British Journal of Anaesthesia, Vol 81, Issue 2 188-192, Copyright © 1998 by The Board of Management and Trustees of the British Journal of Anaesthesia
K. G. Allman, A. P. Stoddart and J. D. Young
Excess production of nitric oxide contributes to the refractory hypotension
associated with sepsis and is dependent upon precursor availability,
L-arginine. Endothelial uptake of L-arginine by the y+ transporter can be
inhibited by another cationic amino acid, L-lysine. This study was
undertaken to determine the effects of L-lysine in an anaesthetized ovine
model of endotoxaemia in which nitric oxide production is known to be
limited by L-arginine availability. The haemodynamic effects of i.v.
L-lysine (500 mg kg-1) were compared with those of a known inhibitor of
nitric oxide synthase, NG-nitro-L- arginine-methyl ester, L-NAME (25 mg
kg-1) and with control animals (n = 6 per group). Serum nitrates, the
stable end metabolite of nitric oxide production, were also measured.
L-NAME administration caused a significant increase in systemic and
pulmonary vascular resistance (P < 0.0001), mean arterial pressure (P
< 0.0001) and a reduction in serum nitrate concentrations (P <
0.0001). The administration of L-lysine had no effect on systemic or
pulmonary vascular resistance, mean arterial pressure or serum nitrate
concentrations. We conclude that the administration of L-lysine does not
inhibit nitric oxide production in this model.
LABORATORY INVESTIGATIONS
Effect of L-lysine on nitric oxide production in ovine endotoxaemia
Nuffield Department of Anaesthetics, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE
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