Endogenous heparin decreases the thrombotic response to hemorrhagic shock in rabbits

Purpose: The purpose of this study was to determine if endogenous heparin r elease would modulate the hemostatic response to hemorrhagic shock in rabbi ts. Materials and Methods Anesthetized rabbits (n = 13) underwent hemorrhagic s hock (MAP 30-40 mm Hg) for 60 minutes. Blood samples obtained before and 60 minutes after hemorrhagic shock had thrombelastographic variables (R, reac tion time [min]; angle, alpha [degrees]; and G [dynes/cm(2)]) determined. H emostatic function was assessed by modified thrombelastography under four c onditions: (1) unmodified sample; (2) platelet inhibition with cytochalasin D; (3) heparinase I exposure; and (4) platelet inhibition and heparinase I exposure. Results: Thrombelastographic variable values in samples without platelet in hibition or heparinase exposure did not significantly change after hemorrha ge (before hemorrhage: R = 22.01 +/- 0.7 min, alpha = 43.6 +/- 1.3 degrees, G = 7,089 +/- 379 dyne/cm(2); after hemorrhage: R = 22.1 +/- 2.4, alpha = 41.6 +/- 3.9, G = 5,662 +/- 564; mean +/- SEM). However, blood samples expo sed to heparinase after hemorrhage demonstrated enhanced hemostatic functio n with thrombelastographic values (R = 13.4 +/- 1.5, alpha = 56.0 +/- 3.4, G = 7012 +/- 565) significantly different (P < .05) from samples not expose d to heparinase. Samples with platelet inhibition demonstrated a similar pa ttern. Conclusion: Hemorrhagic shock significantly increased circulating endogenou s heparin activity, attenuating the thrombotic response to hemorrhage in ra bbits. Heparin-mediated regulation of hemostasis may serve as a protective mechanism in shock states. Copyright (C) 2001 by W.B. Saunders Company.