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LIOR DAYAN, SERGEI SALMAN, DORON NORMAN, JEAN-JACQUE VATINE, EDWARD CALIF, and GIRIS JACOB

ABSTRACT.

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. (J Rheumatol First Release May 1 2008)

Key Indexing Terms:

COMPLEX REGIONAL PAIN SYNDROME
VASOCONSTRICTION
ENDOTHELIAL FUNCTION
VASCULAR REFLEXES

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.

Supported in part by a grant from the Yahel Foundation.

L. Dayan, MD, MSc; S. Salman, MD, J. Recanati Autonomic Dysfunction Center, Orthopedic Department B, Rambam Medical Center; D. Norman, MD, Orthopedic Department B, Rambam Medical Center; J-J. Vatine, MD, Outpatient and Research Division, Reuth Medical Center, Sackler Faculty of Medicine; E. Calif, MD, Orthopedic Department B, Rambam Medical Center; G. Jacob, MD, DSc, Professor of Medicine and Physiology, J. Recanati Autonomic Dysfunction Center, Orthopedic Department B, Rambam Medical Center.

Address reprint requests to Dr. G. Jacob, J. Recanati Autonomic Dysfunction Center, Rambam Medical Center, Haifa 31096, Israel. E-mail: g_jacob@rambam.health.gov.il

Accepted for publication February 7, 2008.