Nitric oxide decreases coagulation protein function in rabbits as assessedby thromboelastography

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.