مرکز منطقه ای اطلاع رساني علوم و فناوري - تغيير در پروفيل گيرنده هاي آلفا و بتا- آدرنرژيك عروق مفصل زانوي خرگوش به علت التهاب حاد

چكيده لاتين :

Background: This experiment was planned to investigate the nature of a and (i adrenoceptor in blood vessels supplying the posterior capsule of the acutely inflamed rabbit knee joint, and results were compared to findings from previous experiments on the normal joint, to assess any alteration which may occur in the adrenoceptor profile due to the inflammation process. Materials and Methods: This study was conducted with 30 white New Zealandian rabbits under pentobarbital induced general anesthesia. They were divided into two a and Beta groups. Blood flow of posterior articular nerve of knees was measured by laser flowmeter. a and Beta agonist drugs were injected intra-arterial in the presence and absence of their antagonists. Acute inflammation was induced by intra-articular Carrageenan. Posterior articular nerve was stimulated by nerve stimulator. Results: Electrical stimulation of the posterior articular nerve resulted in vasoconstriction which was reversed to vasodilatation by phentolamine and yohimbine. The dose - response curves intraarterial injection of a adrenoceptor agonists showed a rank-order potency of: adrenaline= phenylephrine= clonidine. The adrenaline dose-response curve was shifted to the right by administration of antagonists with a rank-order potency of: phentolamine= yohimbine= prazosin. At this stage of the experiment there was an equal response of alpha1-and alpha2- adrenoceptors in blood vessels of the acutely inflamed rabbit knee joint. In other two groups of animals the neurally mediated vasodilatation, (which appeared after administration of phentolamine), was completely blocked by propranolol, and was reduced to about 50% by atenolol. The dose-response curves in intra -arterial injection of Beta adrenoceptor agonists showed a rank-order potency of: isoprenaline> salbutamol = dobutamine. The isoprenaline dose- response curve was shifted to the right by administration of antagonists with a rank-order potency of: propranolol> atenolol. This experiment also showed an almost equal response of Beta1-and Beta 2- adrenoceptors in blood vessels of the acutely inflamed rabbit knee joint. Overall, compared to previous experiments on the normal joint in which alphal-and Beta1-adrenoceptor responses predominated, acute inflammation resulted in a shift from alpha2-towards alphal- and from Beta1-towards Beta 2- adrenoceptors responses. Conclusion: Generally in comparison to previous experiments on the normal joint in which al and Beta1 receptor responses predominated, acute inflammation resulted in a shift from alpha2 towards al and Beta1 towards Beta2 - receptor responses.