onset of anesthesia in the Group RecDex was significantly later and of a shorter duration than in the Group IPDEx (p < 0.05). In the Group RecDex, the administration of dexmedetomidine induced mild–moderate losses of mucosal architecture in the colon and rectum, 2 h after rectal inoculation. Conclusion Although 100 μg kg −1 dexmedetomidine administered rectally to rats achieved a significantly longer duration of anesthesia compared with the rectal administration of saline, our histopathological evaluations showed that the rectal administration of 100 μg kg −1 dexmedetomidine led to mild–moderate damage to the mucosal structure of the rectum. [ABSTRACT FROM AUTHOR]

The article presents a study which examined the action of demineralized bovine bone matrix on bone neoformation in rats presented to experimental alcoholism. The goal of the study is to determine whether demineralized bovine bone (Gen-ox) changes bone formation in rats submitted to alcoholism. The study was authorized by the Ethics Committee in Animal Experimentation at the Universidade Estadual Experimentation in Brazil.

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The article evaluates the effects of semicarbazide on the testicular morphology of rats. Results of the study showed normal testicular architecture in rats not treated with semicarbazide. However, rats treated with the agent showed testicular atrophy accompanied by the degeneration of the seminiferous tubules with shrunken and greatly depleted germ cells.

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The article investigates the effects of the use of nandrolone decanoate with vincristine sulphate in the brain and lipid peroxidation in rats. Results of the study indicate that lipid peroxidation increased with the isolated use of vincristine and nandrolone decanoate and with vincristine associated to the highest dose of the ester as well. This suggest that nandrolone when used with vincristine protect the organism from the damaging process involved in free radical production.

Copyright of Revista Odonto Ciencia is the property of EDIPUCRS - Editora Universitaria da PUCRS and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The article discusses research on the interference of age and repetition of similar noxious stimulus on the expression of hyperalgesia. The study procedure included the collection of 60 rats and their arrangement in three groups including a group of three-month-old rats, a group of six-month-old rats, and a group of nine-month-old rats. A formalin solution was injected in the plantar face of the hind paw of the subjects under anesthesia. Results revealed a difference between the hyperalgesia thresholds of younger and older rats.

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista da Faculdade de Odontologia is the property of UFRGS-Faculdade de Odontologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archivos Latinoamericanos de Nutrición is the property of Sociedad Latinoamericana de Nutricion and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)