Visceral ischemia-reperfusion injury promotes tumor necrosis factor (TNF) and interleukin-1 (IL-1) dependent organ injury in the mouse

M. Burress Welborn, Wade G. Douglas, Zaher Abouhamze, Troy Auffenburg, Amer S. Abouhamze, Julie Baumhofer, James M. Seeger, Jeffrey H. Pruitt, Paul D. Edwards, Richard Chizzonite, David Martin, Lyle L. Moldawer, Timothy R S Harward

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Acute visceral ischemia and subsequent reperfusion injury, which accompanies the surgical repair of a thoracoabdominal aorta aneurysm, is associated with high rates of morbidity and mortality. The purpose of the present study was to determine whether endogenous tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) production contributes to organ dysfunction in animals subjected to viscera! ischemia secondary to 30 min of supraceliac aortic occlusion. C57BL6/j mice were treated with either a TNF binding protein (TNF-bp-10 mg/kg) or an anti-IL-1 receptor type 1 antibody (150 μg) 2 h prior to 30 min of supraceliac aortic occlusion. An additional group of mice received 30 min of infrarenal aortic occlusion to determine the contribution of lower torso ischemia-reperfusion injury to the changes seen following supraceliac aortic occlusion. Visceral organ ischemia for 30 min produced by supraceliac aortic occlusion followed by 2 h of reperfusion produced measurable TNF-α in 38% of untreated mice, but TNF-α was undetectable in both sham-operated mice and following infrarenal aortic occlusion. After 2 h of reperfusion, lung myeloperoxidase levels were significantly elevated in the mice experiencing visceral ischemia-reperfusion compared with either a sham operation or infrarenal ischemia-reperfusion (11.6 ± 1.3 U/g vs. 3.4 ±.2 U/g and 3.7 ± 1.0 U/g, respectively, p < .05). Pretreatment with TNF-bp and anti-IL-1 antibody decreased lung neutrophil recruitment (7.2 ± 1.2 U/g and 4.6 ± 1.1 U/g) and capillary membrane permeability changes in mice following visceral ischemia-reperfusion. The present study demonstrates that brief (30 min) clinically relevant visceral ischemia produces TNF-α and IL-1 dependent lung injury.

Original languageEnglish (US)
Pages (from-to)171-176
Number of pages6
JournalShock
Volume6
Issue number3
StatePublished - Sep 1996

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Reperfusion Injury
Interleukin-1
Tumor Necrosis Factor-alpha
Ischemia
Reperfusion
Wounds and Injuries
Interleukin-1 Type I Receptors
Torso
Lung
Viscera
Neutrophil Infiltration
Antibodies
Capillary Permeability
Lung Injury
Peroxidase
Aneurysm
Aorta
Carrier Proteins
Morbidity
Membranes

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Physiology

Cite this

Burress Welborn, M., Douglas, W. G., Abouhamze, Z., Auffenburg, T., Abouhamze, A. S., Baumhofer, J., ... Harward, T. R. S. (1996). Visceral ischemia-reperfusion injury promotes tumor necrosis factor (TNF) and interleukin-1 (IL-1) dependent organ injury in the mouse. Shock, 6(3), 171-176.

Visceral ischemia-reperfusion injury promotes tumor necrosis factor (TNF) and interleukin-1 (IL-1) dependent organ injury in the mouse. / Burress Welborn, M.; Douglas, Wade G.; Abouhamze, Zaher; Auffenburg, Troy; Abouhamze, Amer S.; Baumhofer, Julie; Seeger, James M.; Pruitt, Jeffrey H.; Edwards, Paul D.; Chizzonite, Richard; Martin, David; Moldawer, Lyle L.; Harward, Timothy R S.

In: Shock, Vol. 6, No. 3, 09.1996, p. 171-176.

Research output: Contribution to journalArticle

Burress Welborn, M, Douglas, WG, Abouhamze, Z, Auffenburg, T, Abouhamze, AS, Baumhofer, J, Seeger, JM, Pruitt, JH, Edwards, PD, Chizzonite, R, Martin, D, Moldawer, LL & Harward, TRS 1996, 'Visceral ischemia-reperfusion injury promotes tumor necrosis factor (TNF) and interleukin-1 (IL-1) dependent organ injury in the mouse', Shock, vol. 6, no. 3, pp. 171-176.
Burress Welborn M, Douglas WG, Abouhamze Z, Auffenburg T, Abouhamze AS, Baumhofer J et al. Visceral ischemia-reperfusion injury promotes tumor necrosis factor (TNF) and interleukin-1 (IL-1) dependent organ injury in the mouse. Shock. 1996 Sep;6(3):171-176.
Burress Welborn, M. ; Douglas, Wade G. ; Abouhamze, Zaher ; Auffenburg, Troy ; Abouhamze, Amer S. ; Baumhofer, Julie ; Seeger, James M. ; Pruitt, Jeffrey H. ; Edwards, Paul D. ; Chizzonite, Richard ; Martin, David ; Moldawer, Lyle L. ; Harward, Timothy R S. / Visceral ischemia-reperfusion injury promotes tumor necrosis factor (TNF) and interleukin-1 (IL-1) dependent organ injury in the mouse. In: Shock. 1996 ; Vol. 6, No. 3. pp. 171-176.
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abstract = "Acute visceral ischemia and subsequent reperfusion injury, which accompanies the surgical repair of a thoracoabdominal aorta aneurysm, is associated with high rates of morbidity and mortality. The purpose of the present study was to determine whether endogenous tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) production contributes to organ dysfunction in animals subjected to viscera! ischemia secondary to 30 min of supraceliac aortic occlusion. C57BL6/j mice were treated with either a TNF binding protein (TNF-bp-10 mg/kg) or an anti-IL-1 receptor type 1 antibody (150 μg) 2 h prior to 30 min of supraceliac aortic occlusion. An additional group of mice received 30 min of infrarenal aortic occlusion to determine the contribution of lower torso ischemia-reperfusion injury to the changes seen following supraceliac aortic occlusion. Visceral organ ischemia for 30 min produced by supraceliac aortic occlusion followed by 2 h of reperfusion produced measurable TNF-α in 38{\%} of untreated mice, but TNF-α was undetectable in both sham-operated mice and following infrarenal aortic occlusion. After 2 h of reperfusion, lung myeloperoxidase levels were significantly elevated in the mice experiencing visceral ischemia-reperfusion compared with either a sham operation or infrarenal ischemia-reperfusion (11.6 ± 1.3 U/g vs. 3.4 ±.2 U/g and 3.7 ± 1.0 U/g, respectively, p < .05). Pretreatment with TNF-bp and anti-IL-1 antibody decreased lung neutrophil recruitment (7.2 ± 1.2 U/g and 4.6 ± 1.1 U/g) and capillary membrane permeability changes in mice following visceral ischemia-reperfusion. The present study demonstrates that brief (30 min) clinically relevant visceral ischemia produces TNF-α and IL-1 dependent lung injury.",
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