Nitric oxide (NO) is administered via infusion of donors such as nitroglyce
rin or in inhaled form for treatment of ischemia and pulmonary hypertension
, respectively. In rabbits, the NO donor, DETANONOate, decreases whole bloo
d clotting function as assessed by thromboelastographic variables (R, react
ion time; alpha, angle; and G, a measure of clot strength). I hypothesized
that DETANONOate-derived NO would adversely affect coagulation protein and
platelet function. Blood obtained from ear arteries of conscious rabbits (n
= 8) anticoagulated with sodium citrate. The blood was then incubated with
0 or 10mM DETANONOate for 30 min. After incubation and recalcification, th
romboelastography was performed for 60 min under four conditions: 1) 0mM DE
TANONOate, 2) 0mM DETANONOate with platelet inhibition with cytochalasin D,
3) 10mM DETANONOate, and 4) 10mM DETANONOate with platelet inhibition. DET
ANONOate significantly (P < 0.05) increased R and decreased or and G in sam
ples with or without platelet inhibition, compared with samples not exposed
to DETANONOate. Lastly, the percentage of total G (G(T) attributable to pl
atelet function (G(P) was significantly more in the absence of DETANONOate
(G(P) = 92.3% +/- 1.6%; mean +/- so) than after exposure to DETANONOate (G(
P) = 90.2% +/- 2.3%). DETANONOate-derived NO significantly decreased coagul
ation protein function and platelet function. Coagulation protein function
may be similarly affected in clinical situations involving the administrati
on of NO or NO donors.