Spatial variation in sympathetic influences on the vasculature of the synovium and medial collateral ligament of the rabbit knee joint.
1. Laser Doppler perfusion imaging was used to assess the role of the sympathetic nervous system in the control of blood flow to the medial collateral ligament and capsule (synovium and overlying fibrous tissues) of the rabbit knee joint. 2. Electrical stimulation of the saphenous nerve (width 1 ms; amplitude 20V; 1-30 Hz) produced a frequency-dependent vasoconstriction of knee joint vasculature. The response was maximal at 30 Hz and gave the greatest fall in perfusion at the femoral insertion of the ligament (by 33.8 +/- 7.4%, mean +/- S.E.M.; n = 5-6) and the smallest decrease at the tibial insertion of the ligament (by 10.6 +/- 2.9%). 3. Topical application of phentolamine (10(-6) mol) had no significant effect on basal knee joint blood flow. However, it abolished the nerve-mediated constrictor responses in all regions of the medial collateral ligament and synovium at all frequencies. 4. Topical administration of adrenaline (10(-14) to 10(-7) mol) caused a dose-dependent decrease in knee joint blood flow with the highest dose producing > 75% reduction in perfusion at all areas. 5. There was no evidence of a reactive hyperaemia in the 5 min following a 5 min period of femoral artery occlusion. Artificial manipulation of arterial blood pressure by intravenous infusion or withdrawal of blood caused a proportional change in ligament and synovial blood flow. These observations may indicate a lack of autoregulation in the joint and its exclusion from baroreflex modulation. 6. These results suggest a potential role for the sympathetic nervous system in the control of knee joint blood flow. Neuromodulation of ligament perfusion appears to predominate at the femoral insertion and this could prove to have functional significance.
McDougall
J J
JJ
McCaig Centre for Joint Injury & Arthritis Research, Department of Surgery, University of Calgary, Canada. mcdougaj@acs.ucalgary.ca
Ferrell
W R
WR
Bray
R C
RC
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D017885:Collateral Ligaments / Q000098:blood supply / Q000294:innervation / Q000502:physiology*; D004558:Electric Stimulation; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006614:Hindlimb / Q000098:blood supply / Q000294:innervation / Q000502:physiology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D007596:Joints / Q000098:blood supply / Q000294:innervation / Q000502:physiology*; D010646:Phentolamine / Q000494:pharmacology; D011817:Rabbits; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D013583:Synovial Membrane / Q000098:blood supply / Q000294:innervation / Q000502:physiology*
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D004837:Epinephrine; D010646:Phentolamine