Nitric oxide is produced endogenously to inhibit platelet activation and aggregation until an injury indicates the need for a clot. Inhaled nitric oxide has the same effect and places the patient at risk for bleeding due to inhibition of platelet aggregation. It does not place the patient at risk for clotting due to instigation of platelet aggregation. It also does not destroy platelets. The build-up of nitrogen dioxide as a metabolite is a complication of inhaled nitric oxide therapy, but this is not related to clotting.