Am. J. Respir. Cell Mol. Biol., Vol 13, No. 6, 12 1995, 712-718.
Surfactant incorporation markedly alters mechanical properties of a fibrin clot
A Gunther, M Kalinowski, S Rosseau and W Seeger
Department of Internal Medicine, Justus Liebig University, Giessen, Germany.
Intra-alveolar clot formation is a common finding in acute and chronic
inflammatory lung diseases. Incorporation of lipophilic surfactant
components into a growing fibrin clot has recently been reported (Am. J.
Respir. Cell Mol. Biol. 1993; 9:213-220). In the present study, we
investigated the influence of such surfactant incorporation on the elastic
properties and water permeability of the fibrin polymer. Thrombelastography
and compaction experiments were employed for assessment of the elastic
properties, and the permeability characteristics of the clot material were
addressed in fibrin-packed columns. Two calf lung surfactant extracts (CLSE
and Alveofact), Curosurf, and a synthetic phospholipid mixture
(dipalmitoylphosphatidylcholine, phosphatidylglycerol, and palmitic acid at
a ratio of 68.5:22.5:9 [wt/wt]) were used. The presence of surfactant did
not affect the cleavage of fibrinopeptide A upon incubation of fibrinogen
with thrombin (enzyme-linked immunosorbent assay technique). Similarly,
kinetics and extent of factor XIII-induced covalent crosslinkage of the
fibrin network remained unchanged in the presence of surfactant (sodium
dodecyl sulfate polyacrylamide gel electrophoresis and D-Dimer
quantification upon subsequent clot lysis). All surfactants, however,
dose-dependently decreased the elastic modulus of the arising fibrin
polymer. The maximal amplitude in thrombelastography was reduced, and the
recovery of fluid after centrifugation of the fibrin clot increased. Fibrin
clots embedding natural surfactant material displayed reduced permeability
for saline as compared with control fibrin polymers. Subsequent washout of
lipids from these clots with Triton X-100 resulted in increased hydraulic
conductivity. This was accompanied by an increase in pore size, suggesting
altered architecture of the fibrin matrix generated in the presence of
surfactant.(ABSTRACT TRUNCATED AT 250 WORDS)
This article has been cited by other articles:

|
 |

|
 |
 
P. Prabhakaran, L. B. Ware, K. E. White, M. T. Cross, M. A. Matthay, and M. A. Olman
Elevated levels of plasminogen activator inhibitor-1 in pulmonary edema fluid are associated with mortality in acute lung injury
Am J Physiol Lung Cell Mol Physiol,
July 1, 2003;
285(1):
L20 - L28.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. IDELL, A. P. MAZAR, P. BITTERMAN, S. MOHLA, and A. L. HARABIN
Fibrin Turnover in Lung Inflammation and Neoplasia
Am. J. Respir. Crit. Care Med.,
February 1, 2001;
163(2):
578 - 584.
[Full Text]
|
 |
|

|
 |

|
 |
 
A. GÜNTHER, P. MOSAVI, S. HEINEMANN, C. RUPPERT, H. MUTH, P. MARKART, F. GRIMMINGER, D. WALMRATH, B. TEMMESFELD-WOLLBRÜCK, and W. SEEGER
Alveolar Fibrin Formation Caused by Enhanced Procoagulant and Depressed Fibrinolytic Capacities in Severe Pneumonia . Comparison with the Acute Respiratory Distress Syndrome
Am. J. Respir. Crit. Care Med.,
February 1, 2000;
161(2):
454 - 462.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
A. Günther, P. Markart, M. Kalinowski, C. Ruppert, F. Grimminger, and W. Seeger
Cleavage of Surfactant-Incorporating Fibrin by Different Fibrinolytic Agents . Kinetics of Lysis and Rescue of Surface Activity
Am. J. Respir. Cell Mol. Biol.,
December 1, 1999;
21(6):
738 - 745.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
A. Elssner, G. Mazur, and C. Vogelmeier
Inhibition of factor XIIIa-mediated incorporation of fibronectin into fibrin by pulmonary surfactant
Am J Physiol Lung Cell Mol Physiol,
April 1, 1999;
276(4):
L625 - L630.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
M. Ikegami, C. M. Rebello, and A. H. Jobe
Surfactant inhibition by plasma: gestational age and surfactant treatment effects in preterm lambs
J Appl Physiol,
December 1, 1996;
81(6):
2517 - 2522.
[Abstract]
[Full Text]
[PDF]
|
 |
|
Copyright © 1995 American Thoracic Society.
|
|
|