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Bowel Ischemia

The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform

Patrick Sorkine – 1st expert on this subject based on the ideXlab platform

  • gut decontamination reduces Bowel Ischemia induced lung injury in rats
    Chest, 1997
    Co-Authors: Patrick Sorkine, Oded Szold, Pinhas Halpern, Mordechai Gutman, Mazal Greemland, Valery Rudick, Gideon Goldman

    Abstract:

    Objective To evaluate the effects of gut decontamination on endotoxin, tumor necrosis factor (TNF) levels, and the associated lung injury in a rat model of Bowel Ischemia. Design Summary background data:Gut Ischemia induces disruption of the intestinal mucosal barrier, allowing translocation of bacteria and endotoxin into the blood, which may trigger a systemic inflammatory response and lung injury. Methods Thirty anesthetized rats were randomized into three groups: (1) Ischemia-reperfusion (I/R) alone (a 60-min superior mesenteric artery occlusion and 4 h of reperfusion, n=10); (2) rats that underwent gut decontamination prior to Ischemia (I/R+GD, n=10); and (3) control rats (sham operated, n=10). Serum levels of lipopolysaccharide (LPS) and TNF were measured at the end of the experiment. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Results One hour of Bowel Ischemia and 4 h of reperfusion (I/R) led to elevations of blood LPS and TNF levels of 0.33±0.005 EU/mL and 173±56 pg/mL, which were higher than the sham group (p Conclusions Our data suggest that gut decontamination can reduce the generation of LPS, TNF, and the severity of lung damage that often follows Ischemia and reperfusion of the intestine in rats.

  • Soluble tumor necrosis factor receptors reduce Bowel Ischemia-induced lung permeability and neutrophil sequestration.
    Critical Care Medicine, 1995
    Co-Authors: Patrick Sorkine, Pinhas Halpern, Valery Rudick, Arik Setton, Ariel Miller, Sylvia Marmor, Joseph M. Klausner, Guideon Goldman

    Abstract:

    Objectives : To evaluate the possible role of tumor necrosis factor (TNF) in the development of lung injury after Bowel Ischemia, and the ability of TNF-soluble receptors to negate TNF toxicity, using a rat small Bowel Ischemia and reperfusion model. Design : Prospective, randomized, controlled laboratory study. Setting : Research laboratory. Subjects : Forty adult male Sprague-Dawley rats weighing ∼300 g. Interventions : The rats were divided equally into four groups : a) Ischemia and reperfusion alone ; b) those animals receiving TNF antibodies (1 mL) before reperfusion ; and c) those animals receiving 200 μg of human recombinant TNF soluble receptors. These 30 anesthetized rats underwent 60 mins of superior mesenteric artery occlusion per 4 hrs of reperfusion. The remaining ten animals were sham operated (laparotomy), serving as controls. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Measurements and Main Results : Thirty and 60 mins after declamping and reperfusion, plasma TNF concentrations increased to 830 ± 66 and 173 ± 56 pg/mL, respectively, compared with 10 pg/mL before Ischemia (p < .001). In sham-operated control rats, TNF concentrations did not increase from baseline concentrations. Four hours after reperfusion, sequestration of neutrophils in the pulmonary microcirculation was noted (319 ± 60 vs. 84 ± 13 neutrophils/10 high-power fields in sham-operated rats [p

  • soluble tumor necrosis factor receptors reduce Bowel Ischemia induced lung permeability and neutrophil sequestration
    Critical Care Medicine, 1995
    Co-Authors: Patrick Sorkine, Pinhas Halpern, Valery Rudick, Arik Setton, Ariel Miller, Sylvia Marmor, Joseph M. Klausner, Guideon Goldman

    Abstract:

    Objectives : To evaluate the possible role of tumor necrosis factor (TNF) in the development of lung injury after Bowel Ischemia, and the ability of TNF-soluble receptors to negate TNF toxicity, using a rat small Bowel Ischemia and reperfusion model. Design : Prospective, randomized, controlled laboratory study. Setting : Research laboratory. Subjects : Forty adult male Sprague-Dawley rats weighing ∼300 g. Interventions : The rats were divided equally into four groups : a) Ischemia and reperfusion alone ; b) those animals receiving TNF antibodies (1 mL) before reperfusion ; and c) those animals receiving 200 μg of human recombinant TNF soluble receptors. These 30 anesthetized rats underwent 60 mins of superior mesenteric artery occlusion per 4 hrs of reperfusion. The remaining ten animals were sham operated (laparotomy), serving as controls. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Measurements and Main Results : Thirty and 60 mins after declamping and reperfusion, plasma TNF concentrations increased to 830 ± 66 and 173 ± 56 pg/mL, respectively, compared with 10 pg/mL before Ischemia (p < .001). In sham-operated control rats, TNF concentrations did not increase from baseline concentrations. Four hours after reperfusion, sequestration of neutrophils in the pulmonary microcirculation was noted (319 ± 60 vs. 84 ± 13 neutrophils/10 high-power fields in sham-operated rats [p <.04]). Pulmonary microvascular leak also occurred, as measured by translocation of radiolabeled albumin into the bronchoalveolar space and expressed as the ratio of bronchoalveolar lavage to blood concentrations. This ratio was 5.3 ± 0.8 in ischemic control animals compared with 1.1 ± 0.3 in sham animals (p <.03). Treatment with antibodies to TNF before reperfusion attenuated the pulmonary injury (75 ± 6 neutrophils/10 high-power fields, permeability index 1.6 ± 0.1) less than in ischemic controls (p <.005). A similar protection was achieved with soluble TNF receptors, which prevented Bowel Ischemia-induced lung neutrophil sequestration (117 ± 35 neutrophils/10 high-power fields, pulmonary vascular leak ratio of 2.3 ± 0.1, p <.05). Conclusions : The results of this study show that Ischemia and subsequent reperfusion of the intestine in rats produce lung injury. This injury is mediated, at least in part, by TNF. Soluble TNF receptors are an effective tool in preventing lung TNF injury after intestinal Ischemia. (Crit Care Med 1995 ; 23 :1377-1381)

Guideon Goldman – 2nd expert on this subject based on the ideXlab platform

  • Soluble tumor necrosis factor receptors reduce Bowel Ischemia-induced lung permeability and neutrophil sequestration.
    Critical Care Medicine, 1995
    Co-Authors: Patrick Sorkine, Pinhas Halpern, Valery Rudick, Arik Setton, Ariel Miller, Sylvia Marmor, Joseph M. Klausner, Guideon Goldman

    Abstract:

    Objectives : To evaluate the possible role of tumor necrosis factor (TNF) in the development of lung injury after Bowel Ischemia, and the ability of TNF-soluble receptors to negate TNF toxicity, using a rat small Bowel Ischemia and reperfusion model. Design : Prospective, randomized, controlled laboratory study. Setting : Research laboratory. Subjects : Forty adult male Sprague-Dawley rats weighing ∼300 g. Interventions : The rats were divided equally into four groups : a) Ischemia and reperfusion alone ; b) those animals receiving TNF antibodies (1 mL) before reperfusion ; and c) those animals receiving 200 μg of human recombinant TNF soluble receptors. These 30 anesthetized rats underwent 60 mins of superior mesenteric artery occlusion per 4 hrs of reperfusion. The remaining ten animals were sham operated (laparotomy), serving as controls. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Measurements and Main Results : Thirty and 60 mins after declamping and reperfusion, plasma TNF concentrations increased to 830 ± 66 and 173 ± 56 pg/mL, respectively, compared with 10 pg/mL before Ischemia (p < .001). In sham-operated control rats, TNF concentrations did not increase from baseline concentrations. Four hours after reperfusion, sequestration of neutrophils in the pulmonary microcirculation was noted (319 ± 60 vs. 84 ± 13 neutrophils/10 high-power fields in sham-operated rats [p

  • soluble tumor necrosis factor receptors reduce Bowel Ischemia induced lung permeability and neutrophil sequestration
    Critical Care Medicine, 1995
    Co-Authors: Patrick Sorkine, Pinhas Halpern, Valery Rudick, Arik Setton, Ariel Miller, Sylvia Marmor, Joseph M. Klausner, Guideon Goldman

    Abstract:

    Objectives : To evaluate the possible role of tumor necrosis factor (TNF) in the development of lung injury after Bowel Ischemia, and the ability of TNF-soluble receptors to negate TNF toxicity, using a rat small Bowel Ischemia and reperfusion model. Design : Prospective, randomized, controlled laboratory study. Setting : Research laboratory. Subjects : Forty adult male Sprague-Dawley rats weighing ∼300 g. Interventions : The rats were divided equally into four groups : a) Ischemia and reperfusion alone ; b) those animals receiving TNF antibodies (1 mL) before reperfusion ; and c) those animals receiving 200 μg of human recombinant TNF soluble receptors. These 30 anesthetized rats underwent 60 mins of superior mesenteric artery occlusion per 4 hrs of reperfusion. The remaining ten animals were sham operated (laparotomy), serving as controls. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Measurements and Main Results : Thirty and 60 mins after declamping and reperfusion, plasma TNF concentrations increased to 830 ± 66 and 173 ± 56 pg/mL, respectively, compared with 10 pg/mL before Ischemia (p < .001). In sham-operated control rats, TNF concentrations did not increase from baseline concentrations. Four hours after reperfusion, sequestration of neutrophils in the pulmonary microcirculation was noted (319 ± 60 vs. 84 ± 13 neutrophils/10 high-power fields in sham-operated rats [p <.04]). Pulmonary microvascular leak also occurred, as measured by translocation of radiolabeled albumin into the bronchoalveolar space and expressed as the ratio of bronchoalveolar lavage to blood concentrations. This ratio was 5.3 ± 0.8 in ischemic control animals compared with 1.1 ± 0.3 in sham animals (p <.03). Treatment with antibodies to TNF before reperfusion attenuated the pulmonary injury (75 ± 6 neutrophils/10 high-power fields, permeability index 1.6 ± 0.1) less than in ischemic controls (p <.005). A similar protection was achieved with soluble TNF receptors, which prevented Bowel Ischemia-induced lung neutrophil sequestration (117 ± 35 neutrophils/10 high-power fields, pulmonary vascular leak ratio of 2.3 ± 0.1, p <.05). Conclusions : The results of this study show that Ischemia and subsequent reperfusion of the intestine in rats produce lung injury. This injury is mediated, at least in part, by TNF. Soluble TNF receptors are an effective tool in preventing lung TNF injury after intestinal Ischemia. (Crit Care Med 1995 ; 23 :1377-1381)

Valery Rudick – 3rd expert on this subject based on the ideXlab platform

  • gut decontamination reduces Bowel Ischemia induced lung injury in rats
    Chest, 1997
    Co-Authors: Patrick Sorkine, Oded Szold, Pinhas Halpern, Mordechai Gutman, Mazal Greemland, Valery Rudick, Gideon Goldman

    Abstract:

    Objective To evaluate the effects of gut decontamination on endotoxin, tumor necrosis factor (TNF) levels, and the associated lung injury in a rat model of Bowel Ischemia. Design Summary background data:Gut Ischemia induces disruption of the intestinal mucosal barrier, allowing translocation of bacteria and endotoxin into the blood, which may trigger a systemic inflammatory response and lung injury. Methods Thirty anesthetized rats were randomized into three groups: (1) Ischemia-reperfusion (I/R) alone (a 60-min superior mesenteric artery occlusion and 4 h of reperfusion, n=10); (2) rats that underwent gut decontamination prior to Ischemia (I/R+GD, n=10); and (3) control rats (sham operated, n=10). Serum levels of lipopolysaccharide (LPS) and TNF were measured at the end of the experiment. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Results One hour of Bowel Ischemia and 4 h of reperfusion (I/R) led to elevations of blood LPS and TNF levels of 0.33±0.005 EU/mL and 173±56 pg/mL, which were higher than the sham group (p Conclusions Our data suggest that gut decontamination can reduce the generation of LPS, TNF, and the severity of lung damage that often follows Ischemia and reperfusion of the intestine in rats.

  • Soluble tumor necrosis factor receptors reduce Bowel Ischemia-induced lung permeability and neutrophil sequestration.
    Critical Care Medicine, 1995
    Co-Authors: Patrick Sorkine, Pinhas Halpern, Valery Rudick, Arik Setton, Ariel Miller, Sylvia Marmor, Joseph M. Klausner, Guideon Goldman

    Abstract:

    Objectives : To evaluate the possible role of tumor necrosis factor (TNF) in the development of lung injury after Bowel Ischemia, and the ability of TNF-soluble receptors to negate TNF toxicity, using a rat small Bowel Ischemia and reperfusion model. Design : Prospective, randomized, controlled laboratory study. Setting : Research laboratory. Subjects : Forty adult male Sprague-Dawley rats weighing ∼300 g. Interventions : The rats were divided equally into four groups : a) Ischemia and reperfusion alone ; b) those animals receiving TNF antibodies (1 mL) before reperfusion ; and c) those animals receiving 200 μg of human recombinant TNF soluble receptors. These 30 anesthetized rats underwent 60 mins of superior mesenteric artery occlusion per 4 hrs of reperfusion. The remaining ten animals were sham operated (laparotomy), serving as controls. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Measurements and Main Results : Thirty and 60 mins after declamping and reperfusion, plasma TNF concentrations increased to 830 ± 66 and 173 ± 56 pg/mL, respectively, compared with 10 pg/mL before Ischemia (p < .001). In sham-operated control rats, TNF concentrations did not increase from baseline concentrations. Four hours after reperfusion, sequestration of neutrophils in the pulmonary microcirculation was noted (319 ± 60 vs. 84 ± 13 neutrophils/10 high-power fields in sham-operated rats [p

  • soluble tumor necrosis factor receptors reduce Bowel Ischemia induced lung permeability and neutrophil sequestration
    Critical Care Medicine, 1995
    Co-Authors: Patrick Sorkine, Pinhas Halpern, Valery Rudick, Arik Setton, Ariel Miller, Sylvia Marmor, Joseph M. Klausner, Guideon Goldman

    Abstract:

    Objectives : To evaluate the possible role of tumor necrosis factor (TNF) in the development of lung injury after Bowel Ischemia, and the ability of TNF-soluble receptors to negate TNF toxicity, using a rat small Bowel Ischemia and reperfusion model. Design : Prospective, randomized, controlled laboratory study. Setting : Research laboratory. Subjects : Forty adult male Sprague-Dawley rats weighing ∼300 g. Interventions : The rats were divided equally into four groups : a) Ischemia and reperfusion alone ; b) those animals receiving TNF antibodies (1 mL) before reperfusion ; and c) those animals receiving 200 μg of human recombinant TNF soluble receptors. These 30 anesthetized rats underwent 60 mins of superior mesenteric artery occlusion per 4 hrs of reperfusion. The remaining ten animals were sham operated (laparotomy), serving as controls. Lung permeability was measured using bovine serum albumin labeled with 125 I, and organ injury was assessed histologically. Measurements and Main Results : Thirty and 60 mins after declamping and reperfusion, plasma TNF concentrations increased to 830 ± 66 and 173 ± 56 pg/mL, respectively, compared with 10 pg/mL before Ischemia (p < .001). In sham-operated control rats, TNF concentrations did not increase from baseline concentrations. Four hours after reperfusion, sequestration of neutrophils in the pulmonary microcirculation was noted (319 ± 60 vs. 84 ± 13 neutrophils/10 high-power fields in sham-operated rats [p <.04]). Pulmonary microvascular leak also occurred, as measured by translocation of radiolabeled albumin into the bronchoalveolar space and expressed as the ratio of bronchoalveolar lavage to blood concentrations. This ratio was 5.3 ± 0.8 in ischemic control animals compared with 1.1 ± 0.3 in sham animals (p <.03). Treatment with antibodies to TNF before reperfusion attenuated the pulmonary injury (75 ± 6 neutrophils/10 high-power fields, permeability index 1.6 ± 0.1) less than in ischemic controls (p <.005). A similar protection was achieved with soluble TNF receptors, which prevented Bowel Ischemia-induced lung neutrophil sequestration (117 ± 35 neutrophils/10 high-power fields, pulmonary vascular leak ratio of 2.3 ± 0.1, p <.05). Conclusions : The results of this study show that Ischemia and subsequent reperfusion of the intestine in rats produce lung injury. This injury is mediated, at least in part, by TNF. Soluble TNF receptors are an effective tool in preventing lung TNF injury after intestinal Ischemia. (Crit Care Med 1995 ; 23 :1377-1381)