Anesth Analg 2001;92:314-319
© 2001 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
PentaLyte® Does Not Decrease Heparinoid Release but Does Decrease Circulating Thrombotic Mediator Activity Associated with Aortic Occlusion-Reperfusion in Rabbits
Vance G. Nielsen, MD*,
Valerie E. Armstead, MD ,
Brian T. Geary, BS*, and
Irina L. Opentanova, MS
*Department of Anesthesiology, Division of Cardiothoracic Anesthesia, The University of Alabama at Birmingham, Birmingham Alabama; and Department of Anesthesiology, Thomas Jefferson University, Philadelphia, Pennsylvania
Address correspondence and reprint requests to Vance G. Nielsen, MD, Department of Anesthesiology, The University of Alabama at Birmingham, 619 S. 19th St., Birmingham, AL 35249. Address e-mail to vance.nielsen{at}ccc.uab.edu
Hemorrhage and thrombosis are associated with major vascular and trauma surgery. Release of heparinoids and thrombotic mediators may contribute to these complications and have been described in rabbits after aortic occlusion-reperfusion. We hypothesized that the resuscitative fluid used could reduce heparinoid and thrombotic mediator release after aortic occlusion-reperfusion in rabbits as assessed by thromboelastographic variables (R, reaction time; , angle; and G, a measure of clot strength). Anesthetized rabbits were administered lactated Ringers solution (n = 8) or PentaLyte® (n = 8) at reperfusion after 30 min of ischemia. Blood was obtained before ischemia and after 30 min of reperfusion for thromboelastography under four conditions: 1) unmodified sample, 2) platelet inhibition, 3) heparinase, and 4) platelet inhibition and heparinase. During reperfusion, unmodified samples demonstrated a significant increase in R and decrease in and G that was not affected by PentaLyte®. In the presence of heparinase, no significant fluid-specific thromboelastographic differences were noted. However, thrombotic mediator release (discerned by a decrease in R and an increase in ) during reperfusion in samples with platelet inhibition and heparinase was significantly attenuated by PentaLyte®. PentaLyte® administration does not decrease heparinoid release but does decrease thrombotic mediator release after aortic occlusion-reperfusion.
Implications: PentaLyte® administration does not decrease the heparinoid release associated with aortic occlusion-reperfusion but does decrease the elaboration of a thrombotic mediator. This study serves as a rational basis to determine whether coadministration of PentaLyte® with a heparin antagonist (e.g., protamine or heparinase) may maintain hemostasis after aortic occlusion-reperfusion.
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