Reflex inhibition of monosynaptic reflexes by stimulation of type J pulmonary endings

1. Monosynaptic reflexes, evoked from flexor and extensor hind limb muscle nerves in cats anaesthetized with pentobarbitone sodium, were depressed for several seconds after right intra-atrial injection of phenyl diguanide. Injection of the drug close to the aortic valves did not produce the same effect on the reflex. There was no obvious depression of polysynaptic reflexes on intra-atrial injection of phenyl diguanide.2. This depression of the monosynaptic reflex was present even after the administration of atropine, which lessened the hypotension due to phenyl diguanide. The blood gas tensions were also measured after the administration of phenyl diguanide, and were not altered to a degree where one would expect the depression to be secondary to a change in arterial gas tensions. The depression was also present in paralysed and artificially ventilated cats.3. The afferent pathway causing this depression of the monosynaptic reflex runs in the vagus nerve, as shown by experiments done before and after vagotomy. Intercollicular decerebration also abolished this inhibition of the monosynaptic reflex.4. Prior intravenous injection of strychnine (0.1 mg/kg) abolished the effect of intra-atrial administration of phenyl diguanide.5. It was concluded that stimulation of type J pulmonary endings causes a reflex inhibition of monosynaptic reflexes lasting for several seconds via regions of the brain cephalad to the intercollicular level.