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

Abstract

SUIMMARY1. 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 (01 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.

Sinoaortic baroreceptor reflex arc modulation of nociception in spontaneously hypertensive and normotensive rats

“…Electrophysiological data showing that stimulation of vagal C-fibers in normotensive rats inhibits neural activity evoked by noxious stimulation at several levels of the neuroaxis, including cunneate nucleus and spinoreticular tracts, are compatible with this view (Dell, 1972;Gahery & Vigier, 1974;Thies & Foreman, 1981). However, these findings do not preclude the possibility that activation cardiopulmonary baroreceptors produces such behaviors through influences on motor excitability (Deshpande & Devanandan, 1970;Ginzel, 1973aGinzel, , 1973b.…”

“…Activation of either cardiopulmonary (Deshpande & Devanandan, 1970;Ginzel, 1973aGinzel, , 1973b or carotid sinus (Coleridge, Coleridge, & Rosenthal, 1976) baroreceptors produces a decrease in motor excitability, for example, inhibition of both flexor and extensor reflexes in cats. Thus, if resetting of sinoaortic baroreceptors in the SHR resulted in an augmentation of motor excitability, then the outcomes of the flinch-jump assay would be consistent with an interpretation based upon motor excitability.…”

Changes in respiratory sensations induced by lobeline after human bilateral lung transplantation

“…These reflex changes occur in many species including the cat whether it is decerebrate, anaesthetised, or awake (Ginzel & Eldred, 1969, 1970Paintal, 1969Paintal, , 1970Paintal, , 1973Deshpande & Devanandan, 1970;Schiemann & Schomburg, 1972;Kalia, 1973;Kalia et al 1973;Ginzel, 1973;Anand & Paintal, 1980;Pickar et al 1993).…”

Prolonged inactivation of cortical pyramidal tract neurones in cats by distension of the carotid sinus

“…Stimulation of the central end of the vagus nerve, for example, produces depression of the knee jerk in the cat (Schweitzer & Wright, 1937). Stimulation of the endings of afferent vagal C-fibres in the lungs by phenyldiguanide and other chemicals inhibits a and y motor activity, diminishes decerebrate rigidity and depresses spinal monosynaptic reflexes (Ginzel & Eldred, 1969;Deshpande & Devanandan, 1970;Ginzel, 1973); it also depresses PT-cell firing (F. Rosenthal, H. M. Coleridge & J. C. G. Coleridge, unpublished). The inhibitory effects of afferent vagal stimulation are also of very long duration.…”