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- W2002075075 abstract "Comment The ability of nitric oxide to inhibit platelet aggregation is predictable from the effects of nitric oxide on intraplatelet guanylate cyclase. Because of increased cyclic guanosine monophosphate, a protein kinase is stimulated that results in a reduction in fibrinogen binding to glycoprotein receptors on the platelets. This should induce an inhibition of platelet aggregation, and that is exactly what the authors found. Thus, the authors tested a logical scientific hypothesis, and it proved correct. What is rather surprising, however, is that this inhibited platelet aggregation ex vivo did not prolong Ivy bleeding time in patients. Although the authors did not definitively explain these relatively contradictory effects, they suggested several possible mechanisms in their paper. The reader is urged to review this manuscript for interesting details, but the take-home message for the clinician is that if there is a preexisting clotting defect, nitric oxide may not be a benign drug. On the other hand, because surgery and the acute respiratory distress syndrome can induce a hypercoa-gulable state, perhaps nitric oxide will prevent some unwanted clotting in vital organs of patients without preexisting coagulation disorders." @default.
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- W2002075075 date "1996-10-01" @default.
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- W2002075075 title "Inhibition of Platelet Aggregation by Inhaled Nitric Oxide in Patients with Acute Respiratory Distress Syndrome" @default.
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