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Vascular resistance and endothelial function in cyclosporine-treated lung transplant recipients

Journal article
Authors Martin Silverborn
Anneli Ambring
Folke Nilsson
Peter Friberg
Anders Jeppsson
Published in Transpl Int
Volume 19
Issue 12
Pages 974-81
ISSN 0934-0874 (Print)
Publication year 2006
Published at Institute of Medicine
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 974-81
Language en
Links www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Adult, Antigens/analysis, Blood Pressure, Cyclosporine/*therapeutic use, Endothelial Cells/*physiology, Endothelin-1/blood, Female, Heart Rate, Humans, *Lung Transplantation/adverse effects, Male, Middle Aged, Nitric Oxide/physiology, Nitric Oxide Synthase/antagonists & inhibitors, *Vascular Resistance
Subject categories Surgery

Abstract

The majority of patients undergoing solid organ transplantation develop hypertension, to which vasoconstriction and impaired endothelial function have been suggested to contribute. We compared basal vascular resistance and nitric oxide-mediated endothelial-dependent and independent vasoreactivity between cyclosporine-treated lung transplant recipients and healthy subjects. Forearm blood flow was measured by venous occlusion plethysmography at rest and during acetylcholine, glyceryltrinitrate and N(G)-monomethyl-L-arginine acetate (L-NMMA) infusion in 11 lung transplant recipients 3-5 years after transplantation and in eight healthy subjects. Forearm vascular resistance (FVR) was calculated. Plasma levels of endothelin-1 (ET-1) and von Willebrand factor (vWf) were analysed. Basal vascular resistance was 40% lower in transplant recipients than in healthy subjects (P = 0.021). Endothelial-dependent and independent vasodilation did not differ. Plasma levels of ET-1 and vWf were higher in transplant recipients (P = 0.009 and P < 0.001 respectively). There was a significant correlation between ET-1 levels and FVR in healthy subjects (r = 0.83, P = 0.042), but not in transplant recipients (r = -0.14, P = 0.70). The findings oppose the theory of generalized vasoconstriction and impaired endothelial function in the pathogenesis of hypertension after transplantation. Increased plasma levels of ET-1 do not cause increased FVR in lung transplant recipients.

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