Vascular relaxation of canine visceral arteries after ischemia by means of supraceliac aortic cross-clamping followed by reperfusion

<p>Abstract</p> <p>Background</p> <p>The supraceliac aortic cross-clamping can be an option to save patients with hipovolemic shock due to abdominal trauma. However, this maneuver is associated with ischemia/reperfusion (I/R) injury strongly related to oxidative stress and reduction of nitric oxide bioavailability. Moreover, several studies demonstrated impairment in relaxation after I/R, but the time course of I/R necessary to induce vascular dysfunction is still controversial. We investigated whether 60 minutes of ischemia followed by 30 minutes of reperfusion do not change the relaxation of visceral arteries nor the plasma and renal levels of malondialdehyde (MDA) and nitrite plus nitrate (NOx).</p> <p>Methods</p> <p>Male mongrel dogs (n = 27) were randomly allocated in one of the three groups: sham (no clamping, n = 9), ischemia (supraceliac aortic cross-clamping for 60 minutes, n = 9), and I/R (60 minutes of ischemia followed by reperfusion for 30 minutes, n = 9). Relaxation of visceral arteries (celiac trunk, renal and superior mesenteric arteries) was studied in organ chambers. MDA and NOx concentrations were determined using a commercially available kit and an ozone-based chemiluminescence assay, respectively.</p> <p>Results</p> <p>Both acetylcholine and calcium ionophore caused relaxation in endothelium-intact rings and no statistical differences were observed among the three groups. Sodium nitroprusside promoted relaxation in endothelium-denuded rings, and there were no inter-group statistical differences. Both plasma and renal concentrations of MDA and NOx showed no significant difference among the groups.</p> <p>Conclusion</p> <p>Supraceliac aortic cross-clamping for 60 minutes alone and followed by 30 minutes of reperfusion did not impair relaxation of canine visceral arteries nor evoke biochemical alterations in plasma or renal tissue.</p

Microstructural analysis of deformation-induced hypoxic damage in skeletal muscle

Deep pressure ulcers are caused by sustained mechanical loading and involve skeletal muscle tissue injury. The exact underlying mechanisms are unclear, and the prevalence is high. Our hypothesis is that the aetiology is dominated by cellular deformation (Bouten et al. in Ann Biomed Eng 29:153–63, 2001; Breuls et al. in Ann Biomed Eng 31:1357–364, 2003; Stekelenburg et al. in J App Physiol 100(6):1946–954, 2006) and deformation-induced ischaemia. The experimental observation that mechanical compression induced a pattern of interspersed healthy and dead cells in skeletal muscle (Stekelenburg et al. in J App Physiol 100(6):1946–954, 2006) strongly suggests to take into account the muscle microstructure in studying damage development. The present paper describes a computational model for deformation-induced hypoxic damage in skeletal muscle tissue. Dead cells stop consuming oxygen and are assumed to decrease in stiffness due to loss of structure. The questions addressed are if these two consequences of cell death influence the development of cell injury in the remaining cells. The results show that weakening of dead cells indeed affects the damage accumulation in other cells. Further, the fact that cells stop consuming oxygen after they have died, delays cell death of other cells

A atividade respiratória mitocondrial é um bom parâmetro para a lesão por isquemia e reperfusão hepática? Is the mitochondrial respiratory activity a good parameter for hepatic ischemia and reperfusion injury?

RACIONAL: A atividade respiratória das mitocôndrias está associada à lesão por isquemia e reperfusão do fígado. OBJETIVO: Investigar in vitro se há obrigatoriedade de impedimento da respiração mitocondrial para que a lesão por isquemia e reperfusão do fígado possa ser detectada. MATERIAIS E MÉTODOS: Vinte e quatro cães de ambos os gêneros foram divididos nos seguintes grupos: controle, cães operados sem sofrer isquemia ou reperfusão hepática; I60, cães submetidos a 60 minutos de isquemia do fígado; I30/R60, cães submetidos a 30 minutos de isquemia e 60 minutos de reperfusão do fígado e I45/R120, cães submetidos a 45 minutos de isquemia e 120 de reperfusão do fígado. Amostras de fígado foram obtidas para dosagem de malondialdeído, para estudo da respiração mitocondrial por meio de traços polarográficos e para avaliação do potencial de membrana mitocondrial. Sangue foi obtido para dosagem de transaminases e desidrogenase lática. RESULTADOS: O grupo I45/R120 apresentou evidente aumento dos valores de transaminases, desidrogenase lática, aumento dos valores de malondialdeído e tendência à diminuição da respiração mitocondrial estimulada por adenosina difosfato, sem haver prejuízo irreversível para a fosforilação oxidativa ou para o potencial de membrana mitocondrial. CONCLUSÃO: A lesão por isquemia e reperfusão do fígado do cão pode ser documentada sem que haja prejuízo demonstrável para a função mitocondrial. Dados referentes à respiração mitocondrial podem não mostrar diferenças significativas em relação aos controles, mesmo em situações de evidente lesão tecidual por isquemia e reperfusão do fígado.<br>BACKGROUND: Mitochondrial respiratory activity is associated with hepatic ischemia/reperfusion injury. AIM: To determine in vitro whether hepatic ischemia/reperfusion injury may be detected regardless mitochondrial respiratory activity. MATERIAL AND METHODS: Twenty-four heartworm-free mongrel dogs of either sex were randomized in the following groups: control, sham-operated dogs; I60, dogs subjected to 60 min of liver ischemia; I30/R60, dogs subjected to 30 min of ischemia e 60 min of reperfusion of liver; I45/R120 animals subjected to 45 min of ischemia and 120 min of reperfusion of liver. Blood and liver samples were taken after surgery to be processed. Mitochondrial respiratory activity was measured with a Clark-type oxygen electrode and mitochondrial membrane potential was calculated. lactic dehydrogenase, aspartate amino transferase and alanine aminotrasferase activities were determinated using laboratory kits, and malondialdehyde content in liver samples was estimated. RESULTS: The group I45/R120 showed increases of serum aminotransferase, lactic dehydrogenase and malondialdehyde in liver samples. Whereas no changes were registered in mitochondrial respiratory activities and mitochondrial membrane potential, a tendency of decrease in the rate of active respiration (state 3) could be observed. CONCLUSION: Under the conditions of this study, the results suggest the data from mitochondrial respiratory activity could show no significance difference among groups in hepatic ischemia/reperfusion injury. Hepatic ischemia reperfusion injury can be detected regardless mitochondrial respiratory activity