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      Effect of different periods of hyperbaric oxygen on ischemia-reperfusion injury of rat small bowel.

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          Abstract

          To determine whether hyperbaric oxygen (HBO) could effectively protect the small intestine mucosa against an ischemic insult, according to different periods of application.

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          Most cited references15

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          Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen.

          S Thom (1990)
          The effects of oxygen at 1, 2, and 3, atmospheres absolute (ATA) were assessed on brain lipid peroxidation caused by carbon monoxide (CO) poisoning in a rat model. Oxygen at 3 ATA, but not 1 ATA, was found to prevent brain lipid peroxidation when administered to rats for 45 min, beginning 45 min subsequent to CO poisoning. Oxygen at 2 ATA had an intermediate effect. The action of hyperbaric oxygen could not be attributed to a more rapid diminution of carboxyhemoglobin, and appears to occur at the level of the brain tissue.
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            Effects of hyperbaric oxygen treatment on neutrophil activation and pulmonary sequestration in intestinal ischemia-reperfusion in rats.

            Treatment with hyperbaric oxygen (HBO) has shown promising results in some models of ischemia, the major effect being a reduction in the local ischemic damage. The present study investigated the effects of HBO treatment on neutrophil activation and leukosequestration during reperfusion following intestinal ischemia in a rat model. The superior mesenteric artery was clamped for 2 h and subsequently reperfused for 90 min. One group of male Sprague-Dawley rats (n = 9) was given HBO and another group (n = 9) served as controls. Prior to ischemia, leukocytes and erythrocytes were separated, radiolabelled with 111ln and 51Cr, respectively, and reinfused. Leukocyte transit factor, the ratio between the mean passage time of leukocytes and erythrocytes was used to quantitate leukosequestration and the fraction of circulating, spontaneously nitroblue tetrazolium (NBT)-reducing neutrophils was used to measure the degree of neutrophil preactivation. HBO treatment reduced the level of leukocyte pooling significantly, especially in the lungs but also, to a minor degree, in the systemic vascular bed. The percentage of NBT-positive cells increased in all animals after reperfusion, but the increase was significantly reduced by HBO treatment. In conclusion, HBO treatment reduces leukosequestration and neutrophil preactivation following intestinal ischemia-reperfusion.
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              Metabolic effects of hyperbaric oxygen in postischemic muscle.

              In traumatic injuries to the extremities, with a circulatory insufficiency, the resultant ischemia leads to decreasing levels of the energy-rich compounds adenosine triphosphate (ATP) and phosphocreatine (PCr) and increasing levels of lactate in muscle. A tourniquet model for temporary ischemia was used to determine if hyperbaric oxygen treatment could enhance the cellular metabolic restitution when the circulation was restored. The circulation of the rat hindlimb was interrupted for 1.5 and 3 hours. After 1.5 hours of ischemia, the levels of adenosine triphosphate, phosphocreatine, and lactate were restored to normal in muscle biopsies taken 5 hours after the ischemia. After 3 hours of ischemia, there were marked reductions of adenosine triphosphate and phosphocreatine and elevated lactate values in the postischemic muscle, indicating severe ischemic damage. Hyperbaric oxygen treatment at 2.5 atm for 45 minutes reduced these changes significantly. A certain number of hyperbaric oxygen treatments were necessary to maintain this effect. It is concluded that repeated hyperbaric oxygen treatments in the postischemic phase stimulate aerobic metabolism.
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                Author and article information

                Journal
                Acta Cir Bras
                Acta cirurgica brasileira
                0102-8650
                0102-8650
                February 19 2008
                : 23
                : 1
                Affiliations
                [1 ] University of Grande Dourados, Mato Grosso do Sul, Brazil. bertoletto@terra.com.br
                Article
                S0102-86502008000100003
                18278387
                e0106468-1e09-44b2-8aba-ef5275c41788
                History

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