Endogenous heparin decreases the thrombotic response to hemorrhagic shock in rabbits

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Abstract

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 thrombelastographic variables (R, reaction time [min], angle, α [°]; and G [dynes/cm2]) 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, α = 43.6 ± 1.3°, G = 7,089 ± 379 dyne/cm2; after hemorrhage: R = 22.1 ± 2.4, α = 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, α = 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.

Original languageEnglish (US)
Pages (from-to)64-68
Number of pages5
JournalJournal of Critical Care
Volume16
Issue number2
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Heparin Lyase
Hemorrhagic Shock
Heparin
Hemorrhage
Rabbits
Hemostatics
Blood Platelets
Thrombelastography
Cytochalasin D
Hemostasis
Shock

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Endogenous heparin decreases the thrombotic response to hemorrhagic shock in rabbits. / Nielsen, Vance G.

In: Journal of Critical Care, Vol. 16, No. 2, 2001, p. 64-68.

Research output: Contribution to journalArticle

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abstract = "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 thrombelastographic variables (R, reaction time [min], angle, α [°]; and G [dynes/cm2]) 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, α = 43.6 ± 1.3°, G = 7,089 ± 379 dyne/cm2; after hemorrhage: R = 22.1 ± 2.4, α = 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, α = 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.",
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AB - 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 thrombelastographic variables (R, reaction time [min], angle, α [°]; and G [dynes/cm2]) 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, α = 43.6 ± 1.3°, G = 7,089 ± 379 dyne/cm2; after hemorrhage: R = 22.1 ± 2.4, α = 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, α = 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.

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