Literature DB >> 7385023

Production of acute pulmonary injury by leukocytes and activated complement.

D C Hohn, A J Meyers, S T Gherini, A Beckmann, R E Markison, A M Churg.   

Abstract

The adult respiratory distress syndrome (ARDS) frequently occurs after sepsis and major trauma. Since both sepsis and trauma may cause activation of the complement system, we have infused rabbits with complement-activated plasma (AP) and have studied the effects on leukocyte counts, respiratory rate, PaO2, and lung morphology. Sustained AP infusion caused: (1) early granulocytopenia, (2) progressive hypoxemia and tachypnea, and (3) pulmonary vascular plugging by aggregates of degenerating granulocytes with interstital edema and endothelial injury. These changes were not observed in control animals infused with unactivated plasma or in animals rendered leukopenic with nitrogen mustard. Complement activation in patients with sepsis and trauma may be an etiologic factor in the development of ARDS.

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Year:  1980        PMID: 7385023

Source DB:  PubMed          Journal:  Surgery        ISSN: 0039-6060            Impact factor:   3.982


  24 in total

1.  Acute generalized microvascular injury by activated complement and hypoxia: the basis of the adult respiratory distress syndrome and multiple organ failure?

Authors:  J K Nuytinck; R J Goris; J G Weerts; P H Schillings; J H Stekhoven
Journal:  Br J Exp Pathol       Date:  1986-08

Review 2.  Current concepts in the management of the adult respiratory distress syndrome.

Authors:  J A Weigelt
Journal:  World J Surg       Date:  1987-04       Impact factor: 3.352

Review 3.  Mechanisms of membrane damage and surfactant depletion in acute lung injury.

Authors:  S Westaby
Journal:  Intensive Care Med       Date:  1986       Impact factor: 17.440

Review 4.  Organ dysfunction after cardiopulmonary bypass. A systemic inflammatory reaction initiated by the extracorporeal circuit.

Authors:  S Westaby
Journal:  Intensive Care Med       Date:  1987       Impact factor: 17.440

5.  Complement levels and C3 breakdown products in open-heart surgery: association of C3 conversion with the postpericardiotomy syndrome.

Authors:  S Meri; K Verkkala; A Miettinen; V Valtonen; E Linder
Journal:  Clin Exp Immunol       Date:  1985-06       Impact factor: 4.330

6.  Complement and the damaging effects of cardiopulmonary bypass.

Authors:  S Westaby
Journal:  Thorax       Date:  1983-05       Impact factor: 9.139

7.  Alterations in activities of anaphylatoxin inactivator and chemotactic factor inactivator during hemodialysis.

Authors:  J R McCormick; D L Kreutzer; H J Keating; J Hupp; A Despins; M Moore
Journal:  Am J Pathol       Date:  1982-12       Impact factor: 4.307

8.  Complement conversion and leukocyte kinetics in open heart surgery.

Authors:  J Utoh; T Yamamoto; T Kambara; H Goto; Y Miyauchi
Journal:  Jpn J Surg       Date:  1988-05

9.  Corticosteroids block binding of chemotactic peptide to its receptor on granulocytes and cause disaggregation of granulocyte aggregates in vitro.

Authors:  K M Skubitz; P R Craddock; D E Hammerschmidt; J T August
Journal:  J Clin Invest       Date:  1981-07       Impact factor: 14.808

10.  Intravascular activation of complement and acute lung injury. Dependency on neutrophils and toxic oxygen metabolites.

Authors:  G O Till; K J Johnson; R Kunkel; P A Ward
Journal:  J Clin Invest       Date:  1982-05       Impact factor: 14.808

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