Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation

S. D. Ross, C. G. Tribble, Jr Gaughen, K. S. Shockey, P. E. Parrino, I. L. Kron

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Background. There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. Methods. Using an isolated, whole blood-perfused, ventilated rabbit lung model, we sought to characterize the pattern of reperfusion injury and investigate the contribution of neutrophils to this injury. Donor rabbits underwent lung harvest after pulmonary arterial prostoglandin E1 injection and Euro-Collins preservation solution flush. Group I lungs (n = 8) were immediately reperfused without ischemic storage. Group II lungs (n = 8) were stored for 18 h at 4°C before reperfusion. Group III lungs (n = 10) underwent 18 h of ischemic storage and were reperfused with whole blood that was first passed through a leukocyte-depleting filter. All lungs were reperfused for 2 h. Results. Arterial oxygenation in group III progressively improved, and was significantly higher than that of group II after 2 h of reperfusion (272.58 ± 58.97 vs 53.58 ± 5.34 mm Hg, p = 0.01). Both pulmonary artery pressure and pulmonary vascular resistance were significantly reduced in group III when compared with group II (27.85 ± 1.45 vs 44.15 ± 4.77 mm Hg, p = 0.002; and 30,867 ± 2,323 vs 52,775 ± 6,386 dynes · sec · cm-5, p = 0.003, respectively). Microvascular permeability in group III lungs was reduced to 73.98 ± 6.15 compared with 117.16 ± 12.78 ng Evans blue dye/g tissue in group II (p = 0.005). Group III myeloperoxidase activity was 56.92 ± 6.31 ΔOD/g/min compared with 102.84 ±10.41 ΔOd/g/min in group II (p = 0.002). Conclusions. Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.

Original languageEnglish (US)
Pages (from-to)1428-1433
Number of pages6
JournalAnnals of Thoracic Surgery
Volume67
Issue number5
DOIs
StatePublished - Jul 20 1999
Externally publishedYes

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Neutrophil Infiltration
Lung Injury
Reperfusion Injury
Transplantation
Lung
Reperfusion
Neutrophils
Capillary Permeability
Leukocytes
Rabbits
Evans Blue
Vascular Resistance
Pulmonary Artery
Peroxidase
Coloring Agents
Transplants
Pressure

ASJC Scopus subject areas

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation. / Ross, S. D.; Tribble, C. G.; Gaughen, Jr; Shockey, K. S.; Parrino, P. E.; Kron, I. L.

In: Annals of Thoracic Surgery, Vol. 67, No. 5, 20.07.1999, p. 1428-1433.

Research output: Contribution to journalArticle

Ross, S. D. ; Tribble, C. G. ; Gaughen, Jr ; Shockey, K. S. ; Parrino, P. E. ; Kron, I. L. / Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation. In: Annals of Thoracic Surgery. 1999 ; Vol. 67, No. 5. pp. 1428-1433.
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abstract = "Background. There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. Methods. Using an isolated, whole blood-perfused, ventilated rabbit lung model, we sought to characterize the pattern of reperfusion injury and investigate the contribution of neutrophils to this injury. Donor rabbits underwent lung harvest after pulmonary arterial prostoglandin E1 injection and Euro-Collins preservation solution flush. Group I lungs (n = 8) were immediately reperfused without ischemic storage. Group II lungs (n = 8) were stored for 18 h at 4°C before reperfusion. Group III lungs (n = 10) underwent 18 h of ischemic storage and were reperfused with whole blood that was first passed through a leukocyte-depleting filter. All lungs were reperfused for 2 h. Results. Arterial oxygenation in group III progressively improved, and was significantly higher than that of group II after 2 h of reperfusion (272.58 ± 58.97 vs 53.58 ± 5.34 mm Hg, p = 0.01). Both pulmonary artery pressure and pulmonary vascular resistance were significantly reduced in group III when compared with group II (27.85 ± 1.45 vs 44.15 ± 4.77 mm Hg, p = 0.002; and 30,867 ± 2,323 vs 52,775 ± 6,386 dynes · sec · cm-5, p = 0.003, respectively). Microvascular permeability in group III lungs was reduced to 73.98 ± 6.15 compared with 117.16 ± 12.78 ng Evans blue dye/g tissue in group II (p = 0.005). Group III myeloperoxidase activity was 56.92 ± 6.31 ΔOD/g/min compared with 102.84 ±10.41 ΔOd/g/min in group II (p = 0.002). Conclusions. Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.",
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T1 - Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation

AU - Ross, S. D.

AU - Tribble, C. G.

AU - Gaughen, Jr

AU - Shockey, K. S.

AU - Parrino, P. E.

AU - Kron, I. L.

PY - 1999/7/20

Y1 - 1999/7/20

N2 - Background. There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. Methods. Using an isolated, whole blood-perfused, ventilated rabbit lung model, we sought to characterize the pattern of reperfusion injury and investigate the contribution of neutrophils to this injury. Donor rabbits underwent lung harvest after pulmonary arterial prostoglandin E1 injection and Euro-Collins preservation solution flush. Group I lungs (n = 8) were immediately reperfused without ischemic storage. Group II lungs (n = 8) were stored for 18 h at 4°C before reperfusion. Group III lungs (n = 10) underwent 18 h of ischemic storage and were reperfused with whole blood that was first passed through a leukocyte-depleting filter. All lungs were reperfused for 2 h. Results. Arterial oxygenation in group III progressively improved, and was significantly higher than that of group II after 2 h of reperfusion (272.58 ± 58.97 vs 53.58 ± 5.34 mm Hg, p = 0.01). Both pulmonary artery pressure and pulmonary vascular resistance were significantly reduced in group III when compared with group II (27.85 ± 1.45 vs 44.15 ± 4.77 mm Hg, p = 0.002; and 30,867 ± 2,323 vs 52,775 ± 6,386 dynes · sec · cm-5, p = 0.003, respectively). Microvascular permeability in group III lungs was reduced to 73.98 ± 6.15 compared with 117.16 ± 12.78 ng Evans blue dye/g tissue in group II (p = 0.005). Group III myeloperoxidase activity was 56.92 ± 6.31 ΔOD/g/min compared with 102.84 ±10.41 ΔOd/g/min in group II (p = 0.002). Conclusions. Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.

AB - Background. There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. Methods. Using an isolated, whole blood-perfused, ventilated rabbit lung model, we sought to characterize the pattern of reperfusion injury and investigate the contribution of neutrophils to this injury. Donor rabbits underwent lung harvest after pulmonary arterial prostoglandin E1 injection and Euro-Collins preservation solution flush. Group I lungs (n = 8) were immediately reperfused without ischemic storage. Group II lungs (n = 8) were stored for 18 h at 4°C before reperfusion. Group III lungs (n = 10) underwent 18 h of ischemic storage and were reperfused with whole blood that was first passed through a leukocyte-depleting filter. All lungs were reperfused for 2 h. Results. Arterial oxygenation in group III progressively improved, and was significantly higher than that of group II after 2 h of reperfusion (272.58 ± 58.97 vs 53.58 ± 5.34 mm Hg, p = 0.01). Both pulmonary artery pressure and pulmonary vascular resistance were significantly reduced in group III when compared with group II (27.85 ± 1.45 vs 44.15 ± 4.77 mm Hg, p = 0.002; and 30,867 ± 2,323 vs 52,775 ± 6,386 dynes · sec · cm-5, p = 0.003, respectively). Microvascular permeability in group III lungs was reduced to 73.98 ± 6.15 compared with 117.16 ± 12.78 ng Evans blue dye/g tissue in group II (p = 0.005). Group III myeloperoxidase activity was 56.92 ± 6.31 ΔOD/g/min compared with 102.84 ±10.41 ΔOd/g/min in group II (p = 0.002). Conclusions. Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.

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