Exaggerated Vasoconstriction in Complex Regional Pain Syndrome-1 Is Associated with Impaired Resistance Artery Endothelial Function and Local Vascular Reflexes, Dayan L, Salman S, Norman D, Vatine JJ, Calif E, Jacob G.
Journal of Rheumatoly 2008 May 1.
From the J. Recanati Autonomic Dysfunction Center, Orthopedic Department B, Rambam Medical Center and Faculty of Medicine, Technion-IIT, Haifa; and Outpatient and Research Division, Reuth Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
OBJECTIVE: Local regulatory mechanisms and microvascular function play a major role in the pathogenesis of hemodynamic and trophic changes in patients with complex regional pain syndrome-1 (CRPS). Venoarteriolar and venoarteriolar-myogenic reflexes (VAR, VMR, respectively) as well as endothelial-dependent vasodilatation are important contributors to local vasoregulation. We examined whether VAR and VMR as well as resistance artery endothelial function are damaged in affected limbs of patients with CRPS.
METHODS: We measured reactive hyperemic response as an index of resistance artery endothelial function, VAR and VMR in extremity soft-tissue vasculature in patients with CRPS. RESULTS: Baseline blood flow values were not different between CRPS affected and unaffected upper and lower limbs. Resistance artery endothelial function indices, i.e., values of maximal flow after ischemia and the area under the flow-time curve (AUC), were significantly higher in the unaffected versus CRPS-affected upper limbs (19 +/- 3 vs 16 +/- 3 ml*min(-1)*dl(-1) and 373 +/- 71 vs 319 +/- 70 units, for maximal flow AUC, respectively) and lower limbs (9 +/- 2 vs 6 +/- 1.5 ml*min(-1)*dl(-1) and 160 +/- 51 vs 130 +/- 42 units, for maximal flow and AUC, respectively). Flow indices reflecting VAR were lower in the lower, but not upper CRPS-affected limbs compared with unaffected contralaterals (2 +/- 0.24 vs 1.55 +/- 0.3 ml*min(-1)*dl(-1); p = 0.027). Microvascular myogenic reflex-VMR indices, however, were not different in the upper or in the lower CRPS-affected limbs compared with their unaffected contralaterals.
CONCLUSION: Impaired balance exists in CRPS-affected limbs between vascular regulation systems responsible for vasoconstriction and vasodilation.
http://www.ncbi.nlm.nih.gov/pubmed/18464300
__________________________________________________ __________________________________________________ _______________
Continuous intra-arterial application of substance P induces signs and symptoms of experimental complex regional pain syndrome (CRPS) such as edema, inflammation and mechanical pain but no thermal pain, Gradl G, Finke B, Schattner S, Gierer P, Mittlmeier T, Vollmar B,
Neuroscience 2007 Sep 7;148(3):757-65. Epub 2007 Aug 8.
Institute for Experimental Surgery, University of Rostock, Schillingallee 69a, 18055 Rostock, Germany.
Substance P is involved in nociception in both the peripheral nervous system and the CNS and has been documented to play a crucial role in the complex regional pain syndrome (CRPS). So far, however, most experimental animal models are restricted to the effect of neurokinin-1 receptor blockers to inhibit substance P and do not directly evaluate its action. Thus, this study was conducted to test the hypothesis that local application of substance P causes signs and symptoms of CRPS. For this purpose rats received a continuous infusion of either substance P or saline over 24 h delivered by a mini-osmotic pump connected to an intrafemoral catheter. Animals were analyzed at either day 1 (n=6, each group) or day 4 (n=5, each group) after start of infusion. Substance P application caused a significant and long-lasting decrease in paw withdrawal thresholds upon mechanical stimulation, while animals did not present with thermal allodynia at days 1 and 4 after onset of infusion. In addition, severe s.c. edema was observed in all animals receiving substance P. In vivo fluorescence microscopy of the extensor digitorum longus muscle of the affected hind paw revealed enhanced leukocyte-endothelial cell interaction with a significant rise in the number of leukocytes both rolling along and firmly adhering to the wall of postcapillary venules, while saline-exposed animals were free of this local inflammatory response. Muscle cell apoptosis, as assessed by in vivo bisbenzimide staining, terminal deoxynucleotidyl transferase nick end labeling analysis and caspase 3-cleavage, could not be observed in either of the animals. In summary, the present study indicates that substance P is responsible for neurogenic inflammation, including local cell response, edema formation and mechanical pain, while it seems not to contribute to the generation of thermal allodynia.
http://www.sciencedirect.com/science...56267685a9ecbb