Biomedical subjects

M Fallert

Publications and source records attributed to M Fallert.

At least 37 records · Page 2Linked to original sources

PubMed1976

Metabolic control of respiratory neuronal activity and the accompanying changey-expiratory neurons.

Expiratory-related neurons have been classified according to their phase relation within the respiratory cycle, their response to lung distension and collapse (alpha- and beta-type), and to hyperventilation (tonic firing denoted by "+", cessation of activity by "-"). The dorsal surface of the medulla oblongata was superfused with a metabolite-containing CSF solution and the activity of expiratory (E) and inspiratory-expiratory (IE) neurons was extracellulary recorded. The neuronal sub-types established by their functional behaviour could equally be distinguished by their differential response to one or several metabolites. In contrast to inspiratory (I) neurons, Ealpha- Ebeta-, Ebeta- and IEbeta- neurons are inhibited by 3.5 mM AMP, but are activated by 10 mM citrate (with the exception of Ebeta+ units). Furthermore I cells are activated by ATP, while Ealpha and Ebeta units become inhibited. Vagotomy in some instances affected the response of some IEbeta units. An increase in spike density of IEbeta+ and Ealpha- cells is paralleled by a reduction of both the respiratory rate and the tidal volume, while a lower spike density in IEbeta+, IEbeta- and Ealpha- units is accompanied by increases in respiratory rate and tidal volume. In the case of Ebeta+ and Ebeta- cells lower activity is associated with an increased tidal volume. No metabolite-induced changes could be obtained with cardiovascular or unspecific reticular neurons.

Adenosine Monophosphate↗

PubMed1976

Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit. III. Phase shifts in respiratory neurons induced by inflation and collapse of the lung, hyperventilation, or metabolic modifiers.

Phase shifts between inspiratory-related and expiratory-related discharge patterns can be reversibly induced in respiratory neurons following volume changes of the lung, hypocapnic apnea as a result of hyperventilation, or superfusion with certain metabolic modifiers. Phase-spanning expiratory-inspiratory or inspiratory-expiratory discharges are frequently induced in those neurons which are activated either by pulmonary stretch receptors or collapse afferents. The same is true for regulatory effectors which activate key steps of the neuronal metabolism such as ADP, 3-phosphoglycerate, L-glutamine, fructose-6-phosphate and fructose-1,6-diphosphate. In contrast, inhibitory vagal inputs or superfusion with citrate, an inhibitory metabolic modifier, revert preexisting expiratory-inspiratory discharges into a phase-coupled inspiratory pattern. It is postulated that the respiratory neuronal networks represents a time-optimal control system which strives to adjust to a new equilibrium value in a minimum of time, following a given mechanical or chemical perturbation. Following the hypothesis advanced by Cohen (1974) that the phase-spanning units modulate the activity of the in-phase neurons, it is suggested that the additional recruitment of expiratory-inspiratory and inspiratory-expiratory units provides a measure of the quality of time-optimal control and hence a performance index of the system.

Animals↗

PubMed1976

The bulbar respiratory centre in the rabbit. I. Changes of respiratory parameters caused by intermittent electrical bulbar stimulation during inspiration or expiration.

In anesthetized rabbits, spirogram and diaphragmatic activity were examined during electrical stimulation of regions of the medulla oblongata. The stimulating volleys were triggered by the phase transitions of the animal's own respiration. 1. Each early inspiratory volley of 120 ms duration at 100 pulses per second caused an immediate and transient inhibition of the diaphragmatic activity. Respiration was slowed down due to prolongation of inspiration. The tidal volume increased above control. Stimuli delivered after 30-40% of a control inspiration had elapsed cut short this phase and entailed a shortening of the following expiration, too. Respiration was thus accelerated. 2. Each early expiratory volley caused an inspiratory twitch after a short latency. The respiratory rate was slightly increased due to shortening of expiration. The spirogram exhibited a distinct inspiratory effect (elevation of the end-inspiratory and end-expiratory levels). Stimuli delivered after 60--70% of a control expiration had elapsed slowed down respiration due to prolongation of inspiration but did not alter the end-expiratory level. The expiration remained almost unaltered. The effects were still observed while an artificial state of lung distension or collapse was maintained. 3. Volleys of increasing duration were delivered, starting with onset of expiration. The initial respiratory acceleration (shortening of both phases) and elevation of the end-expiratory level, observed when short volleys were applied, changed into slowing down of respiration (prolongation of both phases) and a shift of the end-expiratory level towards active expirations when the duration of the volley was somewhat longer than a normal expiration. The end-inspiratory level remained slightly elevated. Results suggest that during inspiration a progressively increasing inhibitory state is built up. During expiration, both an increasing inspiratory and an expiratory tendency are present as revealed by mixed inexpiratory stimulation effects.

Animals↗

PubMed1976

The bulbar respiratory centre in the rabbit. II. Responses of respiratory neurons to intermittent electrical bulbar stimulation during in- or expiration.

In anesthetized rabbits, spirogram and diaphragmatic activity were examined during electrical stimulation of the bulbar lateral reticular formation. The activity of bulbar respiratory neurons was recorded contra- or ipsilaterally to the stimulation site. One volley of repetitive stimuli per breath was delivered during either inspiration of expiration. 1. Each volley of about 120 ms duration at 100 pulses per second, delivered early in inspiration, caused an immediate and transient inhibition of the diaphragmatic activity. An inspiratory rebound comprising lengthening of inspiration and increase in tidal volume occurred. a) "Inspiratory" and "expiratory-inspiratory" phase-spanning neurons exhibited inhibition during the volley. The burst discharge was lengthened and the spike density increased after stimulus. The same was true of some "inspiratory-expiratory" phase-spanning units. b) The discharge of most of the "inspiratory-expiratory neurons was not inhibited. "Expiratory" units were excited. In both types of cells activation occurred which outlasted the volley. 2. When applied during expiration, the volley caused a short inspiratory twitch. a) "Inspiratory" and "expiratory-inspiratory" neurons exhibited a short post-stimulus firing and the spike density was increased. In some units of the latter type, however, the burst discharge was shortened. b) Most of the "expiratory" and "inspiratory-expiratory" neurons were not inhibited by the volley. Cells of the former type often produced post-stimulus after-discharge; the burst discharge of units belonging to the latter type was shortened. The effects of expiratory stimuli upon neuronal activity, however, were less consistent than those elicited by inspiratory volleys. 3. During spontaneous irregularities of single inspirations (short interruptions), EI and I neurons exhibited comparable burst pattern changes. The changes in pattern of IE and E units were also comparable and differed distinctly from the behaviour of the EI and I cells. No major differences in behaviour were observed between neurons which were inhibited during lung inflation (alpha units) and those which were activated during inflation (beta cells). The findings are in accord with the effects observed during electrical bulbar stimulation, suggesting that EI and I units are inspiratory-activating cells, whereas IE and E neurons may have an inspiratory-inhibitory function. 4. The conclusion is drawn that the effects of bulbar stimulation on the respiratory movements are the result of manipulation on intrinsic rhythmogenesis.

Animals↗

PubMed1976

A window amplitude discriminator with adjustable upper and lower thresholds.

An amplitude window discriminator is described which permits selection of spikes from a multi-unit recording, provided the signal-to-noise ratio is high enough. The device can be built at relatively low cost and time. The circuitry permits analysis of the positive or the negative deflections of the recorded signals. In Part One of the circuitry, the signals are pre-amplified and may be inverted in polarity. In Part Two, the pulses are compared to a variable lower threshold voltage, and low amplitude noise is eliminated. Part Three depicts a logic circuit for elimination of disturbing high-amplitude signals, whose output delivers digital pulses, each corresponding to an original signal (e.g. a neuronal spike) of a certain amplitude.

Amplifiers, Electronic↗

PubMed1975

Inspiratory inhibition and rebound activation elicited by intermittent electrical bulbar stimulation in various states of pulmonary afferent vagal excitation.

In anesthetized rabbits spirogram and diaphragmatic activity were examined during electrical stimulation of regions of the medulla oblongata. The volleys were triggered by the animal's own respiration. 1. One volley of 120 msec duration at 100 pulses p.s., applied during inspiratory, caused an immediate and transient inhibition of the diaphragmatic activity. After the end of the volley and inspiratory rebound appeared: the tidal volume was increased and the inspiration was prolonged by some 150 msec. The respiratory rate decreased. 2. Continuous low or high frequency electrical stimulation of pulmonary stretch afferents caused an inspiratory or an expiratory effect respectively. In both conditions the effects of additional intermittent bulbar stimulation remained essentially unaltered. 3. By means of specially designed spirometer both pulmonary collapse and marked lung distension were produced. At low lung volume collapse afferents were excited. Inspiratory inhibition and rebound activation upon central stimulation persisted throughout the whole range of lung volume investigated; the rebound increase in tidal volume consecutive to the stimulus volley, however, was minimal in extreme lung distension. 4. Results suggest that the stimulation effects were the consequence of manipulation on intrinsic mechansims of the bulbar respiratory centre.

Animals↗

PubMed1975

A device to trigger automatically electrical stimulation at different states of in- or expiration on the background of variable lung inflation in the rabbit.

A device is described which permits to obtain a signal at the beginning of in- or expiration respectively. This signal may be used to trigger an electrical stimulator. To permit studies at different states of lung inflation the tracheal cannula is connected to a spirometer circuit. To produce constant positive or negative air pressure this bellows-type spirometer is loaded with exchangeable metal weights. The tracheal pressure is recorded by means of a pressure transducer, the output of which is taken as signal. The device allows accurate compensation of the DC-component of the transducer output resulting from spirometer operation at a maintained positive or negative pressure.

Animals↗

PubMed1974