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.