Neurogenic inflammation and reflex sympathetic dystrophy (in vivo and in vitro assessment in an experimental model).

In the chronic constriction injury (CCI) model, signs and symptoms similar to those observed in reflex sympathetic dystrophy (RSD) can be induced by loosely ligating a rat sciatic nerve. Skin microcirculatory (inflammation-like) disorders may result from release of vasoactive neuropeptides at peripheral endings of antidromically acting nociceptive nerve fibers. These antidromic mechanisms may account for vasodilation and polymorphonuclear leukocyte (PMN) accumulation in the ligated hindpaw. We assessed skin blood flow (SBF) on the ligated side, by means of laser Doppler flowmetry, before as well as at day 4 after ligation. Postligation SBF measurements were performed before and after selective (capsaicin) conduction blockade of the ligated sciatic nerve. The extent of PMN accumulation was determined by measuring myeloperoxidase (MPO) activity in muscle biopsies obtained from the ligated and contralateral nonligated side. As compared to preligation SBF values, we observed an increase at day 4. SBF returned to preligation values consequent to capsaicin application. MPO activity, when compared to the nonligated side, was higher in biopsies obtained from the ligated side. These findings indicate that in the CCI-model, antidromically acting C-nociceptor nerve fibres increase SBF at 4 days after ligation. In addition, these antidromic mechanisms may induce an inflammatory response in the ipsilateral hindpaw, mediated by release of neuropeptides from the peripheral endings of antidromically acting C-nociceptor nerve fibers. This inflammatory response may account for various signs and symptoms as observed in the CCI model and may mirror pathophysiological mechanisms of RSD.