S-Nitrosoglutathione inhibits platelet activation and deposition in coronary artery saphenous vein grafts in vitro and in vivo
- aDepartment of Gynecology, Obstetrics and Pharmacology, University of Alberta, Edmonton, Canada, bDepartment of Cardiology, King’s College Hospital, London, UK, cDepartment of Cardiothoracic Surgery, King’s College Hospital, dCruciform Project, University College, London, UK
- Dr A J de Belder, Department of Cardiology, King’s College Hospital, Denmark Hill, London SE5 9RS, UK.
- Accepted 4 March 1998
Abstract
Objective To investigate platelet activation and deposition in human saphenous vein and internal mammary artery grafts following coronary artery bypass in vitro and in vivo, as well as inhibition of activation by the platelet selective nitric oxide donor S-nitrosoglutathione (GSNO).
Design Controlled in vitro and in vivo studies.
Setting Tertiary cardiac centre.
Patients 24 patients undergoing coronary artery bypass surgery requiring vein and artery grafts.
Interventions In vitro: human platelet rich plasma was perfused through segments of vein and artery, with or without GSNO 10-6 M, and the platelet count was measured in the effluent. In vivo: indium-111 labelled antibody against the platelet α granule protein GMP-140 was injected at the end of coronary bypass grafting and γ counts were compared between vein and artery grafts with or without systemic infusion of GSNO (40 nmol/min).
Results In vitro: platelet count in perfused vein (< 70% of baseline) decreased more than in artery segments (89–94% of baseline) (p < 0.001). The platelet count was unchanged with GSNO in vein and artery segments. In vivo: γ counts were greater at all time points over vein than artery grafts (p < 0.05), and were reduced by infusion of GSNO (p < 0.05).
Conclusions Platelet activation is greater in vein than in artery grafts in vitro and in vivo. Activation, which contributes to early vein graft failure, was inhibited by GSNO.
