SUMMARY1. The experiments reported here have examined some temporal characteristics of the inspiration-related sympathetic discharge of the cat in control conditions and during forcing of the respiratory oscillator into marked deviations from its natural frequency. The purpose of these experiments was to establish whether or not the relation of sympathetic to phrenic nerve activity shows properties consistent with the hypothesis that the inspiration-related sympathetic discharge is driven by a neural oscillator, independent of, but coupled and stably entrained to, the brain-stem respiratory oscillator.2. The electrical activity of the whole cervical sympathetic trunk (n = 26) or of small strands of the cervical trunk containing single units (n = 20) and of the phrenic nerve was recorded in pentobarbitone-anaesthetized, paralysed, artificially ventilated, sino-aortic denervated cats. Most of the cats were bilaterally vagotomized.3. The onset of the inspiratory burst of the sympathetic preganglionic neurones had a fixed delay from the onset of the phrenic nerve burst. The level of activity within the burst, in whole cervical trunk recording, reached a maximum in early inspiration and then was maintained at approximately this level for the rest of inspiration (twenty-two out of twenty-six cats). In four cats the activity level increased throughout the burst. Individual sympathetic preganglionic neurones displaying inspiration-related burst firing were characteristically recruited in early inspiration and thereafter maintained an approximately constant firing frequency for the rest of inspiration.4. Electrical stimulation of afferents in the superior laryngeal nerve during various phases of the respiratory cycle caused equivalent, phase-dependent, resetting patterns of both phrenic nerve and inspiration-related sympathetic discharge.5. In cats with intact vagus nerves, entrainment of the brain-stem respiratory oscillator to the frequency of the respiratory pump was used to change the frequency of the former, within limits, by changing the frequency of the latter. Over the range of frequencies tested, the pump-to-phrenic delay varied as a function of frequency, while the delay between phrenic and sympathetic burst onset was essentially independent of frequency.6. In hyperthermic, hypocapnic cats phrenic nerve burst frequency increased up to about 300 bursts/min from a value of 15 bursts/min in normothermia-18 PHY 385 M. BACHOO AND C. POLOSA normocapnia. At all frequencies within this range the sympathetic burst maintained a delay, with respect to the phrenic burst, which was essentially independent of frequency.7. The fact that phrenic nerve and sympathetic burst maintained a 1: 1 relation with essentially constant delay over all frequencies tested is inconsistent with the known behaviour of coupled neural oscillators. Therefore, the equality of period of phrenic nerve burst and inspiration-related sympathetic discharge is unlikely to result from the activity of an autonomous sympathetic oscillator coupled to the bra...

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1. In the anesthetized, scopolamine-treated cat, the compound action potential (CAP) evoked by a single supramaximal shock to the third thoracic white ramus (T3WR) was recorded in the inferior cardiac nerve (ICN). The CAP was depressed in a dose-dependent manner by the intravenous administration of the nicotinic antagonist hexamethonium (C6). 2. During steady intravenous infusion of C6, which reduced the amplitude of the CAP by 80-90%, a short train of stimuli (few seconds, 10-40 Hz) to the sympathetic trunk just below T4WR potentiated the CAP for periods of tens of minutes to 1-2 h (heterosynaptic long-term potentiation, LTP). An LTP of similar time course was obtained when both train and single shock were applied to T3WR (homosynaptic LTP). Magnitude and duration of the heterosynaptic LTP were dependent on number, frequency, and intensity of the stimuli. No LTP was produced by a train to the ICN. Heterosynaptic LTP was also observed in the absence of C6. Because of the limited subliminal fringe of the test input under this condition, the LTP was of small magnitude. Heterosynaptic LTP also of the heart rate (HR) response to a test stimulus was observed after a conditioning train. 3. The conditioning train produced a displacement to the right of the dose-response curve for C6. The intravenous dose of C6 required for 50% attenuation of the test CAP increased from 0.84 +/- 0.15 (SE) mg/kg pretrain to 2.56 +/- 0.46 mg/kg posttrain (n = 5, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

SUMMARY1. The properties of sympathetic preganglionic neurone activity during expiration were studied in pentobarbitone-anaesthetized (n = 26) and in non-anaesthetized, mid-collicular decerebrate (n = 5), paralysed, artificially ventilated cats in which the electrical activity of the phrenic nerve and of the cervical sympathetic trunk was recorded.2. In control conditions (end-tidal Pco, between 35 and 40 mmHg, zero endexpiratory pressure) sympathetic activity during expiration was either steady at a low level (n = 11) or showed a modest progressive increase from a low level in early expiration (n = 17). Very infrequently (n = 3), it showed a transient increase during the second half of expiration.3. Artificial ventilation with positive end-expiratory pressures in the range from 2-1 +0 4 (mean+ S.D.) to 6-7 +0-6 cmH2O caused, in cats with intact vagus nerves, an increase in sympathetic neurone activity during the second half of expiration. Within this range of pressures, the magnitude of the increase was related to the magnitude of the positive end-expiratory pressure. This effect reversed at higher positive end-expiratory pressures. Pressures in excess of 10-2 + 1-8 cmH2O caused inhibition of sympathetic activity.4. The sympatho-excitatory effect of positive end-expiratory pressure disappeared after bilateral cervical vagotomy. With intact vagus nerves, it also disappeared at levels of systemic hypocapnia (end-tidal PCO2 < 15 mmHg) which abolished phrenic nerve activity. In hypocapnia, artificial ventilation with peak tracheal pressures greater than 7-2 + I1 cmH2O caused inhibition of sympathetic activity, while ventilation with lower end-expiratory pressures had no effect on sympathetic activity. It may be concluded that the sympatho-excitatory effect of positive end-expiratory pressure is mediated by vagal afferents and requires a certain level of brain-stem respiratory neurone activity.5. Sympatho-excitation during expiration was also observed, in normocapnic conditions, during short-duration static lung inflation with tracheal pressures in the range from 2-5 + 0-3 to 7-0 + 0-8 cmH2O as well as during artificial ventilation with zero end-expiratory pressure when lung inflation occurred in expiration. These responses were abolished by bilateral cervical vagotomy and during systemic hypocapnia.6. Sympatho-excitation during expiration was also observed when systemic M. BACHOO AND C. POLOSA hypercapnia was produced in vagotomized cats by artificial ventilation with gas mixtures containing 5 or 10 % CO2.7. These results can be explained by the hypothesis that some brain-stem expiratory neurones are a source of facilitatory synaptic input to sympathetic neurones. The activity of brain-stem expiratory neurones is known to be enhanced by moderate degrees of lung inflation and by increased chemical drive. Under these conditions sympathetic neurone activity would be expected to increase during expiration.

SUMMARY1. The background discharge of sympathetic preganglionic neurones shows a marked inspiration-synchronous component which is known to originate from within the central nervous system. The contribution of this component to total neurogenic vasoconstrictor tone is unknown.2. In order to estimate its extent we have exploited the inspiration-suppressing effect of a group of low threshold afferent fibres in the superior laryngeal nerve.3. The electrical activities of the cervical sympathetic trunk and of the phrenic nerve were recorded in pentobarbitone-anaesthetized, paralysed, artificially ventilated, sino-aortic denervated and vagotomized cats, together with the perfusion pressure of an innervated hind limb perfused at a constant flow rate.4. Repetitive stimulation of the superior laryngeal nerve at an intensity just sufficient to suppress phrenic nerve activity inhibited the inspiration-synchronous sympathetic discharge and caused hind limb vasodilatation. This vasodilatation was abolished by hexamethonium or phentolamine, but was not affected by atropine or propranolol.5. Following the elimination ofphrenic nerve activity and inspiration-synchronous sympathetic discharge by systemic hypocapnia, repetitive stimulation of the superior laryngeal nerve either failed to affect the residual sympathetic activity and hind limb perfusion pressure, or caused an increase of both.6. Stimulation of the superior laryngeal nerve with short (02 s) trains of stimuli, delivered at selected times of the respiratory cycle for several consecutive cycles, had similar effects on phrenic nerve bursts, inspiration-synchronous sympathetic discharge and hind limb perfusion pressure. Stimulation at progressively earlier times during inspiration produced a graded reduction in all three variables, while stimulation during late inspiration or early expiration had no effect on any of them.7. The results suggest that the vasodilator reflex, elicited by inspiration-suppressing afferents in the superior laryngeal nerve, results from selective abolition of the excitatory input which causes the inspiration-synchronous discharge of sympathetic neurones. The magnitude of the hind limb vasodilatation can therefore be taken as an indication of the extent of control of hind limb vasoconstrictor tone exerted by this particular input. By comparing the magnitude of the reflexly evoked vasodilatation with that of the vasodilatation resulting from ganglionic blockade, it was M. BACHOO AND C. POLOSA estimated that 24-2 % of the neurogenic vasoconstrictor tone of the hind limb was attributable to the inspiration-synchronous component of sympathetic discharge.