Biomedical subjects

Walter M St -John

Publications and source records attributed to Walter M St -John.

5 recordsLinked to original sources

PubMed2004

Phrenic, vagal and hypoglossal activities in rat: pre-inspiratory, inspiratory, expiratory components.

During eupnea in an in situ perfused preparation of the rat, inspiratory activities of the hypoglossal and vagal nerves commence before the phrenic; the vagus also discharges in expiration. The hypoglossal discharge has a prominent "pre-inspiratory" component. Power spectral analysis indicated that peak frequencies of oscillations in phrenic, hypoglossal and vagal inspiratory and expiratory activities were the same during eupnea. "Pre-inspiratory" hypoglossal activity had significantly lower peak frequencies. In gasping, "pre-inspiratory" hypoglossal activity ceased and all neural activities became purely inspiratory. High frequency oscillations of phrenic and vagal activities during gasping were shifted upward, compared to those in eupnea, whereas that of the hypoglossal was unaltered. In gasping, the temporal patterns of activities of the phrenic, hypoglossal and vagal nerves, and the level of coherence between these activities implies a restricted and shared set of pre-motor neurons. During eupnea, the activity patterns in the phrenic, hypoglossal and vagal nerves seem to originate from different sets of pre-motor neurons.

Action Potentials↗

PubMed2003

Defining eupnea.

To describe a pattern of rhythmic activity as "breathing" or "respiration" inevitably leads to the conclusion that this rhythmic activity is "normal" or "eupneic". Initially, it must be noted that, by strictest definition, "eupnea" can only be applied to "breathing" in an unanesthetized preparation. Any experimental perturbation, including anesthesia, changes eupnea, primarily by reducing the frequency of "breathing". However, a "eupneic pattern", in terms of the pattern of airflow of individual breaths, remains. Also remaining are patterns of neural and neuronal activities which are characteristic of individual breaths of eupnea. In this commentary, we consider these patterns of activities, which define a eupneic pattern and contrast these with patterns during apneusis and gasping. It has long been recognized that these three different patterns of "respiratory activity", eupnea, apneusis and gasping, can be generated in preparations in which all of the central nervous system has been removed, exclusive of the brainstem and spinal cord.

Animals↗

PubMed2003

Tonic pulmonary stretch receptor feedback modulates both eupnea and gasping in an in situ rat preparation.

The perfused in situ juvenile rat preparation produces phrenic discharge patterns comparable to eupnea and gasping in vivo. These ventilatory patterns of eupnea and gasping differ in multiple aspects, including most prominently the rate of rise of inspiratory activity. Because gasping, but not eupnea, appeared similar after vagotomy in spontaneous breathing preparations, it has been assumed that gasping was unresponsive to afferent stimuli from pulmonary stretch receptors. In the present study, efferent activity of the phrenic nerve was recorded during eupnea and gasping in the in situ juvenile rat preparation. Gasping was induced in hypoxic-hypercapnia or ischemia. An increase in the pressure of tonic lung inflation from 1 to 10 cmH2O caused a prolongation of the duration between phrenic bursts in both eupnea or gasping. Bilateral vagotomy eliminated these changes. We conclude that the neural substrate mediating the Hering-Breuer reflex is retained in the in situ preparation and that the brain stem circuitry generating the respiratory patterns responds to tonic activation of pulmonary stretch receptors in a similar manner in eupnea and gasping. These findings support the homology of eupnea-like phrenic discharge patterns in the reduced in situ preparation and eupnea in vivo and disprove the common supposition that gasping is insensitive to vagal afferent feedback from pulmonary stretch receptor mechanisms.

Adaptation, Physiological↗

PubMed2002

Influence of levels of carbon dioxide and oxygen upon gasping in perfused rat preparation.

In vivo, the augmenting pattern of integrated phrenic nerve discharge of eupnea is altered to the decrementing pattern of gasping in severe hypoxia or ischaemia. Identical alterations in phrenic discharge are found in perfused in situ preparations of the juvenile rat. In this preparation, gasping was produced by equilibration of the perfusate with various levels of carbon dioxide and oxygen. The duration of the phrenic burst, the interval between bursts and the burst amplitude were not significantly different following equilibration with 21-6%O(2) at 5% CO(2) or with 0-9% CO(2) at 6% O(2), with the exception that the burst amplitude was significantly greater in hypercapnic-hypoxia (9% CO(2) at 6% O(2)). It is proposed that hypoxia-induced gasping results from the release of an endogenous pacemaker activity of rostral medullary neurons. This release is caused by cellular mechanisms that change the balance between membrane ionic currents. Moreover, these cellular mechanisms may be explicitly induced by alterations in the ionic and metabolic homeostasis.

Animals↗

PubMed2002

Potential switch from eupnea to fictive gasping after blockade of glycine transmission and potassium channels.

This study evaluated possible neuronal mechanisms responsible for the transition from normal breathing (eupnea) to gasping. We hypothesized that a blockade of both inhibitory glycinergic synaptic transmission and potassium channels, combined with an increase in extracellular concentration of potassium, would induce a switch from an eupneic respiratory pattern to gasping. Efferent activities of the phrenic, vagal, and hypoglossal nerves were recorded during eupnea and ischemia-induced gasping in a perfused in situ preparation of the juvenile rat (4-6 wk of age). To block potassium channels, 4-aminopyridine (4-AP, 1-10 microM) was administered. Strychnine (0.2-0.6 microM) was used to block glycinergic neurotransmission. After administrations of 4-AP, excess extracellular potassium (10.25-17.25 mM), and strychnine, the incrementing pattern of eupneic phrenic activity was altered to a decrementing discharge. Hypoglossal and vagal activities became concentrated to the period of the phrenic burst with expiratory activity being reduced or eliminated. These changes in neural activities were similar to those in ischemia-induced gasping. Results are consistent with the concept that the elicitation of gasping represents a switch from a network-based rhythmogenesis for eupnea to a pacemaker-driven mechanism.

4-Aminopyridine↗