Adherent neutrophils mediate permeability after atelectasis

G. Goldman, R. Welbourn, R. Rothlein, M. Wiles, L. Kobzik, C. R. Valeri, D. Shepro, H. B. Hechtman, D. S. Mulder, B. A. Pruitt, David Herndon, A. H. Harken, A. Naji

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Abstract

Re-expansion of atelectatic lung is associated with increased permeability. This study tests whether neutrophils mediate this event. Right middle lobar atelectasis was induced in anesthetized rabbits (n = 18) by intraluminal obstruction of the bronchus after a 20-minute ventilation with 100% O2. After 1 hour of bronchial obstruction and 20 minutes after lobar re-expansion, leukopenia was noted, 2870 ± 210 white blood cells (WBC)/mm3, relative to control animals treated with a noninflated balloon catheter, 6500 ± 410 WBC/mm3 (p < 0.05). Three hours after re-expansion, neutrophils were sequestered in the previously atelectatic region 78 ± 7 polymorphonuclear leukocytes (PMN)/10 high-power field (HPF), as well as in nonatelectatic areas, 40 ± 3 PMN/10 HPF, higher than control values of 26 ± 3 PMN/10 HPF (p < 0.05). In the atelectatic region, neutrophil sequestration was associated with increased protein concentration in lobar bronchoalveolar lavage (BAL) of 1370 ± 100 μg/mL, higher than control values of 270 ± 20 μg/mL (p < 0.05). Re-expansion also induced increases in lung wet-to-dry weight ratio (W/d) of 6.2 ± 0.2, higher than control values of 4.3 ± 0.1 (p < 0.05). Rendering rabbits neutropenic (n = 18) (0 to 4 PMN/mm3) limited the atelectasis-induced protein accumulations in BAL (520 ± 60 μg/mL) and increase in lung W/d (5.2 ± 0.1) (both p < 0.05). Intravenous (I.V.; treatment of another group (n = 18) with an anti-CD 18 monoclonal antibody (R 15.7, 1 mg/kg) before balloon deflation prevented leukopenia (6550 ± 560 WBC/mm3), minimized neutrophil sequestration (36 ± 2 PMN/10 HPF), and attenuated protein leak (710 ± 95 μg/mL) and the increased lung W/d (5.6 ± 0.1) (all p < 0.05). A final atelectatic group (n = 9) was treated I.V. with the antiintercellular adhesion molecule-1 monoclonal antibody (RR 1/1, 1 mg/kg), which also prevented leukopenia and showed similar protection of microvascular barrier function. These data indicate that adherent neutrophils in large part mediate lung permeability and edema after atelectasis and re- expansion. Adhesion receptors of both neutrophils and endothelial cells regulate this event.

Original languageEnglish (US)
Pages (from-to)372-380
Number of pages9
JournalAnnals of Surgery
Volume216
Issue number3
StatePublished - 1992
Externally publishedYes

Fingerprint

Pulmonary Atelectasis
Permeability
Neutrophils
Leukopenia
Lung
Leukocytes
Bronchoalveolar Lavage
Monoclonal Antibodies
Rabbits
Proteins
Pulmonary Edema
Bronchi
Ventilation
Edema
Catheters
Endothelial Cells

ASJC Scopus subject areas

  • Surgery

Cite this

Goldman, G., Welbourn, R., Rothlein, R., Wiles, M., Kobzik, L., Valeri, C. R., ... Naji, A. (1992). Adherent neutrophils mediate permeability after atelectasis. Annals of Surgery, 216(3), 372-380.

Adherent neutrophils mediate permeability after atelectasis. / Goldman, G.; Welbourn, R.; Rothlein, R.; Wiles, M.; Kobzik, L.; Valeri, C. R.; Shepro, D.; Hechtman, H. B.; Mulder, D. S.; Pruitt, B. A.; Herndon, David; Harken, A. H.; Naji, A.

In: Annals of Surgery, Vol. 216, No. 3, 1992, p. 372-380.

Research output: Contribution to journalArticle

Goldman, G, Welbourn, R, Rothlein, R, Wiles, M, Kobzik, L, Valeri, CR, Shepro, D, Hechtman, HB, Mulder, DS, Pruitt, BA, Herndon, D, Harken, AH & Naji, A 1992, 'Adherent neutrophils mediate permeability after atelectasis', Annals of Surgery, vol. 216, no. 3, pp. 372-380.
Goldman G, Welbourn R, Rothlein R, Wiles M, Kobzik L, Valeri CR et al. Adherent neutrophils mediate permeability after atelectasis. Annals of Surgery. 1992;216(3):372-380.
Goldman, G. ; Welbourn, R. ; Rothlein, R. ; Wiles, M. ; Kobzik, L. ; Valeri, C. R. ; Shepro, D. ; Hechtman, H. B. ; Mulder, D. S. ; Pruitt, B. A. ; Herndon, David ; Harken, A. H. ; Naji, A. / Adherent neutrophils mediate permeability after atelectasis. In: Annals of Surgery. 1992 ; Vol. 216, No. 3. pp. 372-380.
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abstract = "Re-expansion of atelectatic lung is associated with increased permeability. This study tests whether neutrophils mediate this event. Right middle lobar atelectasis was induced in anesthetized rabbits (n = 18) by intraluminal obstruction of the bronchus after a 20-minute ventilation with 100{\%} O2. After 1 hour of bronchial obstruction and 20 minutes after lobar re-expansion, leukopenia was noted, 2870 ± 210 white blood cells (WBC)/mm3, relative to control animals treated with a noninflated balloon catheter, 6500 ± 410 WBC/mm3 (p < 0.05). Three hours after re-expansion, neutrophils were sequestered in the previously atelectatic region 78 ± 7 polymorphonuclear leukocytes (PMN)/10 high-power field (HPF), as well as in nonatelectatic areas, 40 ± 3 PMN/10 HPF, higher than control values of 26 ± 3 PMN/10 HPF (p < 0.05). In the atelectatic region, neutrophil sequestration was associated with increased protein concentration in lobar bronchoalveolar lavage (BAL) of 1370 ± 100 μg/mL, higher than control values of 270 ± 20 μg/mL (p < 0.05). Re-expansion also induced increases in lung wet-to-dry weight ratio (W/d) of 6.2 ± 0.2, higher than control values of 4.3 ± 0.1 (p < 0.05). Rendering rabbits neutropenic (n = 18) (0 to 4 PMN/mm3) limited the atelectasis-induced protein accumulations in BAL (520 ± 60 μg/mL) and increase in lung W/d (5.2 ± 0.1) (both p < 0.05). Intravenous (I.V.; treatment of another group (n = 18) with an anti-CD 18 monoclonal antibody (R 15.7, 1 mg/kg) before balloon deflation prevented leukopenia (6550 ± 560 WBC/mm3), minimized neutrophil sequestration (36 ± 2 PMN/10 HPF), and attenuated protein leak (710 ± 95 μg/mL) and the increased lung W/d (5.6 ± 0.1) (all p < 0.05). A final atelectatic group (n = 9) was treated I.V. with the antiintercellular adhesion molecule-1 monoclonal antibody (RR 1/1, 1 mg/kg), which also prevented leukopenia and showed similar protection of microvascular barrier function. These data indicate that adherent neutrophils in large part mediate lung permeability and edema after atelectasis and re- expansion. Adhesion receptors of both neutrophils and endothelial cells regulate this event.",
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T1 - Adherent neutrophils mediate permeability after atelectasis

AU - Goldman, G.

AU - Welbourn, R.

AU - Rothlein, R.

AU - Wiles, M.

AU - Kobzik, L.

AU - Valeri, C. R.

AU - Shepro, D.

AU - Hechtman, H. B.

AU - Mulder, D. S.

AU - Pruitt, B. A.

AU - Herndon, David

AU - Harken, A. H.

AU - Naji, A.

PY - 1992

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N2 - Re-expansion of atelectatic lung is associated with increased permeability. This study tests whether neutrophils mediate this event. Right middle lobar atelectasis was induced in anesthetized rabbits (n = 18) by intraluminal obstruction of the bronchus after a 20-minute ventilation with 100% O2. After 1 hour of bronchial obstruction and 20 minutes after lobar re-expansion, leukopenia was noted, 2870 ± 210 white blood cells (WBC)/mm3, relative to control animals treated with a noninflated balloon catheter, 6500 ± 410 WBC/mm3 (p < 0.05). Three hours after re-expansion, neutrophils were sequestered in the previously atelectatic region 78 ± 7 polymorphonuclear leukocytes (PMN)/10 high-power field (HPF), as well as in nonatelectatic areas, 40 ± 3 PMN/10 HPF, higher than control values of 26 ± 3 PMN/10 HPF (p < 0.05). In the atelectatic region, neutrophil sequestration was associated with increased protein concentration in lobar bronchoalveolar lavage (BAL) of 1370 ± 100 μg/mL, higher than control values of 270 ± 20 μg/mL (p < 0.05). Re-expansion also induced increases in lung wet-to-dry weight ratio (W/d) of 6.2 ± 0.2, higher than control values of 4.3 ± 0.1 (p < 0.05). Rendering rabbits neutropenic (n = 18) (0 to 4 PMN/mm3) limited the atelectasis-induced protein accumulations in BAL (520 ± 60 μg/mL) and increase in lung W/d (5.2 ± 0.1) (both p < 0.05). Intravenous (I.V.; treatment of another group (n = 18) with an anti-CD 18 monoclonal antibody (R 15.7, 1 mg/kg) before balloon deflation prevented leukopenia (6550 ± 560 WBC/mm3), minimized neutrophil sequestration (36 ± 2 PMN/10 HPF), and attenuated protein leak (710 ± 95 μg/mL) and the increased lung W/d (5.6 ± 0.1) (all p < 0.05). A final atelectatic group (n = 9) was treated I.V. with the antiintercellular adhesion molecule-1 monoclonal antibody (RR 1/1, 1 mg/kg), which also prevented leukopenia and showed similar protection of microvascular barrier function. These data indicate that adherent neutrophils in large part mediate lung permeability and edema after atelectasis and re- expansion. Adhesion receptors of both neutrophils and endothelial cells regulate this event.

AB - Re-expansion of atelectatic lung is associated with increased permeability. This study tests whether neutrophils mediate this event. Right middle lobar atelectasis was induced in anesthetized rabbits (n = 18) by intraluminal obstruction of the bronchus after a 20-minute ventilation with 100% O2. After 1 hour of bronchial obstruction and 20 minutes after lobar re-expansion, leukopenia was noted, 2870 ± 210 white blood cells (WBC)/mm3, relative to control animals treated with a noninflated balloon catheter, 6500 ± 410 WBC/mm3 (p < 0.05). Three hours after re-expansion, neutrophils were sequestered in the previously atelectatic region 78 ± 7 polymorphonuclear leukocytes (PMN)/10 high-power field (HPF), as well as in nonatelectatic areas, 40 ± 3 PMN/10 HPF, higher than control values of 26 ± 3 PMN/10 HPF (p < 0.05). In the atelectatic region, neutrophil sequestration was associated with increased protein concentration in lobar bronchoalveolar lavage (BAL) of 1370 ± 100 μg/mL, higher than control values of 270 ± 20 μg/mL (p < 0.05). Re-expansion also induced increases in lung wet-to-dry weight ratio (W/d) of 6.2 ± 0.2, higher than control values of 4.3 ± 0.1 (p < 0.05). Rendering rabbits neutropenic (n = 18) (0 to 4 PMN/mm3) limited the atelectasis-induced protein accumulations in BAL (520 ± 60 μg/mL) and increase in lung W/d (5.2 ± 0.1) (both p < 0.05). Intravenous (I.V.; treatment of another group (n = 18) with an anti-CD 18 monoclonal antibody (R 15.7, 1 mg/kg) before balloon deflation prevented leukopenia (6550 ± 560 WBC/mm3), minimized neutrophil sequestration (36 ± 2 PMN/10 HPF), and attenuated protein leak (710 ± 95 μg/mL) and the increased lung W/d (5.6 ± 0.1) (all p < 0.05). A final atelectatic group (n = 9) was treated I.V. with the antiintercellular adhesion molecule-1 monoclonal antibody (RR 1/1, 1 mg/kg), which also prevented leukopenia and showed similar protection of microvascular barrier function. These data indicate that adherent neutrophils in large part mediate lung permeability and edema after atelectasis and re- expansion. Adhesion receptors of both neutrophils and endothelial cells regulate this event.

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