Made available in DSpace on 2014-06-11T19:29:17Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-06-19Bitstream added on 2014-06-13T18:59:01Z : No. of bitstreams: 1 marques_co_me_botfm.pdf: 378901 bytes, checksum: 2a06b8e8fb2e48ad5f6c9ce7c12f4c38 (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Choque hemorrágico reduz o fluxo sanguíneo e a oxigenação teciduais, bem como a remoção de produtos de degradação. A hipóxia tecidual provoca alteração na síntese e liberação de citocinas pró-inflamatórias. A glibenclamida, antagonista dos canais KATP, em rins de ratos anestesiados com sevoflurano e que sofreram hemorragia, preservou mais a histologia e a função renais. O objetivo deste estudo foi verificar se houve alterações da concentração sérica e da expressão renal das citocinas IL-1 e TNF- em ratos que receberam sevoflurano e glibenclamida e que sofreram hemorragia, sem reposição adequada da volemia. Dois grupos de ratos Wistar (n=10) anestesiados com sevoflurano: G1, controle, e G2, com glibenclamida, 1μg/g iv, submetidos à hemorragia de 30% da volemia (10% a cada 10 min), com reposição por Ringer lactato, 5mL/kg/h. Estudaram-se as concentrações séricas de IL-1 e TNF- : na primeira hemorragia (M1) e 50 min após (M2). Em M2, estudou-se a expressão renal dessas citocinas. Em G1, TNF- sérico (normal de 143pg/ml): M1=178,6pg/mL ± 33,5 e M2=509,2pg/mL ± 118,8 e IL-1 sérica (normal de 158pg/mL): M1=148,8pg/mL ± 31,3 e M2=322,6pg/mL ± 115,4. Em G2, TNF- sérico: M1=486,2pg/mL ± 83,6 e M2=261,8pg/mL ± 79,5 e IL-1 sérica: M1=347,0pg/mL ± 72,0 e M2=327,3pg/mL ± 90,9. Houve expressão de TNF- e IL-1 nas células tubulares e glomerulares renais, mais marcantes em G2. A hemorragia e glibenclamida aumentaram a concentração sérica e a imunomarcação renal das citocinas IL-1 e TNF- , mas G2 enfrentou a hipotensão conseqüente à hemorragia com vasodilatação (provável ação do TNF- ) e melhor perfusão, resultando em alguma proteção / Hemorrhagic shock reduces blood flow and tissue oxygenation, as well as the removal of degradation products. Tissue hypoxia causes changes in the synthesis and release of proinflammatory cytokines. Treatment with the KATP channel antagonist glibenclamide in sevoflurane-anesthetized rats that suffered from hemorrhaging preserved more renal function and histology. The objective of this study was to verify if there were changes in the serum concentration and renal expression of the IL-1 and TNF- cytokines in rats that received sevoflurane and glibenclamide and had hemorrhaging with inadequate volemia replacement. Two groups of sevofluraneanesthetized Wistar rats (n=10): G1 (control) and G2 (with glibenclamide, 1 μg/g i.v.) were subjected to 30% blood volume hemorrhaging (10% every 10 min), with replacement using Ringer’s lactate, 5 ml/kg/h. The IL-1 and TNF- serum concentrations were studied in the first hemorrhage (M1) and then 50 min later (M2). At M2, the renal expression of these cytokines was also studied. In G1, serum TNF- (normal range around 143 pg/mL) was M1=178.6 ± 33.5 pg/mL and M2=509.2 ± 118.8 pg/mL, while serum IL-1 (normal range around 158 pg/mL) was M1=148.8 ± 31.3 pg/mL and M2=322.6 ±115.4 pg/mL. In G2, serum TNF- was M1=486.2 ± 83.6 pg/mL and M2=261.8 ± 79.5 pg/mL, and serum IL-1 was M1=347.0 ± 72.0 pg/mL and M2=327.3 ±90.9 pg/mL. The expression of TNF- and IL-1 in the renal glomerular and tubular cells was more abundant in the G2 group. Hemorrhage and glibenclamide increased the serum concentration and renal immunoreactions of the TNF- and IL-1 cytokines, but the G2 group experienced hypotension resulting from the hemorrhage with vasodilatation, probably due to TNF- , and better perfusion, resulting in some protection

A clinical trial was undertaken using three different inhalant anaesthetic agents and one intravenous anaesthetic agent in dogs undergoing routine desexing surgery. Healthy adult dogs undergoing either ovariohysterectomy or castration were assessed as to their demeanour, with the more excitable dogs being placed in groups receiving premedication with acepromazine and morphine. All dogs were then randomly assigned an anaesthetic agent for induction of general anaesthesia. The agents were the inhalants halothane, isoflurane and sevoflurane, and the intravenous agent propofol. Inhalant inductions were undertaken using a tight fitting mask attached to a standard anaesthetic machine with a rebreathing circuit, with the maximum dose of inhalant available from a standard vaporiser. Propofol inductions were undertaken via intravenous catheter. Dogs induced with propofol were randomly assigned one of the three inhalant agents for maintenance. Those induced by inhalant agent were maintained using the same agent. The surgical procedure was undertaken in standard fashion, as was recovery from anaesthesia. All dogs received the non-steroidal anti-inflammatory agent meloxicam. Data collection was divided into three stages: induction, maintenance, and recovery from anaesthesia. Variables measured at induction of anaesthesia were time to intubation, number of intubation attempts, tolerance of mask, quality of induction and quality of transfer to the maintenance stage. Standard variables for monitoring of anaesthesia were recorded throughout the maintenance of anaesthesia. Variables measured at recovery were time to righting, time to standing and quality of recovery. The mean time to intubation when using the newer inhalant sevoflurane (196.2 � 14.8sec, mean � SE) was not significantly different to that for halothane (221.4 � 14.0sec) or isoflurane (172.4 � 15.0sec). Time to intubation with isoflurane was significantly faster than with halothane. Mean time to intubation with propofol (85.4 � 7.7sec) was significantly faster than that for any of the three inhalants. Choice of inhalant had no effect on quality of induction. The use of premedication significantly improved the quality of induction. The use of propofol for induction likewise significantly improved the quality of induction. Standard cardiorespiratory variables measured during the maintenance phase of anaesthesia remained within normal clinical ranges for all three inhalants, and were therefore not further analysed. Choice of inhalant agent had no significant effect on the time to righting or standing in recovery. The use of propofol for induction had no effect on these variables. Animals placed in groups receiving premedication had significantly longer times to righting and standing. The oesophageal temperature at the end of the procedure had a significant effect on times to righting and standing, with lower temperatures contributing to slower recoveries. Independent of procedure time, male dogs had shorter times to righting than female dogs.

A clinical trial was undertaken using three different inhalant anaesthetic agents and one intravenous anaesthetic agent in dogs undergoing routine desexing surgery. Healthy adult dogs undergoing either ovariohysterectomy or castration were assessed as to their demeanour, with the more excitable dogs being placed in groups receiving premedication with acepromazine and morphine. All dogs were then randomly assigned an anaesthetic agent for induction of general anaesthesia. The agents were the inhalants halothane, isoflurane and sevoflurane, and the intravenous agent propofol. Inhalant inductions were undertaken using a tight fitting mask attached to a standard anaesthetic machine with a rebreathing circuit, with the maximum dose of inhalant available from a standard vaporiser. Propofol inductions were undertaken via intravenous catheter. Dogs induced with propofol were randomly assigned one of the three inhalant agents for maintenance. Those induced by inhalant agent were maintained using the same agent. The surgical procedure was undertaken in standard fashion, as was recovery from anaesthesia. All dogs received the non-steroidal anti-inflammatory agent meloxicam. Data collection was divided into three stages: induction, maintenance, and recovery from anaesthesia. Variables measured at induction of anaesthesia were time to intubation, number of intubation attempts, tolerance of mask, quality of induction and quality of transfer to the maintenance stage. Standard variables for monitoring of anaesthesia were recorded throughout the maintenance of anaesthesia. Variables measured at recovery were time to righting, time to standing and quality of recovery. The mean time to intubation when using the newer inhalant sevoflurane (196.2 � 14.8sec, mean � SE) was not significantly different to that for halothane (221.4 � 14.0sec) or isoflurane (172.4 � 15.0sec). Time to intubation with isoflurane was significantly faster than with halothane. Mean time to intubation with propofol (85.4 � 7.7sec) was significantly faster than that for any of the three inhalants. Choice of inhalant had no effect on quality of induction. The use of premedication significantly improved the quality of induction. The use of propofol for induction likewise significantly improved the quality of induction. Standard cardiorespiratory variables measured during the maintenance phase of anaesthesia remained within normal clinical ranges for all three inhalants, and were therefore not further analysed. Choice of inhalant agent had no significant effect on the time to righting or standing in recovery. The use of propofol for induction had no effect on these variables. Animals placed in groups receiving premedication had significantly longer times to righting and standing. The oesophageal temperature at the end of the procedure had a significant effect on times to righting and standing, with lower temperatures contributing to slower recoveries. Independent of procedure time, male dogs had shorter times to righting than female dogs.

Orientador: Yara Marcondes Machado Castiglia / Banca: Sueli Aparecida Calvi / Banca: Antonio Carlos Aguiar Brandão / Resumo: Choque hemorrágico reduz o fluxo sanguíneo e a oxigenação teciduais, bem como a remoção de produtos de degradação. A hipóxia tecidual provoca alteração na síntese e liberação de citocinas pró-inflamatórias. A glibenclamida, antagonista dos canais KATP, em rins de ratos anestesiados com sevoflurano e que sofreram hemorragia, preservou mais a histologia e a função renais. O objetivo deste estudo foi verificar se houve alterações da concentração sérica e da expressão renal das citocinas IL-1 e TNF- em ratos que receberam sevoflurano e glibenclamida e que sofreram hemorragia, sem reposição adequada da volemia. Dois grupos de ratos Wistar (n=10) anestesiados com sevoflurano: G1, controle, e G2, com glibenclamida, 1μg/g iv, submetidos à hemorragia de 30% da volemia (10% a cada 10 min), com reposição por Ringer lactato, 5mL/kg/h. Estudaram-se as concentrações séricas de IL-1 e TNF- : na primeira hemorragia (M1) e 50 min após (M2). Em M2, estudou-se a expressão renal dessas citocinas. Em G1, TNF- sérico (normal de 143pg/ml): M1=178,6pg/mL ± 33,5 e M2=509,2pg/mL ± 118,8 e IL-1 sérica (normal de 158pg/mL): M1=148,8pg/mL ± 31,3 e M2=322,6pg/mL ± 115,4. Em G2, TNF- sérico: M1=486,2pg/mL ± 83,6 e M2=261,8pg/mL ± 79,5 e IL-1 sérica: M1=347,0pg/mL ± 72,0 e M2=327,3pg/mL ± 90,9. Houve expressão de TNF- e IL-1 nas células tubulares e glomerulares renais, mais marcantes em G2. A hemorragia e glibenclamida aumentaram a concentração sérica e a imunomarcação renal das citocinas IL-1 e TNF- , mas G2 enfrentou a hipotensão conseqüente à hemorragia com vasodilatação (provável ação do TNF- ) e melhor perfusão, resultando em alguma proteção / Abstract: Hemorrhagic shock reduces blood flow and tissue oxygenation, as well as the removal of degradation products. Tissue hypoxia causes changes in the synthesis and release of proinflammatory cytokines. Treatment with the KATP channel antagonist glibenclamide in sevoflurane-anesthetized rats that suffered from hemorrhaging preserved more renal function and histology. The objective of this study was to verify if there were changes in the serum concentration and renal expression of the IL-1 and TNF- cytokines in rats that received sevoflurane and glibenclamide and had hemorrhaging with inadequate volemia replacement. Two groups of sevofluraneanesthetized Wistar rats (n=10): G1 (control) and G2 (with glibenclamide, 1 μg/g i.v.) were subjected to 30% blood volume hemorrhaging (10% every 10 min), with replacement using Ringer's lactate, 5 ml/kg/h. The IL-1 and TNF- serum concentrations were studied in the first hemorrhage (M1) and then 50 min later (M2). At M2, the renal expression of these cytokines was also studied. In G1, serum TNF- (normal range around 143 pg/mL) was M1=178.6 ± 33.5 pg/mL and M2=509.2 ± 118.8 pg/mL, while serum IL-1 (normal range around 158 pg/mL) was M1=148.8 ± 31.3 pg/mL and M2=322.6 ±115.4 pg/mL. In G2, serum TNF- was M1=486.2 ± 83.6 pg/mL and M2=261.8 ± 79.5 pg/mL, and serum IL-1 was M1=347.0 ± 72.0 pg/mL and M2=327.3 ±90.9 pg/mL. The expression of TNF- and IL-1 in the renal glomerular and tubular cells was more abundant in the G2 group. Hemorrhage and glibenclamide increased the serum concentration and renal immunoreactions of the TNF- and IL-1 cytokines, but the G2 group experienced hypotension resulting from the hemorrhage with vasodilatation, probably due to TNF- , and better perfusion, resulting in some protection / Mestre

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