Effects of thromboxane A2agonist STA2on rapidly adapting pulmonary stretch receptors in vagotomized rabbits

✍ Scribed by S. Matsumoto; S. Takano; N. Nakahata; T. Shimizu

• Publisher: Springer
• Year: 1994
• Tongue: English
• Weight: 627 KB
• Volume: 172
• Category: Article
• ISSN: 0341-2040
• DOI: 10.1007/bf00164312

✦ Synopsis

We investigated the responses of rapidly adapting pulmonary stretch receptors (RARs) and tracheal pressure (Pa-) to right atrial injections of the thromboxane A 2 (TXA2) stable analogue STA2 (0.3, 1.0, and 3.0 p~g/kg) before and after administration of atropine sulfate (1 mg/kg), isoprenaline (200 ~g/kg), indomethacin (1 mg/kg), or S-145 (0.5 mg/kg) in artificially ventilated, bilaterally vagotomized rabbits. The RARs increased their activity after STA2 administration, and the increase was dose-dependent. However, intraatrial injections of STA 2 at all the doses examined had no significant effect on PT. The excitatory responses of RAR activity to STA 2 (0.3-3.0 ~g/kg) were not significantly altered by administration of atropine sulfate (anticholinergic agent), isoprenaline (bronchodilator), or indomethacin (cyclooxygenase inhibitor). However, S-145 treatment (TXA 2 antagonist) blocked the STAz-induced RAR stimulation. To determine whether or not administration of STA 2 causes release of acetylcholine (ACh), we also examined the effects of vagal efferent stimulation (10-15 V, 10 Hz, 1 ms), STA2 administration (3.0 ~g/kg), and their combination on PT in rabbits associated with both artificial ventilation and bilateral vagotomy. The vagally mediated bronchoconstriction that led to an increase in Pa-was not enhanced by simultaneous administration of STA 2 at 3.0 p~g/kg in all of the tested animals. These results suggest that the stimulation of RARs by STA 2 is not mediated by the release of ACh from the nerve endings but is probably due to a local inflammatory bronchoconstriction that does not significantly alter the value of PT-