Literature DB >> 8058778

Hypothesis: disseminated intravascular inflammation as the inflammatory counterpart to disseminated intravascular coagulation.

B S Bull1, M H Bull.   

Abstract

We have identified a leukocyte activation syndrome that is occasionally associated with the transfusion of intraoperatively recovered erythrocytes. This syndrome appears to result from intravascular damage caused by leukocytes activated during the erythrocyte salvage process. We hypothesize that this syndrome is part of a larger disease grouping: disseminated intravascular inflammation (DII). DII is the analog of the coagulation disorder disseminated intravascular coagulation. In disseminated intravascular coagulation, the organ damage results from uncontrolled activation of the clotting pathway; in DII the damage is caused by leukocytes that have become activated by direct contact with bacteria or in rare instances--such as erythrocyte salvage--in the absence of bacteria and bacterial products. Recent studies of the hazards associated with intraoperative blood salvage indicate that activation of leukocytes can be achieved by exposure to activated platelets alone. If such activated leukocytes are reinfused along with the washed erythrocytes, widespread organ damage may result. The lung is the organ most severely affected by activated leukocytes. Adult respiratory distress syndrome is one outcome. It is likely that DII is a presently unrecognized pathophysiological process that complicates a variety of primary disease states and increases their lethality.

Entities:  

Mesh:

Year:  1994        PMID: 8058778      PMCID: PMC44571          DOI: 10.1073/pnas.91.17.8190

Source DB:  PubMed          Journal:  Proc Natl Acad Sci U S A        ISSN: 0027-8424            Impact factor:   11.205


  15 in total

1.  The salvaged blood syndrome: a sequel to mechanochemical activation of platelets and leukocytes?

Authors:  B S Bull; M H Bull
Journal:  Blood Cells       Date:  1990

2.  Thrombospondin-exposed human monocytes display augmented luminol-enhanced chemiluminescence upon receptor triggering.

Authors:  B J Schüepp; T W Jungi
Journal:  Biochem Biophys Res Commun       Date:  1991-06-28       Impact factor: 3.575

3.  Respiratory burst in adherent human neutrophils: triggering by colony-stimulating factors CSF-GM and CSF-G.

Authors:  C F Nathan
Journal:  Blood       Date:  1989-01       Impact factor: 22.113

4.  Inflammatory particles stimulate thromboplastin production by human monocytes.

Authors:  R T Dean; H Prydz
Journal:  Thromb Res       Date:  1983-05-15       Impact factor: 3.944

5.  Recognition coupled responses of the monocyte: activation of coagulation pathways.

Authors:  T S Edgington
Journal:  Nouv Rev Fr Hematol       Date:  1983

Review 6.  Leukocyte-endothelial interactions.

Authors:  J M Harlan
Journal:  Blood       Date:  1985-03       Impact factor: 22.113

7.  The production and availability of tissue thromboplastin in cellular populations of whole blood exposed to various concentrations of endotoxin. An assay for detection of endotoxin.

Authors:  B Osterud; E Bjørklid
Journal:  Scand J Haematol       Date:  1982-08

Review 8.  Clinical significance of increased thromboplastin activity on the monocyte surface--a brief review.

Authors:  T Lyberg
Journal:  Haemostasis       Date:  1984

9.  Thrombospondin stimulates motility of human neutrophils.

Authors:  P J Mansfield; L A Boxer; S J Suchard
Journal:  J Cell Biol       Date:  1990-12       Impact factor: 10.539

10.  Cytokine-induced respiratory burst of human neutrophils: dependence on extracellular matrix proteins and CD11/CD18 integrins.

Authors:  C Nathan; S Srimal; C Farber; E Sanchez; L Kabbash; A Asch; J Gailit; S D Wright
Journal:  J Cell Biol       Date:  1989-09       Impact factor: 10.539

View more
  2 in total

1.  Activation of human endothelial cells by viable or heat-killed gram-negative bacteria requires soluble CD14.

Authors:  R F Noel; T T Sato; C Mendez; M C Johnson; T H Pohlman
Journal:  Infect Immun       Date:  1995-10       Impact factor: 3.441

2.  Staphylococcal enterotoxin B initiates protein kinase C translocation and eicosanoid metabolism while inhibiting thrombin-induced aggregation in human platelets.

Authors:  Uyen Tran; Thomas Boyle; Jeffrey W Shupp; Rasha Hammamieh; Marti Jett
Journal:  Mol Cell Biochem       Date:  2006-03-21       Impact factor: 3.396

  2 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.