Circulation, Vol 87, 1990-2000, Copyright © 1993 by American Heart Association
IM Lang, JJ Marsh, RG Konopka, MA Olman, BR Binder, KM Moser and RR Schleef
BACKGROUND. Numerous investigators have observed that pulmonary emboli are
rapidly lysed in a canine model system. This study was undertaken to
delineate the unique mechanism that accounts for the rapid dissolution of
pulmonary emboli in mongrel dogs. METHODS AND RESULTS. Canine plasminogen
activator (PA) activity (2.6 +/- 1.1 IU/mL acidified platelet-poor plasma
[PPP], < 0.3 IU/mL acidified whole blood serum [WBS], mean +/- SD; n =
6) and PA inhibitor activity (6.1 +/- 2.6 U/mL PPP, 35.4 +/- 7.8 U/mL WBS;
n = 6) were determined in standard plasminogen-based chromogenic assays.
Analysis of canine PPP, WBS, platelet lysates, and primary canine
endothelial cell (EC) cultures by sodium dodecyl sulfate-polyacrylamide gel
electrophoresis and fibrin autography revealed a plasminogen-dependent
lytic zone at 45-kd relative molecular mass that was shown to be related to
urokinase-type PA (u-PA) by its selective inhibition through amiloride.
Analysis of canine platelets on standard 125I fibrin plate assays revealed
a net fibrinolytic activity. In a clot lysis assay system, canine platelets
were able to stimulate fibrinolysis when layered on the outside of fibrin
clots containing autologous PPP. Moreover, net fibrinolytic activity of
primary canine pulmonary artery endothelial cells was higher than the
activities expressed by canine aortic or carotid artery endothelial cells.
CONCLUSIONS. Rapid lysis of pulmonary emboli in mongrel dogs appears to be
a result of 1) the high u-PA activity in canine PPP and 2) the predominant
association of u-PA activity with canine platelets and canine pulmonary
artery endothelial cells.
ARTICLES
Factors contributing to increased vascular fibrinolytic activity in mongrel dogs
University of California, San Diego.
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