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McCaig Centre for Joint Injury and Arthritis Research, University of Calgary, Calgary, Alberta, Canada
Submitted 21 February 2006 ; accepted in final form 19 October 2006
Chronic inflammation associated with osteoarthritis (OA) may alter normal vascular responses and contribute to joint degradation. Vascular responses to vasoactive mediators were evaluated in the medial collateral ligament (MCL) of the anterior cruciate ligament (ACL)-deficient knee. Chronic joint instability and progressive OA were induced in rabbit knees by surgical transection of the ACL. Under halothane anesthesia, laser speckle perfusion imaging (LSPI) was used to measure MCL blood flow in unoperated control (n = 12) and 6-wk ACL-transected knees (n = 12). ACh, bradykinin, histamine, substance P (SP), and prostaglandin E2 (PGE2) were applied to the MCL vasculature in topical boluses of 100 µl (dose range 1014 to 108 mol). In normal joints, ACh, bradykinin, histamine, and PGE2 evoked a dilatory response. Substance P caused a biphasic response that was dilatory from 1014 to 1011 mol and constricting at higher doses. In ACL-deficient knees, ACh, bradykinin, histamine, and SP decreased perfusion, whereas PGE2 had a biphasic response that decreased perfusion at 1014 to 1011 mol and was dilatory at higher concentrations. Sodium nitroprusside increased perfusion in resting and phenylephrine-precontracted vessels with no significant differences between ACL-transected and control knees. Femoral artery occlusion and release increased perfusion by 74.3 ± 11.1% in control knees but only by 25.8 ± 4.4% in ACL-deficient knees. The altered responsiveness of the MCL vasculature to these inflammatory mediators may indicate endothelial dysfunction in the MCL, which may contribute to the progression and severity of OA and to the adaptation of the joint in an altered mechanical environment.
medial collateral ligament; blood flow; laser speckle imaging
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