Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although previous studies have reported that neutrophils play an important role in mediating the microvascular injury observed after reperfusion of ischemic intestine, the contribution of these phagocytic cells to the mucosal dysfunction remains unclear. Three series of experiments consisting of an untreated group, a short-term monoclonal antibody (MAb) IB4 treatment group (MAb IB4 given on the day of the experiment), and a long-term MAb IB4 treatment group (3-day pretreatment with MAb IB4) were performed using autoperfused segments of cat ileum exposed to 3 hours of ischemia followed by 1 hour of reperfusion. Mucosal myeloperoxidase activity, an index of mucosal granulocyte levels, increased from 12 to 25 U/g wet wt in the untreated group. In the short-term MAb IB4 experiments, baseline values were very similar to those of the untreated group but no increase in myeloperoxidase activity was observed after ischemia/reperfusion. Long-term pretreatment with MAb IB4 reduced baseline values of myeloperoxidase activity to approximately 1 U/g wet wt; the values remained at this level throughout the experiment. The permeability of the mucosal barrier was quantitated by measuring blood-to-lumen clearance to 51Cr-ethyl-enediaminetetraacetic acid (EDTA). The water absorptive capacity of the intestine was also measured. In the untreated group, mucosal permeability to 51Cr-EDTA increased sixfold and water absorption was abolished after reperfusion. Both short-term and long-term administration of MAb IB4 prevented the net fluid loss into the lumen, but only long-term administration of MAb IB4 blunted the increased mucosal permeability induced by ischemia/reperfusion. These data suggest that interstitial granulocytes contribute significantly to the mucosal dysfunction associated with reperfusion of the ischemic intestine.
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PMID:Ischemia/reperfusion-induced feline intestinal dysfunction: importance of granulocyte recruitment. 132 98

We have recently reported that 45 min of gut ischemia causes moderate 125I-albumin lung leak at 6 hr of reperfusion which was reversed at 18 hr. Our purpose was to determine the effect of a second insult, low dose endotoxin (LPS, 2.5 mg/kg), given 6 hr after gut ischemia/reperfusion (I/R) on this lung injury as assessed by 125I-albumin leak, neutrophil influx (myeloperoxidase assay, MPO), histopathology, and mortality. Rats were randomized to either sham laparotomy (LAP) or 45 min of superior mesenteric artery occlusion and 6 hr later were treated with LPS or saline. At 18 hr reperfusion the lungs were harvested, assayed for 125I-albumin leak and MPO, and microscopically examined by an unbiased observer after routine H&E staining. We observed that LPS increased lung neutrophil levels both with or without gut I/R. However, only the combined insult (I/R + LPS) increased 125I-albumin leak at 18 hr of reperfusion. Lung histology confirmed that the sequential combination of I/R + LPS caused marked interstitial edema and neutrophil sequestration accompanied by alveolar edema, hemorrhage, and fibrinous exudate, while I/R or LAP + LPS did not. The mortality rate of I/R + LPS was 39% which was significantly higher than LAP alone (0%), gut I/R alone (0%), or LAP + LPS (4%). In conclusion, a delayed exposure to low dose endotoxin converts moderate gut I/R-induced lung dysfunction into advanced organ failure.
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PMID:Endotoxin after gut ischemia/reperfusion causes irreversible lung injury. 132 81

Injury to nonpulmonary organ systems often initiates systemic processes that cause recruitment of neutrophils to the lung. We found that rats subjected to intestinal ischemia-reperfusion (I/R) had increased transvascular leak of 125I-labeled albumin into lungs and decreased lung ATP levels (P less than 0.05). In addition, rats subjected to intestinal I/R had increased plasma xanthine oxidase (XO) activity, plasma leukotactic activity for neutrophils, and lung neutrophil retention (assessed by morphometry and myeloperoxidase activity) compared with sham-treated rats (P less than 0.05). By comparison, after intestinal I/R, rats fed an allopurinol- or tungsten-enriched diet had decreased plasma and intestinal XO activities, decreased plasma leukotacic and lung myeloperoxidase (MPO) activities, decreased lung leak, and increased lung ATP levels compared with rats fed control diets (P less than 0.05). Further studies suggested a more specific role for circulating rather than tissue XO in mediating lung neutrophil accumulation but not lung leak. Plasma XO, plasma leukotactic, and lung MPO activities, but not lung leak, increased in rats administered purified XO intravenously. In addition, plasma XO, plasma leukotactic, and lung MPO activities, but not lung leak, decreased in rats administered antisera against XO and then subjected to intestinal I/R. We conclude that circulating XO increases acutely and may contribute to pulmonary retention of neutrophils after an ischemic intestinal insult.
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PMID:Circulating xanthine oxidase mediates lung neutrophil sequestration after intestinal ischemia-reperfusion. 132 31

Oxygenated perfluorocarbon emulsion has been shown to preserve feline cerebral function after ischemia. The postulated protective effects of perfluorocarbons include improvement of blood rheology and prevention of neutrophil adherence by nonchemical inhibition of surface receptors. In this study, we used a well-described gracilis muscle model to investigate whether oxygenated perfluorocarbon can minimize skeletal muscle necrosis by mitigating the degree of leuko-sequestration. In eight adult mongrel dogs, both gracilis muscles were weighed and then subjected to 6 hours of normothermic ischemia followed by 48 hours of normothermic reperfusion. However, one randomly selected side (experimental side) was infused with oxygen (O2) Fluosol-DA 20% (4.4 +/- 0.2 mL O2/100 mL) intra-arterially at 12 mL/min for 40 minutes immediately after ischemia. Muscle biopsy specimens were obtained before ischemia and after 1 hour and 48 hours of reperfusion to estimate myeloperoxidase (MPO) activity, a marker of neutrophil infiltration. After 48 hours, both gracilis muscles were harvested and weighed in all animals. Muscle necrosis was measured by serial transections, nitroblue tetrazolium staining, and computerized planimetry. The transmuscular oxygen tension (pO2) of the gracilis muscle on the experimental side increased from 2 to 4 mm Hg during ischemia to 315 +/- 50 mm Hg during O2 Fluosol-DA 20% infusion. The percentage of muscle necrosis on the control side was 48.08% +/- 8.46%, compared with 27.62% +/- 6.96% on the experimental side (p less than 0.001). MPO activity was significantly higher at 48 hours of reperfusion compared with pre-ischemic and 1-hour reperfusion values (5.46 +/- 1.52 U/mg tissue protein versus 0.06 +/- 0.01 U/mg tissue protein and 0.16 +/- 0.06 U/mg tissue protein, respectively, in the control group; 1.78 +/- 0.60 U/mg tissue protein versus 0.16 +/- 0.08 U/mg tissue protein and 0.27 +/- 0.10 U/mg tissue protein, respectively, in the experimental group, p less than 0.05). However, MPO activity at 48 hours of reperfusion in the experimental group was significantly lower than in the control group (p less than 0.05). There was no difference in the percentage of weight gain between the control and the experimental groups (38.31% +/- 9.36% and 28.34% +/- 7.35%, respectively, p greater than 0.05). These data show that perfluorocarbons minimize the extent of skeletal muscle necrosis in this canine model. Based on our data on MPO activity, we believe t hat the protective effect of perfluorocarbons is in part due to th e decreased leuko-sequestration in the muscle during the the periods of ischemia and reperfusion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reduction of the extent of ischemic skeletal muscle necrosis by perfusion with oxygenated perfluorocarbon. 132 72

Superoxide production was measured as the superoxide dismutase (SOD)-inhibitable portion of nitro blue tetrazolium (NBT) reduction after cerebral ischemia-reperfusion in anesthetized cats equipped with cranial windows. Significant superoxide production was found in the early reperfusion period and continued for more than 1 h after ischemia. Superoxide was not detected in control animals not subjected to ischemia, during ischemia, and at 120 min of reperfusion. After ischemia, the vasoconstrictor response to arterial hypocapnia was reduced. This effect was prevented by pretreatment with SOD plus catalase or by deferoxamine. The response to topical acetylcholine was converted to vasoconstriction after ischemia. The normal vasodilator response reappeared spontaneously at 120 min of reperfusion. The vasodilator response to acetylcholine was preserved in animals pretreated with SOD plus catalase. Blood-brain barrier permeability to labeled albumin and horseradish peroxidase was increased after ischemia. These effects were minimized by pretreatment with SOD and catalase. We conclude that superoxide generation occurs during reperfusion after cerebral ischemia for a fairly long period and that superoxide and its derivatives are responsible at least in part for the vasodilation and the abnormal reactivity as well as for the increase in blood-brain barrier permeability to macromolecules seen after ischemia. Furthermore, the findings suggest that the agent responsible for the vascular abnormalities is hydroxyl radical generated via the iron-catalyzed Haber-Weiss reaction.
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PMID:Oxygen radicals in cerebral ischemia. 133 9

The protective effect of verapamil on the free radical generation in the ischemic myocardium of rabbit has been studied. A significant decrease of the lactate dehydrogenase activity in the ischemic zone was observed compared to the nonischemic control myocardial tissue. The level of malondialdehyde was found to be elevated in the ischemic zone and in other parts of the myocardium. However, there was no alteration in glutathione content in both zones. In addition, an increase in the activity of myeloperoxidase was observed in the ischemic part of the myocardium. At lower doses (30 micrograms/kg), verapamil protected the animals from ischemic changes but did not do so at higher doses (100 micrograms/kg). These results suggest that, in the rabbit, the free radical scavenging mechanism of the heart is not adversely affected during ischemia.
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PMID:Free radical scavenger mechanisms in experimentally induced ischemia in the rabbit heart and protective effect of verapamil. 133 98

Lower torso ischemia and reperfusion leads to both local and remote tissue injuries. The purpose of this study was to assess the role of complement in mediating the local and remote microvascular permeability after bilateral hind limb tourniquet ischemia. Four hours of ischemia and 4 hours of reperfusion produced an increased skeletal muscle permeability index (muscle/blood 125I albumin ratio) of 2.90 +/- 0.35 compared with the index in nonischemic muscle of 0.25 +/- 0.02 (p < 0.01). Muscle wet-to-dry-weight ratio increased from 3.93 +/- 0.04 in sham to 5.55 +/- 0.09 in ischemic muscle (p < 0.0001). Lung permeability rose at 4 hours as indicated by the increased bronchoalveolar lavage (BAL)/blood 125I albumin ratio 4.36 +/- 0.41 x 10(-3) versus sham 2.64 +/- 0.28 x 10(-3) (p < 0.05) and neutrophil sequestration 0.28 +/- 0.02 U/g myeloperoxidase (MPO) versus sham 0.14 +/- 0.02 U/g (p < 0.001). Serum lytic activity of the classical but not the alternate complement pathway was reduced. The soluble complement receptor (sCR1) was used to inhibit complement activity and attenuated the increase in the permeability index after reperfusion in ischemic muscle 1.11 +/- 0.08 (p < 0.01) and reduced the lung BAL/blood 125I albumin ratio to sham levels 2.46 +/- 0.39 x 10(-3) (p < 0.05) at 6 mg/animal, without reducing the lung neutrophil sequestration, 0.24 +/- 0.02 U/g. The authors conclude that complement activation occurred during tourniquet ischemia and mediated permeability changes in the ischemic muscle and the lungs during reperfusion.
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PMID:Blockade of complement activation prevents local and pulmonary albumin leak after lower torso ischemia-reperfusion. 133 45

The influence of oxygen free radical scavengers and anti-inflammatory drugs on postischemic lipid peroxidation and myeloperoxidase activity was shown. The best results were obtained from vitamin E and the antiinflammatory treatment with CP and SUL, whereas an iron elimination only showed slight effects on myeloperoxidase activity above all. In experiments without therapy a linear increase of lipid peroxides dependent on reperfusion durance was found, whereas myeloperoxidase already showed a remarkable increase during ischemia and early reperfusion. This difference can be interpreted by scavenging mechanisms, which are overcharged after an appointed durance of reperfusion.
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PMID:Influence of anti-inflammatory drugs and free radical scavengers on intestinal ischemia induced oxidative tissue damage. 133 51

Reactive oxygen metabolites (ROM) may play a role in the pathophysiology of inflammatory bowel disease (IBD) and ischemia-reperfusion-induced intestinal injury. Although there are many reports of intestinal mucosal injury associated with neutrophil-derived ROM, free radicals themselves have not been reported to induce intestinal mucosal injury. We administered intrarectally 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) to rats, an azo compound that generates free radicals in vitro. Acute mucosal injury was assessed histologically by light microscopy and biochemically by myeloperoxidase (MPO) activity. Intrarectal administration of AAPH (60, 90, 150 mg/kg) caused erythema, edema, and histologically verifiable mucosal inflammation. MPO activity was increased 9- to 18-fold above the control level. The levels of thiobarbituric acid (TBA) reactants and sulfhydryls (SH) were significantly (P less than 0.01) increased and decreased, respectively, by 90 mg/kg AAPH. Sulfasalazine, 5-aminosalicylic acid, the LTB4 receptor antagonist SC-41930, and the antioxidant glutathione prevented the inflammation. This model of mucosal inflammation may be useful in evaluating new therapeutic agents for the treatment of IBD.
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PMID:Induction of colitis in rats by 2-2'-azobis(2-amidinopropane) dihydrochloride. 134 11

Neutrophils play an important role in ischemia-reperfusion (I/R)-induced vascular injury in the small intestine. Monoclonal antibodies against the leukocyte adhesion glycoprotein CD11/CD18 afford protection against I/R-induced microvascular injury. It has been suggested that the response to I/R differs between the various layers of the bowel wall, with relatively few granulocytes accumulating in the mucosa compared with the serosa or mesentery. The objectives of this study were to determine whether I/R-induced neutrophil accumulation is 1) homogenous in the different layers of intestine (mucosa, submucosa, muscle, and mesentery) and 2) dependent on the expression and/or activation of the leukocyte adhesion glycoprotein CD11/CD18. Neutrophil infiltration was monitored by measuring myeloperoxidase activity in mucosa, submucosa, muscle, and mesentery of cat small intestine subjected to 3 h ischemia (blood flow reduced to 20% of control) and reperfusion. I/R elicited a comparable degree of polymorphonuclear (PMN) infiltration in mucosa, submucosa, and mesentery, with the muscularis exhibiting a greater response. Pretreatment with the CD18-specific monoclonal antibody (IB4) significantly attenuated the I/R-induced PMN accumulation in all layers of the bowel wall and mesentery, indicating that the granulocyte accumulation elicited by I/R is dependent on the expression and/or activation of the leukocyte adhesion molecule CD11/CD18.
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PMID:Granulocyte accumulation in postischemic intestine: role of leukocyte adhesion glycoprotein CD11/CD18. 135 Apr 22


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