Centhaquin is intended for use as a small volume hypotensive resuscitative agent. Our objective was to study the influence of centhaquin on blood coagulation and determine its effect on the anticoagulant properties of aspirin and heparin by ex vivo TEG.
Centhaquin will not affect clotting time, clot kinetics, clot strength and clot lysis or alter the effects of aspirin or heparin as measured by TEG.
Citrated fresh whole rat blood was subjected to TEG. In order to study the effect of centhaquin on coagulation we compared centhaquin with vehicle (normal saline). The effect of centhaquin on aspirin induced inhibition of coagulation was studied in aspirin+vehicle and centhaquin+aspirin groups; and the effect of centhaquin on heparin induced inhibition of coagulation was studied in heparin+vehicle and centhaquin+heparin groups. Since aspirin was dissolved in 0.3% DMSO we also examined its effect on TEG. TEG parameters including clotting time (reaction time, R), clot kinetics (K and?), clot strength (maximum amplitude of the TEG tracing, MA) and percent lysis 30 min post MA (LY30) were determined. Values are mean±SEM.
TEG parameters of vehicle treated group (N=5) were R=2.9 ± 0.2 min, K=0.96 ± 0 min,?=76.0 ± 0.7°, MA=71.2 ± 0.7 mm and LY30=0.1 ± 0%. Centhaquin did not alter any parameter. K and? values predominantly reflect fibrin formation and to a lesser extent platelet function; while MA values reflect modest contribution of fibrin but significantly more of platelets to clot strength. Aspirin did not produce any change in R, K,? or LY30 values, but produced an 11% decrease in MA (p<0.01). Centhaquin did not affect the MA change induced by aspirin. DMSO (0.3%) did not alter any parameter. Heparin did not change LY30 values but significantly increased R by 54%, K by 75%, and decreased? by 62% and MA by 10% (p<0.02). Centhaquin did not alter the anticoagulant effects of heparin.
Centhaquin does not inhibit platelet aggregation, fibrin formation or clot lysis. It can be concluded that centhaquin does not affect coagulation or alter the anticoagulant effects of aspirin or heparin.