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This work deals with the application of a pattern recognition method to distinguish the degree of diaphragm paralysis after gradual unilateral sections of phrenic nerve rootlets in anesthetized, spontaneously breathing cats. The data set consisted of the features that characterize breathing pattern and of phrenic nerve amplitude. The method called for stratification of 6-dimensional vectors into three classes: intact, partial, and complete unilateral phrenicotomy, which offers the possibility to construe the classification rule on the basis of the information contained in a set of feature vectors with the known class-membership. This method deals with the use of a distance function as a measure of similarity between two feature points. The results show that the degree of diaphragm paralysis could be recognized with the probability higher than 90%. Distinguishing the severity of diaphragmatic dysfunction and the compensatory strategies of the respiratory system, knowing only a handful of basic values describing breathing pattern, might have a practical meaning in respiratory emergencies.
Stimulation of the raphe pallidus nucleus produces facilitatory effects on respiratory activity. Numerous serotonergic projections from the raphe pallidus have been shown to terminate in the phrenic nucleus. This study was undertaken to examine the role of 5-hydroxytryptamine 1A (5-HT1A) receptors in the phrenic nucleus on the excitatory response of the phrenic nerve activity elicited from the raphe pallidus. We hypothesized that blockade of 5-HT1A receptors in the phrenic nucleus will attenuate raphe-induced facilitation of the phrenic nerve. Chemical stimulation of the raphe pallidus by synaptic excitant D,L-homocysteic acid produced increase in the amplitude of the phrenic nerve activity. After microinjection of the specific 5-HT1A receptor antagonist WAY, N-(2-(4,2-methoxyphenyl)-1-piperazinyl)ethyl)-N-2-pyridinyl-cyclohexane-carboxamide maleate into the phrenic nucleus, the raphe-induced facilitation of the phrenic nerve was attenuated. These data suggest that excitation of the phrenic nerve activity elicited by activation of the neurons in the raphe pallidus is mediated by 5-HT1A receptors in the phrenic nucleus.
The aim of this study was to examine the response of phrenic and hypoglossal motor outputs to hyperoxia and 11% hypoxia during picrotoxin-induced seizures. Adult rats were anesthetized with a mixture of urethane with alpha-chloralose. The animals were bilaterally vagotomized, paralyzed, and artificially ventilated. Picrotoxin was administered intravenously in a cumulative dose until seizures occurred. The response to changes in oxygen tension was studied after the convulsive dose of picrotoxin and compared with the baseline level. The results show that the picrotoxin-induced seizures evoked a complex respiratory response that consisted of an augmentation of phrenic and hypoglossal nerve activities and irregular disturbances in phasic respiratory discharges. The excitation of the hypoglossal activity appeared earlier and showed a more irregular pattern than that of the phrenic activity. Hyperoxia elicited a similar decrease in neural respiratory outputs during the control and seizure conditions, suggesting the unaltered peripheral chemoreceptor mechanism. In the pre-seizure condition, hypoxia caused an initial excitation of the phrenic and hypoglossal outputs followed by some decline of the effect. During seizures, the striking effect of hypoxia was a decrease of the respiratory rate. A biphasic response to hypoxia was maintained in the hypoglossal activity due to stimulation of the hypoglossal amplitude. In contrast, in the phrenic activity the excitatory phase of hypoxia was absent and depression ensued. The mechanism underlying the facilitation of hypoxic respiratory depression during seizures is discussed.
This study investigated the effects of systemic alcohol injections on respiratory activity and short-term potentiation (STP) of the phrenic nerve and hypoglossal nerve activities, evoked by electrical stimulation of the superior laryngeal nerve (SLN), in anesthetized, paralyzed, and artificially ventilated rabbits. Alcohol, in a dose of 500 mg/kg, given singly or in cumulative fractions of 100mg/kg, depressed hypoglossal activity with little or no effect on phrenic activity. SLN stimulation inhibited both phrenic and hypoglossal activities and this effect remained unchanged by either way of alcohol administration. After cessation of stimulation, hypoglossal activity increased above the control level and slowly declined to the baseline, showing signs of STP. The amplitude and duration of the hypoglossal STP decreased following a single dose of alcohol. Cumulative fractions of the alcohol dose evoked a biphasic effect on the respiratory STP. In a lower range, alcohol enhanced the hypoglossal STP and tended to increase the duration of the phrenic STP. This effect gradually declined with increasing cumulative dose of alcohol and finally reversed to the inhibition of the STP of both nerves. The results demonstrate a dose-dependent biphasic effect of alcohol on the induction and maintaining of the hypoglossal STP. A reduction in STP, together with hypoglossal activity depression following alcohol accumulation, may contribute to the facilitation of upper airway obstruction by alcohol.
In three human foetuses aged 15, 17, and 23 weeks the number of axons surrounded by single Schwann cells was counted. These Schwann cell/axon complexes form the Schwann units. The largest Schwann units in the foetus aged 15 weeks contained 232 axons, in the foetus of 17 weeks the number was 140 and in the foetus of 23 weeks the largest units contained 65 axons.
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Short-term depression of inspiratory activity following tonic vagal stimulation

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This study tested the role of inhibitory neurotransmission in the glutaminergic control of short-term depression (STD) of the inspiratory activity initiated by sustained stimulation of the vagus nerve in anesthetized and vagotomized cats. STD, calculated from the integrated phrenic nerve signal, lasted longer when glutaminergic neurotransmission was inhibited by ketamine, a NMDA receptor antagonist. Application of picrotoxin, a GABAA receptor antagonist, reversed the effect of ketamine and shortened the STD duration below that present in the control condition. The results showed that alternation of the neural excitability by antagonists of excitatory and inhibitory neurotransmission modulates the STD of inspiratory activity, evoked by vagal stimulation. The STD depends on the state of neural excitability and is easier accomplished when the excitability is on the high side.
The NADPH-diaphorase (as a neuronal NO-synthase) reactivity in the medullary structures of the respiratory rhythm (RR) generator and the role of NO in the regulation of respiratory activity in the phrenic nerve of artificially superfused semi-isolated medulla-spinal cord preparations were investigated in newborn rats. NADPH-diaphorase positive neurons were found in all nuclei of both dorsal and ventral respiratory groups of neurons. The maximal density of stained cells was present within the rostral part of the ventrolateral medulla (VLM), in the region of the lateral paragigantocellular reticular nucleus. It was found that endogenous NO mediates the mechanism of tonic inhibitory control of the RR frequency located in the rostral VLM under normal and hypoxic conditions, and appears to be involved in generation of the basic RR by the more caudal structures of VLM. It was shown that NO biosynthesis mediates the effect of NMDA receptors activation on the RR.
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