RESUMO
Una actividad económica de exportación importante para Chile es el procesamiento de crustáceos, que tiene la presencia de tareas repetitivas y de carga de materiales y cuyas empresas mantienen caracteristicas similares de tecnología y procesos de trabajo. En esta actividad no existe informacion epidemiologica ni programas ergonómicos establecidos en estos procesos.Este estudio se desarrollo en una empresa de procesamiento de crustáceos en la XII Región de Chile. Se senalaron las tareas criticas desde el punto de vista musculo-esqueletico, a las cuales se les determinó el riesgo de las lesiones de extremidad superior mediante la aplicacion de herramientas ergonómicas como Strain Index, RULA y OCRA. Por otro lado, se reunio la evidencia clinica de riesgo por movimientos repetitivos con un examen fisico y musculo-esqueletico. La percepcion subjetiva de los trabajadores se resgistro con la aplicacion de una encuesta basada en el cuestionario musculo-esqueletico nordico.Este estudio senala el precedente de la existencia de desórdenes musculo-esqueléticos en estas actividades, situación no descrita en la literatura, a partir de lo cual se pueden disenar criticas de formacion continua y vigilancia permanente, en la implementación de un Programa de Vigilancia Epidemiologica que establezca criterios comunes de evaluacion de estas actividades.
Assuntos
Humanos , Masculino , Feminino , Crustáceos , Extremidade Superior/lesões , Indústria de Processamento de Alimentos , Ergonomia , Pesqueiros , Sistema Musculoesquelético/lesões , ChileRESUMO
We have shown previously that rats subjected to tourniquet shock develop an acute form of remote organ injury of the liver that is both Kupffer cell (KC) and polymorphonuclear (PMN) leukocyte dependent. Circulating plasma xanthine oxidase (XO) has been shown to be responsible for the development of endothelial dysfunction and for remote organ injury of the lung and intestine after ischemia-reperfusion protocols. We now hypothesize that XO is released from rat hind limbs upon reperfusion and that it is responsible for KC and PMN leukocyte activation in this shock model. Our results show that about 30% of rat gastrocnemius muscle xanthine dehydrogenase (XD) is converted to XO during the 5-h tourniquet period and that it is released into the femoral vein within 10 min of reperfusion. Total muscle xanthine oxidoreductase activity (XO + XD) decreases within 30 min of reperfusion and is paralleled by a corresponding increase in femoral vein lactic dehydrogenase. In addition, liver tissue XO increases significantly within 30 min of reperfusion without a corresponding conversion of endogenous XD. Conversion of hepatic XD becomes evident 60 min after reperfusion is initiated, as does XO, and alanine aminotransferase (ALT) release into the hepatic vein, presumably from damaged hepatocytes as a consequence of oxidative stress. Tissue myeloperoxidase activity also increases significantly after the 60-min reperfusion period. That XO mediates KC and PMN activation is supported by the following observations: a) the close relationships between plasma XO and the time courses of tumor necrosis factor-alpha TNFalpha release into the hepatic vein and colloidal carbon clearance by KCs; b) that colloidal carbon clearance, TNFalpha and ALT release, loss of tissue free thiols, lipid peroxidation (TBARS), and liver infiltration by PMN neutrophils can also be induced by the administration of exogenous XO to normal rats; and c) pretreatment of rats with allopurinol inhibits KC activation and liver leukocyte infiltration. These results suggest that XO, released from the ischemic limb on reperfusion, is taken up by the liver were it mediates KC and PMN neutrophil activation and thus contributes to the development of multiple system organ failure after hind limb reperfusion.
Assuntos
Membro Posterior/irrigação sanguínea , Isquemia/fisiopatologia , Células de Kupffer/fisiologia , Fígado/fisiopatologia , Neutrófilos/fisiologia , Estresse Oxidativo/fisiologia , Choque/fisiopatologia , Xantina Oxidase/metabolismo , Alanina Transaminase/sangue , Animais , Feminino , L-Lactato Desidrogenase/sangue , Fígado/fisiologia , Ativação de Macrófagos , Músculo Esquelético/fisiopatologia , Ratos , Ratos Sprague-Dawley , Reperfusão , Fatores de Tempo , Torniquetes , Xantina Desidrogenase/metabolismoRESUMO
Küpffer cells (KCs) have been implicated in leukocyte recruitment and microvascular dysfunction associated with liver inflammation. The overall objective of this study was to assess the role of KCs and polymorphonuclear (PMN) leukocytes on the oxidative stress elicited in the liver as a consequence of hind limb reperfusion in rats subjected to tourniquet shock, a shock model that differs from other models in that hepatic injury is a consequence of remote organ damage. Colloidal carbon clearance from blood and its incorporation into KCs demonstrate that these cells are activated after the 2 h hind limb reperfusion period and that they are responsible for the observed oxidative stress and for PMN leukocyte recruitment and activation. Liver oxidative stress in this model is evidenced by increased liver tissue GSSG/GSH ratio, thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, myeloperoxidase (MPO) activity, an index of tissue-associated neutrophil accumulation, and a significant loss in total tissue superoxide dismutase (SOD) activity. Mean arterial blood pressure (MAP), as well as plasma levels of alanine aminotransferase (ALT), an index of hepatic tissue injury, total SOD activity, plasma levels of alpha-tocopherol and beta-carotene, and total plasma nitrite are also affected as a consequence of KC activation after the 2 h hind limb reperfusion period. Inhibition of KC activity by gadolinium chloride (GdCl3) reverted most of the above alterations to values that do no differ from those found in control animals. These results support the hypothesis that hepatic and systemic oxidative stress elicited by hind limb reperfusion in rats subjected to tourniquet shock is both KC and PMN leukocyte dependent.
Assuntos
Células de Kupffer/metabolismo , Fígado/metabolismo , Neutrófilos/metabolismo , Estresse Oxidativo , Choque/fisiopatologia , Alanina Transaminase/metabolismo , Animais , Carbono/metabolismo , Feminino , Gadolínio/farmacologia , Glutationa/metabolismo , Malondialdeído/metabolismo , Ativação de Neutrófilo , Nitritos/sangue , Peroxidase/metabolismo , Pressão , Ratos , Ratos Sprague-Dawley , Reperfusão , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Torniquetes , Vitamina E/sangue , beta Caroteno/sangueRESUMO
The role of nitric oxide (NO) on liver oxidative stress and tissue injury in rats subjected to tourniquet shock was investigated. This shock model differs from others in that injury is a consequence of remote organ damage. Liver oxidative stress becomes evident after hind limb reperfusion, as evidenced by the loss of total tissue thiols; by increases in tissue oxidized glutathione (GSSG), lipid peroxidation (LPO), plasma aminotransferases (alanine aminotransferase (ALT) and (aspartate aminotransferase (AST)), and plasma nitrites; and by a 36% loss in total superoxide dismutase (SOD) activity. Portal blood flow is reduced by 54.1% after 2 h of hind limb reperfusion. Inhibition of NO synthesis with Nomega-nitro-L-arginine methyl ester or L-arginine methyl ester increased mean arterial blood pressure; further reduced portal blood flow; and aggravated liver injury as assessed by further loss in total thiols, increased LPO and GSSG content, and further increases in plasma ALT and AST. Total plasma nitrites were lower than in control animals, and total tissue SOD activity decreased by more than 80%. Treatment with the NO donor sodium nitroprusside reverted the decrease in portal blood flow and also reverted tissue thiol loss, LPO, and GSSG increases, as well as the loss of ALT and AST to plasma and of SOD activity to levels comparable to untreated control shock animals. As expected, plasma nitrites were greater than in tourniquet control animals. These data support the hypothesis that endogenous NO formation protects the rat liver from the consequences of oxidative stress elicited by hind limb reperfusion in rats subjected to tourniquet shock.
Assuntos
Glutationa/metabolismo , Fígado/fisiopatologia , NG-Nitroarginina Metil Éster/farmacologia , Óxido Nítrico Sintase/antagonistas & inibidores , Estresse Oxidativo , Choque Traumático/fisiopatologia , Superóxido Dismutase/metabolismo , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Pressão Sanguínea , Cisteína/metabolismo , Feminino , Dissulfeto de Glutationa/metabolismo , Peroxidação de Lipídeos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Malondialdeído/análise , Nitroprussiato/farmacologia , Ratos , Ratos Sprague-Dawley , Reperfusão , Choque Traumático/metabolismo , Superóxido Dismutase/antagonistas & inibidores , TorniquetesRESUMO
Rats subjected to tourniquet shock suffer a severe form of circulatory shock, tissue and organ oxidative stress, and final multiple system organ failure (MSOF) and death of the animals within 24 h of tourniquet release. The oxidative damage observed in hind-limb muscle tissue after reperfusion does not by itself account for the final systemic and lethal MSOF. We have postulated that organ failure has its genesis in a primary perfusion abnormality, e.g. the hind limbs, which is followed by secondary hypoperfusion of other organs, such as the liver, as has been shown to be the case in several septic shock models. It has also been shown that injured or necrotic tissue can activate neutrophils, Küpffer cells, platelets, and both the complement and coagulation cascades. In turn, complement activation also leads to neutrophil and Küpffer cell activation as assessed by their capacity to generate oxyradicals. Herein we have evaluated the potential protective effect of ibuprofen on hepatic oxygen-derived free radical production, as well as its effects on both polymorphonuclear leucocyte (PMN) activation and liver infiltration. The protective effect of ibuprofen on hepatic oxidative injury was assessed by determining total thiol groups (SH), thiobarbituric acid-reactive substances (TBARS), and by the release of aspartic acid (AsT) and alanine (AIT) aminotransferases in control animals, in animals subjected to 5 h of tourniquets, and in animals after 2 h of hind-limb reperfusion. Liver infiltration by PMNs was determined by histology after staining with eosin-hematoxylin, and PMN activation by their capacity to reduce nitro blue tetrazolium (NBT).(ABSTRACT TRUNCATED AT 250 WORDS)
Assuntos
Ibuprofeno/uso terapêutico , Hepatopatias/prevenção & controle , Espécies Reativas de Oxigênio/metabolismo , Traumatismo por Reperfusão/prevenção & controle , Choque Traumático/metabolismo , Alanina Transaminase/sangue , Animais , Doença Hepática Induzida por Substâncias e Drogas , Estudos de Avaliação como Assunto , Radicais Livres , Hepatopatias/metabolismo , Masculino , Ativação de Neutrófilo/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/complicações , Traumatismo por Reperfusão/metabolismo , Choque Traumático/complicações , Compostos de Sulfidrila/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , TorniquetesRESUMO
We evaluated the role of oxygen free radicals in the induction of acute stress gastric ulcer in rats. After 12 hr of immobility, ulcers of up to 4 mm were observed in the gastric mucosa. Pretreatment with allopurinol, a xanthine oxidase inhibitor, produced a significant reduction in the number and size of lesions (p < 0.0001). No protection was afforded by aluminum hydroxide or ranitidine alone, but enhanced protection was observed when given in association to allopurinol. A secondary role for H ions is suggested by these findings. Our results support the hypothesis of a role of oxygen free radicals in the pathogenesis of stress gastric ulcers. Allopurinol might be used in conditions predisposing to stress in patients.