Resuscitation with Hextend decreases endogenous circulating heparin activity and accelerates clot initiation after hemorrhage in the rabbit.
Hemorrhagic shock can result in a hypercoagulable state and has been associated with both hemorrhagic and thrombotic complications in the perioperative period. The author hypothesized that hemorrhage and resuscitation could result in a hypercoagulable state via changes in the heparin-antithrombin III anticoagulant mechanism in rabbits. Rabbits sedated with ketamine underwent sham operation (n = 8) or hemorrhage (25 mL/kg blood shed) for 60 min, followed by resuscitation with an equal volume of 5% human albumin (n = 8) or Hextend (n = 8). Coagulation analysis with the Thrombelastograph analyzer and determination of endogenous heparin and antithrombin III activity were performed on arterial blood samples obtained before hemorrhage and 30 min after resuscitation. The reaction time significantly decreased by 34% after hemorrhage and resuscitation with Hextend, whereas no other significant changes in Thrombelastograph variables were noted. Antithrombin III activity was significantly less in the Albumin (83% +/- 8% of control, mean +/- SD) and Hextend (88% +/- 8%) Resuscitated groups compared with the Sham-Operated animals. Of interest, only the Hextend-Resuscitated animals demonstrated a significant decrease in heparin activity (53.4 +/- 13.6 mU/mL before hemorrhage, 42.3 +/- 5.6 mU/mL after resuscitation). A Hextend)-mediated decrease of both heparin and antithrombin III activity may explain the acceleration of clot initiation compared with albumin administration after hemorrhage in the rabbit.


CONCLUSIONS
Hemorrhage may result in a hypercoagulable state after resuscitation. Decreases in both endogenous heparin and antithrombin III activity after hemorrhage and Hextend resuscitation in rabbits resulted in a significantly decreased time to clot coagulation analysis initiation without a significant change in the rate of clot formation or final clot strength.
Nielsen
V G
VG
Department of Anesthesiology, Divisions of Cardiothoracic Anesthesia and Anesthesiology Research, The University of Alabama at Birmingham, Birmingham, Alabama 35249-6810, USA. vance.nielsen@ccc.uab.edu
D000818:Animals; D000990:Antithrombin III / Q000378:metabolism; D001778:Blood Coagulation Disorders / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D001792:Blood Platelets / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D002118:Calcium / Q000097:blood; D002245:Carbon Dioxide / Q000097:blood; D006339:Heart Rate / Q000187:drug effects; D006400:Hematocrit; D006470:Hemorrhage / Q000097:blood / Q000188:drug therapy*; D006493:Heparin / Q000097:blood*; D006895:Hydroxyethyl Starch Derivatives / Q000494:pharmacology*; D008297:Male; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D010952:Plasma Substitutes / Q000494:pharmacology*; D011817:Rabbits; D012151:Resuscitation; D012709:Serum Albumin / Q000494:pharmacology
D006895:Hydroxyethyl Starch Derivatives; D010952:Plasma Substitutes; D012709:Serum Albumin; D002245:Carbon Dioxide; D000990:Antithrombin III; D006493:Heparin; D010100:Oxygen; D002118:Calcium