Vg. Nielsen, Resuscitation with Hextend((R)) decreases endogenous circulating heparin activity and accelerates clot initiation after hemorrhage in the rabbit, ANESTH ANAL, 93(5), 2001, pp. 1106-1110
Citations number
30
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Hemorrhagic shock can result in a hypercoagulable state and has been associ
ated with both hemorrhagic and thrombotic complications in the perioperativ
e period. The author hypothesized that hemorrhage and resuscitation could r
esult in a hypercoagulable state via changes in the heparin-antithrombin II
I anticoagulant mechanism in rabbits. Rabbits sedated with ketamine underwe
nt sham operation (n = 8) or hemorrhage (25 mL/kg blood shed) for 60 min, f
ollowed by resuscitation with an equal volume of 5% human albumin (n = 8) o
r Hextend (R) (n = 8). Coagulation analysis with the Thrombelastograph (R)
analyzer and determination of endogenous heparin and antithrombin III activ
ity were performed on arterial blood samples obtained before hemorrhage and
30 min after resuscitation. The reaction time significantly decreased by 3
4% after hemorrhage and resuscitation with Hextend (R), whereas no other si
gnificant changes in Thrombelastograph (R) variables were noted. Antithromb
in III activity was significantly less in the Albumin (83% +/- 8% of contro
l, mean +/- SD) and Hextend (R) (88% +/- 8%) Resuscitated groups compared w
ith the Sham-Operated animals. Of interest, only the Hextend (R) -Resuscita
ted 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
Hextende (R) -mediated decrease of both heparin and antithrombin III activ
ity may explain the acceleration of clot initiation compared with albumin a
dministration after hemorrhage in the rabbit.