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Glutathione reverses
endothelial dysfunction and improves nitric oxide bioavailability
Abhiram Prasad, MBBS, MRCP, Neil P. Andrews, MBBS, MRCP, Feroz A. Padder,
MBBS, Mohsin Husain, BS, Arshed A. Quyyumi, MD, MRCP, FACC
Journal of American College of Cardiology
Vol. 34, No. 2, Aug 1999: 507-514
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ABSTRACT
OBJECTIVES
We investigated whether glutathione (GSH), a reduced thiol that
modulates redox state and forms adducts of nitric oxide (NO), improves
endothelium-dependent vasomotion and NO activity in atherosclerosis.
BACKGROUND
Endothelial dysfunction and reduced NO activity are associated with
atherosclerosis and its clinical manifestations such as unstable angina.
METHODS
In the femoral circulation of 17 patients with atherosclerosis or its
risk factors, endothelium-independent vasodilation with acetylcholine
(ACH), and endothelium-independent vasodilation with nitroglycerin and
sodium nitroprusside were studied before and after GSH. In 10 patients,
femoral vein plasma cyclic guanylate monophosphate (cGMP) levels were
measured during an infusion of ACH before and after GSH. Femoral artery
flow velocity was measured
using a Doppler flow wire and the resistance index (FVRI) calculated as
mean arterial pressure 4 flow velocity.
RESULTS
Glutathione strongly potentiated ACH-mediated vasodilation; at the two
doses, FVRI decreased by 47% and 56% before, and by 61% and 67% after
GSH (p 5 0.003). Glutathione also elevated cGMP levels in the femoral
vein during ACH infusion from 17.6 +/- 3 to 23.3 +/- 3 pmol/ml (p =
0.006). Augmentation of ACH responses was only observed in patients with
depressed endothelial function. Glutathione did not influence
endothelium-independent
vasodilation with either NO donor.
CONCLUSIONS
Thiol supplementation with GSH selectively improves human endothelial
dysfunction by enhancing NO activity. (J Am Coll Cardiol 1999;34:507–14)
© 1999 by the American College of Cardiology
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