Related Experiment Videos
Endogenous heparin decreases the thrombotic response to hemorrhagic shock in rabbits
1Department of Anesthesiology, Division of Cardiothoracic Anesthesia, The University of Alabama at Birmingham, 35249, USA.
Purpose:
The purpose of this study was to determine if endogenous heparin release would modulate the hemostatic response to hemorrhagic shock in rabbits.
Materials And Methods:
Anesthetized rabbits (n = 13) underwent hemorrhagic shock (MAP 30-40 mm Hg) for 60 minutes. Blood samples obtained before and 60 minutes after hemorrhagic shock had thrombelasto-graphic variables (R, reaction time [min]; angle, alpha [ degrees ]; and G [dynes/cm(2)]) determined. Hemostatic function was assessed by modified thrombelastography under four conditions: (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 inhibition or heparinase exposure did not significantly change after hemorrhage (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 exposed to heparinase after hemorrhage demonstrated enhanced hemostatic function with thrombelastographic values (R = 13.4 +/- 1.5, alpha 56.0 +/- 3.4, G = 7012 +/- 565) significantly different (P <.05) from samples not exposed to heparinase. Samples with platelet inhibition demonstrated a similar pattern.
Conclusion:
Hemorrhagic shock significantly increased circulating endogenous heparin activity, attenuating the thrombotic response to hemorrhage in rabbits. Heparin-mediated regulation of hemostasis may serve as a protective mechanism in shock states.