Résumé
It has been shown that inflammation reduces the effectiveness of sympathetic nerves in the regulation of knee joint blood flow, and the joint vascular-beta adrenoceptors are changed due to acute inflammation from a majority of beta-1 to an equality of beta-1 and beta -2 receptors. To investigate the role of sympathetic nerves in nerve induced vasoconstriction and changes in joint vascular beta-adrenoceptors due to chronic inflammation, in 21 NZW rabbits, chronic inflammation of the knee joint was induced by Antigen induced arthritis method, In experiment day animals were anesthetized and the caudal femoral artery, a branch of tibia1 artery, was cannulated to inject the beta -agonists intra-arterially close to the joint. Posterior articular nerve [PAN] was dissected pee for electrical stimulation. Electrical stimulation of PAN resulted in 18.1 +/- 6.2% reduction of blood flow measured by laser Doppler flowmetry technique. Phentolamine completely blocked the constrictor response and reversed it to vasodilation [+8+/- 2.2 %]. Propranolol [nonselective beta-adrenoceptor antagonist] completely blocked this vasodilation response and reverse it to a vasoconstriction. Atenolol [beta l antagonist] no significantly reduced the dilator response but ICI 118551 [beta2 antagonist] reduced 50% of this response. Close intra-arterial injection of different doses of beta-agonists, Isoprinosine [nonselective beta agonist], Dobutamine [beta <1 agonist] and Salbutamol [beta <2 agonist] increased the joint blood flow by the potency rank order of " Isoprenaline > Salbutamole > Dobutamine " .The isoprenaline dose response curve was shifted to the right by J adrenoceptor antagonists by the potency rank order of propranolol> ICI> atenolol. Overall, this study showed that beta 2-adrenoceptor response is stronger and suggested that the shift porn beta l- to beta 2-adrenoceptor subtype started by acute inflammation continued in chronic inflammation and the sympathetic vasoconstrictor response was nearly recovered toward normal compared to acute inflammation