ABSTRACT
Background: Although traditional use of Tridax procumbens aqueous leaf extract (TPALE) in the management of respiratory disorders is documented, validated scientific evidence is scarce. Aim and Objectives: Trachea smooth muscle (TSM) relaxant activity of TPALE ingestion was investigated in the presence or absence of key TSM relaxant agents. This was with the aim at elucidating relaxant activity of TPALE on TSM. Materials and Methods: Contractile activity of TSM excised from TPALE treated (100 mg/kg) and non-treated rats was assessed pre - and post-incubation in salbutamol (10?4 M), theophylline (10?4 M), caffeine (10?4 M), naringin (10?4 M), and naringenin (10?4 M) using organ chamber connected to a force isometric transducer (Model 7004; Ugo-Basile VArese, Italy). Results: TPALE treatment significantly inhibited contractile activity in TSM. TPALE treated rats showed significantly inhibited contractile activity of the TSM pre (45.6%) and post-incubation (35%) in theophylline when compared to control pre (90.6%) and post-incubation (60%). Incubation of TSM from control and TPALE treated rats in salbutamol, significantly inhibited contractile activity (33.2%) and (37.2%), respectively. After incubation in caffeine, TSM from TPALE treated rats showed significant inhibition in the contractile activity (30.7%) as TSM from control postincubation (38.4%). TSM of TPALE-treated group pre-incubation showed significant inhibition in contractile activity (41.8%) when compared to the TSM of TPALE-treated Group (59.3%) and control (64.5%) post-incubation in naringin. However, incubation of TSM of TPALE-treated rats in naringenin significantly inhibited contractile activity (40.4%) when compared to pre-incubation (45%) and control pre - and post-incubation, respectively (52% and 90%). Conclusion: Calcium-activated K+ channels, ?2 adrenergic stimulation, and antioxidant activity contribute to the mediation of relaxant activity by TPALE in TSM.
ABSTRACT
BACKGROUND: Non-depolarizing muscle relaxants have their muscle relaxing effect by competing with acetylcholine (ACh) at the nicotinic receptor level. What are the effects of such muscle relaxants on the tracheal smooth muscle? This present study was set up to address the question as to how vecuronium and pancuronium influence the tracheal smooth muscle. METHODS: Sixty male Sprague-Dawley rat tracheal smooth muscles were isolated at optimal length for isometric force. The preparations were set up in an organ bath containing Tyrode's solution. And isometric force displacement transducer and physiograph were used to record the change in force. After the equilibration period the preparations were contracted with ACh 10(-5) M and carbachol 3x10(-7)M seperately. The preparations were washed with fresh tyrode's solution and allowed to return passively to resting tone. Then the cumulartive effect of ACh (from 3 10(-7) M through 10(-5) M) and carbachol (CCh, from 10(-8) M through 3 10(-6) M) were produced before and after pretreating the preparation with vecuronium (10(-5) M and 10(-6) M) and pancuronium (10(-5) M and 10(-6) M) respectively. Also, we studied the changes of contraction produced by neostigmine before and after pretreatment with vecuronium (10(-5) M and 3 10(-5) M) and pancuronium (3 10(-6) M and 3 10(-5) M). RESULTS: Vecuronium shifted the ACh dose-response curve of the tracheal contraction to the left (p0.05). CONCLUSIONS: Vecuronium inhibits the ACh hydrolyzing enzyme, especially acetylcholinesterase. Therefore it potentiates ACh contraction in the tracheal smooth muscle, but not the CCh contraction, while pancuronium has a different effect in comparison with vecuronium. That is, at a low concentration it reveals an antagonistic effect on the muscarinic M2 receptor and at a higher concentration it has an antagonistic effect on the muscarinic M3 receptor in the tracheal smooth muscle.