ARTERIOVENOUS DIFFERENCES IN PLASMA-CONCENTRATIONS OF CATECHOLS IN RATS WITH NEUROPATHIC PAIN

Background: Alterations in cutaneous temperature, sweating, and cutane ous blood now in patients with pain states, such as reflex sympathetic dystrophy and causalgia, have been interpreted as evidence for exagge rated sympathetic outflow, It was determined whether pain behavior in a rat model of sympathetically maintained pain is associated with alte rations in regional sympathoneural function, Methods: Peripheral neuro pathy was induced in 29 Sprague-Dawley rats by ligation of the left L5 and L6 spinal nerves, Sixteen other rats had sham surgery (nerve expo sure without ligation). Animals were tested for behavioral signs of al lodynia (decreased paw withdrawal thresholds to mechanical stimuli) at 2 and 4 weeks after the surgery. Arterial and iliac venous blood samp les (left, affected; right, control) were obtained at 2 weeks (NP2, n = 14) and 4 weeks (NP4, n = 15) after neuropathic or sham (n = 8 at 2 and 4 weeks) surgery. Plasma concentrations of dihydroxyphenylalanine, dihydroxyphenylacetic acid, dopamine, norepinephrine, and the intrane uronal norepinephrine metabolite, 3,4-dihydroxyphenylglycol, were anal yzed in arterial and left and right iliac venous samples, Results: A d ecrease in paw withdrawal threshold was observed in neuropathic (NP2 a nd NP4) but not sham-operated rats, Affected and control Limbs did not differ in arteriovenous differences in concentrations of dihydroxyphe nylalanine, dihydroxyphenylacetic acid, dopamine, or 3,4-dihydroxyphen ylglycol. No differences were observed between sham-operated and neuro pathic animals in these arteriovenous increments. In contrast, affecte d Limbs of NP2 rats had a reduced arteriovenous increment in norepinep hrine concentrations, compared to that in the control side (P < 0.05). Conclusions: No neurochemical evidence of sympathetic hyperactivity i s observed in the rat model of neuropathic pain; if anything, norepine phrine release is decreased in the affected limb. Autonomic disturbanc es in neuropathic pain are therefore more likely the result of recepto r supersensitivity than increased local sympathoneural traffic.