The potential etiologic role of tumor necrosis factor in mediating multiple organ dysfunction in rats following intestinal ischemia-reperfusion injury

Resuscitation ◽  
1995 ◽  
Vol 29 (2) ◽  
pp. 157-168 ◽  
Author(s):  
Yong-Ming Yao ◽  
Zhi-Yong Sheng(C.Y. Sheng) ◽  
Yan Yu ◽  
Hui-Min Tian ◽  
Ya-Ping Wang ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Etiologic Role ◽  
Intestinal Ischemia Reperfusion ◽  
Necrosis Factor

Role of JNK phosphorylation in intestinal ischemia/reperfusion injury in mice

2010 ◽  
Vol 30 (2) ◽  
pp. 140-143
Author(s):  
De-yi ZHENG ◽  
Jian-ming WNAG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Kai-yang LU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals The role of ischemic preconditioning and pentoxifylline in intestinal ischemia/reperfusion injury of rats

2017 ◽  
Vol 32 (7) ◽  
pp. 559-567 ◽  
Author(s):  
Teresinha Regina Ribeiro de Oliveira ◽  
Geraldo Ferreira de Oliveira ◽  
Ricardo Santos Simões ◽  
Eduardo Hiroshi Tikazawa ◽  
Hugo Pequeno Monteiro ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Role of extracellular nucleotide phosphohydrolysis in intestinal ischemia‐reperfusion injury

2008 ◽  
Vol 22 (8) ◽  
pp. 2784-2797 ◽  
Author(s):  
Melanie L. Hart ◽  
Martina Henn ◽  
David Köhler ◽  
Doris Kloor ◽  
Michel Mittelbronn ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Extracellular Nucleotide ◽  
Intestinal Ischemia Reperfusion

Effects of Prostacyclin on Hemodynamics after Intestinal Ischemia-Reperfusion

1997 ◽  
Vol 5 (1) ◽  
pp. 43-47
Author(s):  
S Fehmi Katircioğlu ◽  
Eser Özgencil ◽  
Birol Yamak ◽  
Tulga Ulus ◽  
Selime Ayaz ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Reperfusion Injury ◽  
Tumor Necrosis ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Venous Pressure ◽  
Control Group ◽  
Central Venous ◽  
Intestinal Ischemia Reperfusion ◽  
Necrosis Factor

Ten rabbits underwent 30 minutes of superior mesenteric artery occlusion to assess the release of tumor necrosis factor, subcellular damage, and hemodynamic changes after intestinal ischemia-reperfusion injury. Five were treated with prostacyclin 5 ng/kg/min 5 minutes before the arterial occlusion. It was increased to 25 ng/kg/min during occlusion, decreased to 5 ng/kg/min for the first 5 minutes of reperfusion, and then discontinued. A control group of 5 rabbits did not receive any pharmacological agent. Specimens were obtained from the small intestine for electron microscopy after 10 minutes and after 60 minutes of reperfusion, while simultaneous blood samples were collected for measurement of tumor necrosis factor. Minimal changes were seen in tissue from the prostacyclin group but severe mitochondrial damage and vacuolation occurred in the control group. The tumor necrosis factor level was 11.97 ± 3.17 U/mL in the control group and 5.06 ± 2.19 U/mL in the prostacyclin group, one hour after the end of mesenteric occlusion ( p < 0.05). Hemodynamic status, assessed by central venous and arterial pressures, was much more affected in the control group than in the prostacyclin group. Mean arterial pressure was 71 ± 5 mm Hg in the control group, and 91 ± 6 mm Hg in the prostacyclin group ( p < 0.05). Central venous pressure was 5.3 ± 0.9 mm Hg in the control group and 2.3 ± 0.7 mm Hg in the prostacyclin group ( p < 0.05). We conclude that intravenous prostacyclin reduced the severity of reperfusion injury occurring during the early period of reperfusion by inhibiting the release of the toxic mediator tumor necrosis factor, thus decreasing distant organ injury.

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