THE THROMBOXANE AZ MIMETIC U-46619 INHIBITS SOMATOMOTOR ACTIVITY VIA A VAGAL REFLEX FROM THE LUNG

Vagal reflexes from the heart and lungs elicit autonomic as well as so matomotor responses. The purpose of the present investigation was to d etermine whether the inflammatory mediator thromboxane A(2) inhibits t he knee-jerk reflex via a vagally mediated reflex from either the hear t or the lung. The thromboxane A(2) mimetic U-46619 (0.8 +/- 0.08 mu g /kg) was injected through a catheter placed near the right atrium (n = 11), near the aortic arch (n = 7), or into the pericardial sac (n = 4 ) in 11 chloralose-anesthetized cats. The knee-jerk reflex, elicited b y striking the patellar tendon with a solenoid-driven hammer, was used to evaluate somatomotor activity. The mean maximum tension produced b y the knee-jerk reflex was 306 +/- 21 g (range 154-471 g). Intravenous U-46619 injection inhibited the knee-jerk reflex by 25 +/- 6% and inc reased peak systolic pressure 53 +/- 7 mmHg on average. Bilateral cerv ical vagotomy abolished the somatomotor inhibition but did not reduce the presser response. Intraarterial U-46619 injection inhibited the kn ee-jerk reflex in two of seven cats and increased peak systolic pressu re by 41 +/- 11 mmHg. Vagotomy abolished the inhibition in one of the two cats but did not reduce the presser response. Intrapericardial U-4 6619 injection did not affect the knee-jerk reflex nor blood pressure. The results indicate that U-46619 inhibited the knee-jerk reflex via a vagal reflex from the lung because the inhibition predominated after intravenous injection and was abolished by vagotomy. Speculation is m ade that the inflammatory mediator thromboxane A(2) may contribute via a vagal reflex to the depression of motor activity associated with si ckness behavior.