Plasminogen activator inhibitor-1 rises after hemorrhage in the
rat.
Yamashita, Masatomo, Daniel N. Darlington, Edwin J. Weeks, Richard O.
Jones, and Donald S. Gann.
Departments of Surgery and Physiology, University of Maryland
School of Medicine, Baltimore, Maryland 21201
APStracts 2:0023E, 1995.
Large hemorrhage leads to hypercoagulability, a phenomenon that has
never been well explained. Because an elevation of plasminogen
activator inhibitor-1 (PAI-1) increases procoagulant activity, we
have determined if plasma PAI activity and tissue PAI-1 mRNA are
elevated after hemorrhage. Sprague-Dawley rats were bled (20 ml/kg or
15 ml/kg) four days after cannulation. Plasma PAI activity was
determined by the capacity of plasma to inhibit tissue-type
plasminogen activator activity. Changes of PAI-1 mRNA in various
tissues were detected by high-performance liquid chromatography after
reverse transcription and polymerase chain reaction. Twenty ml/kg
hemorrhage significantly elevated plasma PAI activity at 0.5, 1, 2,
4, 6, and 8 h after hemorrhage, and PAI-1 mRNA in liver at 1, 2, 4,
and 6 h after hemorrhage. PAI-1 message was also significantly
elevated in lung, heart, and kidney at 4 h after hemorrhage. The
increases of PAI-1 mRNA after 20 ml/kg hemorrhage were significantly
greater than those after 15 ml/kg hemorrhage. These findings indicate
that large hemorrhage can induce the increases in PAI activity and
PAI-1 message and suggest that induction of PAI-1 may be involved in
the thrombogenic responses observed after large hemorrhage.
Received 21 September 1994; accepted in final form 6 February
1995.
APS Manuscript Number E387-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.