Platelet and Neutrophil Distributions in Pump-Oxygenator Circuits. Ii. Influence of Nitric Oxide Gas Infusion

Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

“…Therefore, analysing platelet adhesion molecules on circulating platelets did not reflect the inhibitory effects of gaseous NO in our experiments, confirming other results [24]. We used only small amounts of NO (20 ppm) compared with others (500 and 1000 ppm [25]). It would be interesting to learn whether higher concentrations of NO protect against loss of adhesion receptors.…”

“…Importantly, platelet dysfunction during NO application of 20 ppm was reduced. This contrasts with results after the application of 500 ppm NO during ECC in a pig model, in which both platelet trapping and aggregation were attenuated, possibly reflecting a dose-response effect [25]. Mellgren et al [24] investigated the effects of 40 ppm NO on platelets during CPB.…”

Nitric Oxide Increases Leukocyte Granule Release During Simulated Extracorporeal Circulation1

“…Konishi et al used 100 ppm and 200 ppm to reduce platelet adhesion to oxygenator and found that 200 ppm was more effective [18]. Sly et al showed a decrease in platelet adhesion to the oxygenator when the NO concentration was increased from 500 ppm to 1000 pm in the study group, while the control group did not receive NO [19]. An effect on ROS release may require a higher dose.…”

Cardiac bypass haemostasis: putting blood through the mill

“…If platelet damage in CPB follows the interaction with surface‐adsorbed fibrinogen, blocking it might preserve platelet function during CPB. Platelet adhesion to surfaces can be reduced by nitric oxide (NO) (Radomski, 1987), which also inhibits fibrinogen–platelet binding (Gries et al , 1998); infusion of the NO donor, S‐nitrosoglutathione, did not modify CPB‐induced changes in platelet expression of GpIb or P‐selectin (Langford et al , 1997), but 500 ppm of NO added to the sweep gas reduced platelet adhesion to the oxygenator membrane by 95%, at the cost of 4% methaemoglobinaemia (Sly et al , 1996). This direct approach, taking advantage of the gas transfer function of the platelet‐activating surface itself, looks both elegant and promising; further studies are required.…”