Effects of sympathetic stimulation on C-fibre response after peripheral nerve compression: an experimental study in the rabbit common peroneal nerve

Non-myelinated C-fibre responses during sympathetic trunk stimulation were studied in rabbit common peroneal nerve 2 weeks after the nerve had been subjected to compression at 400 mmHg for 30 min. Our previous studies have demonstrated that during sympathetic trunk stimulation the compound action potential of uninjured somatic C-fibres is characterized by a reduced amplitude and an increased latency. In the present study, nerve compression changed the C-fibre response to sympathetic stimulation. Three out of eight nerves reacted to nerve compression by increased C-fibre compound action potential amplitude in response to sympathetic stimulation. In three other rabbits with compressed nerves the C-fibre action potential amplitude was unchanged, and in the remaining two rabbits the action potential amplitude was decreased during sympathetic stimulation. The action potential latency increased in all tested compressed C-fibres. The phenomenon of increased C-fibre amplitude during sympathetic activation has not been observed in uninjured nerves. As in uninjured nerves, noradrenaline infusion produced an increased C-fibre action potential amplitude and latency in six animals. Sympathetic stimulation did not affect the A-fibre response. These results indicate that sympathetic activity influences the conduction properties in C-fibres of somatic origin and that the response can be changed after a nerve injury. The findings may be of importance for the understanding of pain aggravation in different types of nerve injuries during increased sympathetic activity.     

Renal sympathetic nerve responses to stimulation, inhibition and destruction of the ventrolateral medulla in the rabbit

The role of the sympathetic nervous system in the cardiovascular responses to lesions of the caudal ventrolateral medulla of the rabbit was investigated by measurement of renal sympathetic nerve activity. In addition, the effect of chemical stimulation and inhibition on renal sympathetic nerve activity was assessed. The results show that lesions or chemical inhibition of the caudal ventrolateral medulla result in an increase in sympathetic nerve activity and blood pressure, whilst excitation results in a decrease in blood pressure and nerve activity. These findings contrast with chemical stimulation or inhibition of the rostral ventrolateral medulla in the region of the C1 cells where stimulation results in a rise in blood pressure and renal nerve activity, and inhibition, a fall in blood pressure and nerve activity.     

Hypoglossal responses to macular stimulation in the rabbit

This paper describes preliminary work on the role of the vestibular system in the hypoglossal neurons modulation. Natural stimulation of the otolith organ showed that hypoglossal motoneurons are responsive to gravity stimulation. The spontaneous firing rate of single cells, antidromically identified, was significantly modified during ipsi- or contralateral static tilting of the whole animal. Several response patterns were observed. These results infer that vestibular macular receptors may modulate hypoglossal nucleus activity in response to static head displacement.     

Cardiovascular and electrophysiological responses to sympathetic pathway stimulation.

Anesthetized, vagotomized, and paralyzed cats were used to study the relationship between changes in blood pressure and T2 preganglionic nerve activity elicited by stimulation of descending spinal sympathoexcitatory pathways. While low-frequency stimulation (1-10 Hz) resulted in a depressor response, an attenuation of sympathetic nerve evoked discharges was noted after the second pulse of twin-pulse stimulations with 1,000- to 100-ms intervals between stimuli (corresponding to 1-10 Hz). High-frequency stimulation (greater than 10 Hz) resulted in a pressor response, while preganglionic nerve-evoked discharges were enhanced during twin-pulse stimulations with intervals between stimuli less than 50 ms (corresponding to greater than 20 Hz). These data suggest that the depressor response during low-frequency stimulation may be explained by impulses occurring during the silent period of the previous response. During this time the preganglionic neuron is inexcitable and spontaneous activity is abolished; therefore, the blood pressure falls. High-frequency stimulation may result in a pressor response by increasing the number of preganglionic neurons that are activated. This may be due to a process of temporal summation, with initial stimuli bringing cells closer to their threshold for firing and additional stimuli close in time causing these neurons to discharge.     

Failure of sympathetic stimulation to affect responsiveness of rabbit polymodal nociceptors

The responses of polymodal nociceptors with unmyelinated (C) fibers of the rabbit's great auricular nerve were examined with and without intermittent stimulation of the ipsilateral cervical sympathetic trunk. The receptive field of each polymodal nociceptor was heated twice in a stepwise manner from 30 to 50 or 55 degrees C in 5 degree C steps. For each unit, one heating trial was a control trial and the other was accompanied by sympathetic stimulation. The order of the control and sympathetic stimulation trials and the maximum testing temperature were varied systematically among the units examined. The initial responses of polymodal nociceptors in the first heating trial in the presence of sympathetic stimulation were similar to the responses of units whose first heating was a control trial. Units whose receptive fields were tested to a maximum temperature of 50 degrees C in the first trial displayed enhanced responses to heat in their second trial (sensitization), while units tested initially to 55 degrees C responded less briskly during their second heating trial (depression). However, the occurrence of sympathetic stimulation in the second heating trials had no apparent effect on the responses to heat of sensitized or depressed elements. Alterations in the numbers of impulses, instantaneous frequency, or pattern of impulse activity of individual units could not be attributed to sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

The responses of the left ventricle to left sympathetic burst-like stimulation

This paper attempts to verify experimentally the results of a paper by Greene and Clark (1974) on the modelling of cardiac augmentor function. Three separate stimulation protocols are utilised in this study and model and experimental results are shown to agree.     

Single unit responses in the cervical sympathetic trunk upon somatic nerve stimulation

Pflügers Archiv - European Journal of Physiology -     

Cardiac vagal and sympathetic nerve responses to baroreceptor stimulation in the dog

The effects of ascending stepwise pressure changes in the isolated carotid sinuses on cardiac vagal and sympathetic nerve activities were studied in anesthetized, open chest dogs. The steady state responses of the cardiac vagal and the sympathetic nerve activity and arterial blood pressure were plotted against the sinus pressure and the relations were approximated by the normal distribution function (response curve). The sinus pressure- vs. reflex gain relations (reflex gain curve) were approximated by the normal density function. The maximum gain and the range of change were found to be greater for the vagal than for the sympathetic and arterial pressure responses. The sinus pressure values derived from response curves and reflex gain curves for vagal and sympathetic nerve responses were close to each other, while these values and those obtained from arterial pressure responses were considerably apart. It was concluded that: (1) The cardiac vagal neurons are more sensitive to the baroreceptor input than the sympathetic neurons; (2) The similar type of baroreceptor afferent inputs reach the cardiac vagal and the sympathetic structures which are controlling the autonomic outflows.     

Influence of adenosine on responses to vagal nerve stimulation in the anesthetized rabbit

The influence of local adenosine infusion into the celiac artery on the gastric contractile responses to centrifugal vagal nerve stimulation was studied in anesthetized rabbits, and was compared with the effects of systemic administration of equivalent amounts of adenosine. Close arterial infusion of adenosine caused a marked reduction of gastric contractions induced by nerve stimulation, whereas corresponding responses to close arterial infusions of acetylcholine were enhanced during adenosine. The comparison with systemic adenosine administration revealed that the influence on gastric neurotransmission was not related to the hypotensive effect of the compound. No effects of adenosine were seen on bronchial activity as measured by insufflation pressure. Variable effects were obtained on cardiac responses to vagal stimulation. Gastric smooth muscle contractions elicited in vitro by transmural nerve stimulation were affected by adenosine in a biphasic manner, initial inhibition followed by potentiation of the apparently cholinergic responses. It is suggested that adenosine may modulate cholinergic neurotransmission in vivo by a dual effect, prejunctional inhibition and postjunctional enhancement.     

Cough reflex responses during pulmonary C-fibre receptor activation in anesthetized rabbits

We investigated the changes induced by pulmonary C-fibre receptor activation in the cough reflex evoked by mechanical stimulation of the tracheobronchial tree in pentobarbitone anesthetized, spontaneously breathing rabbits. Phrenic nerve and abdominal muscle activities were monitored along with tracheal and arterial blood pressures. The activation of pulmonary C-fibre receptors by means of right atrial injection of phenylbiguanide (PBG) caused the pulmonary chemoreflex characterized by tachypnea, bradycardia and hypotension. During the pulmonary chemoreflex, the time components (total cycle duration, inspiratory and expiratory times) of the cough motor pattern significantly decreased, whereas no consistent changes in peak phrenic and abdominal activity, peak tracheal pressure and number of coughs evoked by each stimulation trial were observed. At variance with previous findings in cats and dogs, the results show that tracheobronchial cough is not significantly reduced in the rabbit during PBG-induced chemoreflex. This study is the first to provide evidence supporting the hypothesis that the time components of the cough motor pattern are, to some extent, dependent upon the timing characteristics of the ongoing respiratory activity and suggests a novel mechanism leading to cough depression.