Local microvessels of peripheral nerve trunks (vasa nervorum) dilate following
capsaicin-induced
inflammation or local nerve trunk injury. In previous work, we observed that
morphine blocked
capsaicin-induced dilation of vasa nervorum presumably through the action of local
opioid receptors. In the present work, we studied injury-related
hyperemia of the rat sciatic vasa nervorum using
laser Doppler and
hydrogen clearance
microelectrode measurements of local perfusion. Systemic
morphine reversed
hyperemia by vasoconstricting both extrinsic and intrinsic microvessels supplying 48-h-old "
neuroma" preparations or crush zones of peripheral nerve trunks.
Morphine did not constrict microvessels of contralateral uninjured or
sham exposed but uninjured sciatic nerves. In contrast to the injured nerves, contralateral uninjured nerves exposed to
morphine frequently had a rise in local perfusion, indicating vasodilation. The vasoconstrictive actions of
morphine were blocked by pretreatment with
naloxone and were not mimicked by saline
injections alone. Systemic doses of selective
opioid agonists to mu-, kappa-, and
delta-receptors also selectively constricted microvessels of injured nerves. Local blood flow in older experimental
neuromas at 7 days had partial sensitivity to
morphine, whereas at 14 days perfusion flow was not influenced by
morphine. Exogenous
opioids dampen early but not later inflammatory microvasodilation and could have important influences on the nerve regenerative milieu.