Document Detail

The complement regulators C1 inhibitor and soluble complement receptor 1 attenuate acute lung injury in rabbits.
MedLine Citation:
PMID:  10774617     Owner:  NLM     Status:  MEDLINE    
Because activation of the complement system plays a major role in the pathogenesis of acute lung injury, the availability of new specific complement inhibitors represents a promising therapeutic approach. In the present study we investigated pulmonary edema formation and pulmonary artery pressure (PAP) in acute complement-induced lung injury for possible therapeutic impact of the complement regulators C1 inhibitor and soluble complement receptor 1. Eighteen isolated and ventilated rabbit lungs were perfused with pooled normal human serum (NHS, final concentration 35%) in Krebs-Henseleit buffer in a recirculating system. Lung weight gain and PAP were continuously recorded. Complement activation was blocked by the addition of C1 inhibitor (1.0 U/mL, n = 6) or sCR 1 (2.0 microg/mL, n = 6). Lungs that received NHS without inhibitors served as controls (n = 6). This study was performed according to the Helsinki Declaration and approved by the local government. Application of NHS resulted in an increase of PAP within 20 min from 8+/-2 to 42+/-6 mmHg, which was significantly (P < 0.05) decreased by C1-Inh (25+/-5 mmHg) and sCRI (20 +/-3 mmHg). Moreover, pulmonary edema formation after NHS, as assessed by overall weight gain, was reduced by both C1-Inh and sCR1, compared with controls. These findings were paralleled with significantly decreased thromboxane release rates and reduced tissue deposition of C3c and C5b-9. C1 inhibitor and sCR1 attenuate the complement-induced pulmonary capillary leakage and PAP increase, indicating the protective effect of complement inhibition in isolated perfused rabbit lungs.
A Heller; M Kunz; A Samakas; M Haase; M Kirschfink; T Koch
Related Documents :
17669757 - The short-term efficacy of fibrin glue combined with absorptive sheet material in visce...
10774617 - The complement regulators c1 inhibitor and soluble complement receptor 1 attenuate acut...
8335537 - Effect of airway and left atrial pressures on microvascular and interstitial pressures ...
16436847 - Comparative effects of vaporized perfluorohexane and partial liquid ventilation in olei...
15382827 - A computational study of the interaction between coronary blood flow and myocardial mec...
19852677 - Hypertension and its correlates in two communities of dissimilar genetic ancestry in si...
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  13     ISSN:  1073-2322     ISO Abbreviation:  Shock     Publication Date:  2000  
Date Detail:
Created Date:  2000-06-08     Completed Date:  2000-06-08     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  285-90     Citation Subset:  IM    
Department of Anaesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Dresden, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Blood Pressure / drug effects,  physiology*
Complement Activation
Complement C1 Inactivator Proteins / pharmacology*
Complement C3-C5 Convertases / analysis
Complement Membrane Attack Complex / analysis
Complement System Proteins / adverse effects
Lung / drug effects*,  pathology
Pulmonary Artery / drug effects,  physiology*
Pulmonary Edema / etiology,  prevention & control
Receptors, Complement / therapeutic use*
Thromboxane B2 / metabolism
Reg. No./Substance:
0/Complement C1 Inactivator Proteins; 0/Complement Membrane Attack Complex; 0/Receptors, Complement; 150428-53-8/soluble complement inhibitor 1; 54397-85-2/Thromboxane B2; 9007-36-7/Complement System Proteins; EC 3.4.21.-/Complement C3-C5 Convertases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Hepatic injury and lipid peroxidation during ischemia and reperfusion.
Next Document:  A porcine model of sepsis resulting from the combined insults of hemorrhage and peritonitis.