A natural glycoprotein inhibitor (NIF) of CD11b/CD18 reduces leukocyte adhesion in the liver after hemorrhagic shock

• Published in: Shock (Augusta, Ga.) Ga.), 1995-09, Vol.4 (3), p.187-192
• Main Authors: Bauer, C, Siaplaouras, S, Soule, H R, Moyle, M, Marzi, I
• Format: Article
• Language: English
• Subjects: Animals; CD18 Antigens - drug effects; Cell Adhesion - drug effects; Female; Glycoproteins - therapeutic use; Helminth Proteins - therapeutic use; Hemodynamics - drug effects; Leukocytes - drug effects; Leukocytes - metabolism; Leukocytes - pathology; Liver - blood supply; Liver - drug effects; Liver - pathology; Liver Circulation - drug effects; Macrophage-1 Antigen - drug effects; Membrane Proteins; Rats; Rats, Sprague-Dawley; Shock, Hemorrhagic - drug therapy; Shock, Hemorrhagic - pathology; Shock, Hemorrhagic - physiopathology
• ISSN: 1073-2322
• DOI: 10.1097/00024382-199509000-00006

This study was designed to assess the effect of neutrophil inhibitory factor (NIF), a novel specific inhibitor of CD11b/CD18 on hepatic leukocyte trafficking by intravital microscopy 5 h after hemorrhagic shock. Anesthetized rats were instrumented for invasive hemodynamical monitoring. Hemorrhagic shock was induced for 60 min by withdrawal of arterial blood (mean arterial blood pressure = 40 mmHg). Rats were adequately resuscitated for 5 h to achieve a mean arterial blood pressure > 100 mmHg and were randomly assigned to blinded treatment with NIF or placebo control protein administered as a single intravenous bolus (10 mg/kg) at the time of resuscitation. Intrahepatic leukocyte adhesion was evaluated by in vivo fluorescence microscopy. There were no significant differences observed in hemodynamic parameters between the shock groups throughout the study, however, NIF significantly reduced firm leukocyte adhesion in liver sinusoids. The results suggest that NIF may be beneficial in the attenuation of the pathological shock-induced leukocyte adhesion.