Serial changes in leukocyte deformability and whole blood rheology in patients with sepsis or trauma.

BACKGROUND The objective of this study was to investigate serial changes in leukocyte deformability and rheologic properties of whole blood in patients with sepsis or trauma. METHODS Seventeen sepsis patients and 22 trauma patients were enrolled. Leukocyte deformability and rheologic properties of whole blood were determined with the use of a microchannel array etched on a single-crystal silicon tip, simulating the microvasculature. The number of obstructed microchannels (NOM) was used as a measure of leukocyte deformability. Transit time (TT), i.e., the time taken for 100 microL of whole blood to pass through the microchannel array was also used as rheologic measure. Oxidative activity and F-actin content of neutrophils was measured in patients with sepsis. RESULTS NOM and TT significantly increased in patients when sepsis was diagnosed. In survivors, NOM and TT decreased at the time of recovery from sepsis, but in non-survivors values remained high. Oxidative activity and F-actin content of neutrophils increased significantly as leukocyte deformability decreased. In patients with severe trauma, NOM and TT increased after injury and decreased by the time of recovery from the critical stage. CONCLUSION We conclude that leukocyte deformability decreases in patients with sepsis or severe trauma and that this change negatively affects rheologic properties of whole blood.

[1]  G. Nash,et al.  Changes in neutrophil rheology after acute ischemia and reperfusion in the rat hindlimb. , 1996, The Journal of laboratory and clinical medicine.

[2]  E. Elson,et al.  Mechanics of stimulated neutrophils: cell stiffening induces retention in capillaries. , 1989, Science.

[3]  H. Ohki,et al.  Optically accessible microchannels formed in a single-crystal silicon substrate for studies of blood rheology. , 1992, Microvascular research.

[4]  O. Linderkamp,et al.  Impaired deformability of erythrocytes and neutrophils in children with newly diagnosed insulin-dependent diabetes mellitus , 1999, Diabetologia.

[5]  E. Rackow,et al.  Neutrophil rheologic changes in septic shock. , 1997, American journal of respiratory and critical care medicine.

[6]  E. Elson,et al.  Mechanisms of lipopolysaccharide-induced neutrophil retention. Relative contributions of adhesive and cellular mechanical properties. , 1992, Journal of immunology.

[7]  H. Reynolds,et al.  Macrophages and polymorphonuclear neutrophils in lung defense and injury. , 1990, The American review of respiratory disease.

[8]  D. McArthur,et al.  Multiple organ failure: by the time you predict it, it's already there. , 1999, The Journal of trauma.

[9]  Y. Missirlis,et al.  Neutrophil deformability in patients with sepsis, septic shock, and adult respiratory distress syndrome , 2000, Critical care medicine.

[10]  T. Shimazu,et al.  Granulocyte colony-stimulating factor (G-CSF) stiffens leukocytes but attenuates inflammatory response without lung injury in septic patients. , 2001, The Journal of trauma.

[11]  J. Harlan.  Leukocyte-endothelial interactions. , 1985, Blood.

[12]  J. Dormandy,et al.  Changes in the flow properties of white blood cells after acute myocardial infarction. , 1989, British heart journal.

[13]  D. Betticher,et al.  The effect of endotoxin and tumour necrosis factor on erythrocyte and leucocyte deformability in vitro , 1993, British journal of haematology.

[14]  W. Knaus,et al.  Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. , 1992, Chest.

[15]  R S Kronenberg,et al.  Complement and leukocyte-mediated pulmonary dysfunction in hemodialysis. , 1977, The New England journal of medicine.

[16]  G. Lowe,et al.  Impaired filterability of white cells in acute cerebral infarction. , 1989, BMJ.

[17]  H. Sugimoto,et al.  Acceleration of Superoxide Production from Leukocytes in Trauma Patients , 1991, Annals of surgery.

[18]  E. Rackow,et al.  Effects of proinflammatory cytokines and bacterial toxins on neutrophil rheologic properties. , 1998, Critical care medicine.

[19]  C. Haslett,et al.  The pulmonary vascular sequestration of neutrophils in endotoxemia is initiated by an effect of endotoxin on the neutrophil in the rabbit. , 1987, The American review of respiratory disease.

[20]  T. Shimazu,et al.  Changes in granulocyte colony-stimulating factor concentration in patients with trauma and sepsis. , 1996, The Journal of trauma.

[21]  M. Gimbrone,et al.  Interleukin‐8 induces changes in human neutrophil actin conformation and distribution: relationship to inhibition of adhesion to cytokine‐activated endothelium , 1992, Journal of leukocyte biology.

[22]  B Eiseman,et al.  Multiple organ failure. , 1977, Surgery, gynecology & obstetrics.