The effects of nitric oxide on coagulation during simulated extracorporeal membrane oxygenation

Extracorporeal membrane oxygenation (ECMO) is associated with profound alterations in hemostasis, with platelet dysfunction often being implicated as a causative factor for transfusion. Nitric oxide (NO) has shown to be a rapid yet temporary inhibitor of platelet function. The purpose of this study was to evaluate the effects of NO on platelet number and function in an in vitro ECMO model. Eight silicone membrane oxygenators were primed with fresh, heparinized, bovine blood and allowed to circulate for 48 hours. The treatment group (NO) consisted of four oxygenators that had an end concentration of 20 ppm NO applied to the sweep gas. Platelet counts, methemoglobin levels, plasma-free hemoglobin levels, activated clotting times, and thromboelastographic (TEG) studies were performed at baseline, 1, 6, 12, and 24 h. Scanning electron microscopy (SEM) was performed on sample areas from each oxygenator. The treatment group maintained an average of 25% higher platelet counts than the control group (85.1 +/- 32.0, x 10(3) versus 66.5 +/- 30.9 x 10(3)) although statistical significance was not achieved. Methemoglobin levels were significantly elevated in the treatment circuit at hours 12 and 24 (p < .05). This could be attributed to the lack of a biological interaction that would break down this toxic by-product. TEG indices steadily declined in both groups from baseline (-0.4 +/- 3.6) to (-17.2 +/- 3.3 p < .0007) treatment and (-20 +/- 4.5, p < .0001) control, with the treatment circuit maintaining only slightly improved indices over the most of the study. SEM data showed increased fibrin and cellular deposits in the control group (p = .05) when compared with the treatment group. NO added to the sweep gas of a simulated ECMO circuit at 20 ppm had little effect on the maintenance of platelet number and function.