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AJP - Heart and Circulatory Physiology, Vol 258, Issue 3 754-H758, Copyright © 1990 by American Physiological Society
ARTICLES |
M. I. Townsley, S. A. Barman and A. E. Taylor
Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688.
The effect of fibrinolysis inhibition with tranexamic acid on pulmonary microvascular permeability during glass bead embolization was investigated in the isolated lung. Lung lobes from nonheparinized dogs were treated in vivo with the equivalent of 0.6 g/kg 100 microns glass bead emboli alone, emboli after tranexamic acid, tranexamic acid alone, or the bead vehicle alone. After 40-50 min, the lobes were isolated for ex vivo perfusion with heparinized autologous blood. There were no changes in any parameter over the 120-min perfusion period. Blood flow at 120 min was decreased after both emboli alone and emboli with tranexamic acid, reflecting an increase in vascular resistance compared with the Tween or tranexamic acid controls. Furthermore, tranexamic acid increased the ratio of pre- to postcapillary resistance in embolized lobes compared with that after emboli alone or in the Tween or tranexamic acid controls. The isogravimetric capillary pressure and the osmotic reflection coefficient were not significantly decreased by tranexamic acid compared with those after emboli alone; however, it did result in an increase in the capillary filtration coefficient compared with that after emboli alone or in the control groups. We conclude that although fibrinolysis inhibition does not clearly exacerbate the lung injury seen after emboli, the tranexamic acid-induced changes in hemodynamics would tend to accelerate edema formation.
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