Effect of Sulfo Lewis C on smoke inhalation injury in an ovine model.

OBJECTIVE To evaluate the effect of Sulfo Lewis C (SO3-3âGal1-3GlcNAc-O(CH2)8-COOMe), a putative ligand of selectins, on smoke inhalation injury. DESIGN Prospective animal study with concurrent controls. SETTING An animal laboratory. SUBJECTS Twelve 1-yr-old female sheep, weighing 24 to 33 kg. INTERVENTIONS Twelve sheep received nine exposure units of smoke generated by thermolysis of pine woodchips (80 g). Group 1 (n = 6) was untreated. Group 2 (n = 6) was treated with an intravenous infusion of Sulfo Lewis C after smoke exposure. Animals were killed 48 hrs after injury. MEASUREMENTS AND MAIN RESULTS Cardiopulmonary variables and blood gases were measured serially. Granulocyte free-radical production was measured before smoke exposure and at 4 and 48 hrs after injury. Ventilation/perfusion distribution (VA/Q) was analyzed using the multiple inert gas elimination technique. Granulocyte free-radical production was increased after smoke exposure in both groups. Oxygenation was significantly improved by the administration of Sulfo Lewis C. VA/Q analysis demonstrated significantly less blood flow to low VA/Q lung segments in treated animals. CONCLUSIONS Selectin blockade attenuated lung injury after smoke exposure. These data support the hypothesis that neutrophils play a pivotal role in smoke inhalation injury.

[1]  T. Tedder,et al.  Neutrophil margination, sequestration, and emigration in the lungs of L-selectin-deficient mice. , 1997, The Journal of clinical investigation.

[2]  E. Moore,et al.  CD11b blockade prevents lung injury despite neutrophil priming after gut ischemia/reperfusion. , 1995, The Journal of trauma.

[3]  M. Jutila,et al.  A dual-binding antibody to E- and L-selectin attenuates sepsis-induced lung injury. , 1995, American journal of respiratory and critical care medicine.

[4]  A. Beaudet,et al.  P-selectin/ICAM-1 double mutant mice: acute emigration of neutrophils into the peritoneum is completely absent but is normal into pulmonary alveoli. , 1995, The Journal of clinical investigation.

[5]  P. Ward,et al.  Compartmentalized roles for leukocytic adhesion molecules in lung inflammatory injury. , 1995, Journal of immunology.

[6]  J. Hogg,et al.  Leukocyte traffic in the lung. , 1995, Annual review of physiology.

[7]  C. Valeri,et al.  Neutrophil adhesion receptor CD18 mediates remote but not localized acid aspiration injury. , 1995, Surgery.

[8]  A. Mason,et al.  The effect of inhaled nitric oxide on pulmonary ventilation-perfusion matching following smoke inhalation injury. , 1994, The Journal of trauma.

[9]  Amos Etzioni.  Adhesion molecule deficiencies and their clinical significance. , 1994, Cell adhesion and communication.

[10]  P. Ward,et al.  Role of selectins in local and remote tissue injury following ischemia and reperfusion. , 1994, The American journal of pathology.

[11]  R. Korthuis,et al.  Role of neutrophil-endothelial cell adhesion in inflammatory disorders. , 1994, Journal of critical care.

[12]  M. Jutila,et al.  Survival in lung reperfusion injury is improved by an antibody that binds and inhibits L- and E-selectin. , 1994, The Journal of Heart and Lung Transplantation.

[13]  A. Mason,et al.  The effects of pentoxifylline on pulmonary function following smoke inhalation. , 1994, The Journal of surgical research.

[14]  P. Ward,et al.  Requirements for L-selectin in neutrophil-mediated lung injury in rats. , 1994, Journal of immunology.

[15]  W. Hancock,et al.  P-selectin and platelet-activating factor mediate initial endotoxin- induced neutropenia , 1994, The Journal of experimental medicine.

[16]  E. Lightfoot,et al.  Effect of inhibiting leukocyte integrin (CD18) and selectin (L-selectin) on susceptibility to infection with Pseudomonas aeruginosa. , 1993, The Journal of trauma.

[17]  Cioffi,et al.  The effect of inhaled nitric oxide on smoke inhalation injury in an ovine model. , 1993, The Journal of trauma.

[18]  S. Watson,et al.  Protective effects of selectin chimeras in neutrophil-mediated lung injury. , 1993, Journal of immunology.

[19]  D. Herndon,et al.  Is the CD18 adhesion complex of polymorphonuclear leukocytes involved in smoke-induced lung damage? A morphometric study. , 1993, The Journal of burn care & rehabilitation.

[20]  C. Smith,et al.  Role of beta 2 integrins and ICAM-1 in lung injury following ischemia-reperfusion of rat hind limbs. , 1993, The American journal of pathology.

[21]  Z. Zheng,et al.  Protective effects of sialylated oligosaccharides in immune complex- induced acute lung injury , 1993, The Journal of experimental medicine.

[22]  P. Ward,et al.  Protective effects of oligosaccharides in P-selectin-dependent lung injury , 1993, Nature.

[23]  J. Janes.  Mass‐selected ion angular impact energy distributions at the powered electrode in CF4 reactive‐ion etching , 1993 .

[24]  E. Lightfoot,et al.  Inhibition of leukocyte adherence and susceptibility to infection. , 1993, The Journal of surgical research.

[25]  C. Smith,et al.  Role of β1 β2 integrins and ICAM-1 in lung injury after deposition of IgG and IgA immune complexes , 1993 .

[26]  C. Smith,et al.  Role of leukocyte adhesion molecules in complement-induced lung injury. , 1993, Journal of immunology.

[27]  D. Kapelanski,et al.  Lung reperfusion injury is reduced by inhibiting a CD18-dependent mechanism. , 1993, The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation.

[28]  C. Valeri,et al.  A CD18 antibody prevents lung injury but not hypotension after intestinal ischemia-reperfusion. , 1993, Journal of applied physiology.

[29]  T. Paavonen,et al.  Selective expression of sialyl-Lewis x and Lewis a epitopes, putative ligands for L-selectin, on peripheral lymph-node high endothelial venules. , 1992, The American journal of pathology.

[30]  A. C. Stuart,et al.  Novel sulfated ligands for the cell adhesion molecule E-selectin revealed by the neoglycolipid technology among O-linked oligosaccharides on an ovarian cystadenoma glycoprotein. , 1992, Biochemistry.

[31]  C. Valeri,et al.  A Mac-1 antibody reduces liver and lung injury but not neutrophil sequestration after intestinal ischemia-reperfusion. , 1992, Surgery.

[32]  A. Mason,et al.  The morphology of smoke inhalation injury in sheep. , 1991, The Journal of trauma.

[33]  C. Smith,et al.  Role of endothelial-leukocyte adhesion molecule 1 (ELAM-1) in neutrophil-mediated lung injury in rats. , 1991, The Journal of clinical investigation.

[34]  A. Fowler,et al.  Anti-CD18 antibody attenuates neutropenia and alveolar capillary-membrane injury during gram-negative sepsis. , 1991, Surgery.

[35]  D. Herndon,et al.  Administration of a synthetic antiprotease reduces smoke-induced lung injury. , 1990, Journal of applied physiology.

[36]  R. Rodríguez-Roisín,et al.  Clinical relevance of ventilation-perfusion inequality determined by inert gas elimination. , 1990, The European respiratory journal.

[37]  D. Herndon,et al.  The effect of leukocyte depletion on smoke inhalation injury in sheep. , 1988, Surgery.

[38]  E. Pick.  Microassays for superoxide and hydrogen peroxide production and nitroblue tetrazolium reduction using an enzyme immunoassay microplate reader. , 1986, Methods in enzymology.