ANTIPLATELET PROPERTIES OF NITROUS-OXIDE

Nitrous oxide (NO) plays a fundamental part in the haemostatic equilib rium between the endothelium and platelets, an equilibrium of establis hed clinical importance in cardiovascular disease. NO stimulates the e nzyme guanylate cyclase which is responsible for synthesis of GMPc, th e increase of which results in platelet inhibition. Synthesis of NO ma y have an endogenous auto or paracrine origine from platelets or endot helial cells and participates in the local regulation of platelet func tion in association with other products of endothelial or platelet syn thesis. Exogenous administration is common in therapeutics either in m olecules which release NO (nitrate derivatives, sodium nitropruside, m olsidomine, etc) or by NO gas administered by inhalation. The antiplat elet effect of MO has been clearly demonstrated in vitro, in vivo or e x vivo, in animals and humans, and probably explains, at least partial ly, the efficacy of nitrate derivatives in ischaemic coronary artery d isease. Nevertheless, the platelet inhibition observed with intravenou s NO releasing drugs is associated with potentially harmful systemic h ypotension. Platelet inhibition by inhalation of NO could be an altern ative means of avoiding this unwanted effect.