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J Duffin

Publications and source records attributed to J Duffin.

At least 91 records · Page 5Linked to original sources
PubMed1992

Projections to Bötzinger expiratory neurons by dorsal and ventral respiratory group neurons.

Bötzinger complex (BOT) augmenting expiratory neuron efferent connection are well established, but little is known concerning the afferent neural projections to BOT. The dorsal (DRG) and ventral (VRG) respiratory groups were extensively searched in 17 pentobarbital anaesthetized cats for inspiratory neurons that were anti-dromically activated from BOT. Only 1 of the 60 VRG inspiratory neurons with confirmed spinal projection was antidromically activated from BOT. Another 3 VRG inspiratory neurons and 4 of the 30 DRG inspiratory neurons were activated from BOT, but none of these neurons had confirmed spinal cord projections. All 15 early burst neurons were antidromically activated from BOT. Neural projections to BOT from DRG and VRG inspiratory neurons are rare, but neural projections from early burst neurons are common.

Afferent Pathways↗
PubMed1991

Paucity of dorsal inspiratory neuron collateral projections to ventral inspiratory neurons.

The inspiratory region of the ventral respiratory group was mapped in six Nembutal anaesthetized cats. Records multi-unit activity were taken in five or six locations at 0.5 mm spacings. These locations were then used as stimulating sites to test for the antidromic activation of 40 bulbospinal, inspiratory neurons recorded in the ipsilateral, dorsal respiratory group. Only four (10%) were antidromically activated. In a single anatomical experiment, rhodamine labelled microspheres were injected into the ventral group, and Flurogold was injected into the contralateral spinal cord. No neurons in the dorsal group were found to be double-stained. It was concluded that, ipsilateral collaterals from inspiratory dorsal group neurons to the inspiratory region of the ventral group are rare.

Animals↗
PubMed1991

A model of respiratory rhythm generation.

A new hypothesis is proposed to explain the generation of respiratory rhythm by the respiratory neurons of the medulla. The basis of the oscillator is a mutual inhibition between early-burst inspiratory, propriobulbar neurons and Bötzinger complex expiratory, bulbospinal neurons, with only the early burst inspiratory neurons possessing adaptive properties. Only one theoretical connection, unsupported by experimental observations, needs to be assumed for this model, that of an inhibitory connection from Bötzinger complex expiratory neurons to early-burst inspiratory neurons. A mathematical simulation of the model was used to test the hypothesis. The oscillating patterns of activity produced by the model were similar to those observed experimentally in these neurons. It is therefore concluded that, based on reasonable assumptions, the proposed hypothesis will produce oscillations similar to those of respiration.

Animals↗
PubMed1990

The chemoreflex control of breathing and its measurement.

The chemoreflex control of breathing is described in terms of a graphical model. The central chemoreflex, the ventilatory response to carbon dioxide mediated by the central chemoreceptors, is modelled as a straight-line relation between the ventilatory response and the arterial level of carbon dioxide. The peripheral chemoreflex, the ventilatory response to carbon dioxide and hypoxia mediated by the peripheral chemoreceptors, is broken into two relations. First, a straight-line relation between the ventilatory response and the arterial level of carbon dioxide whose slope (sensitivity) increases as the oxygen level varies from hyperoxic to hypoxic. Second, a rectangular hyperbolic relation between the ventilatory response and the arterial level of oxygen with ventilation increasing with increasing hypoxia. The three ventilatory response relations (one central and two peripheral) add to produce the total chemoreflex ventilatory response which forms the feedback part of the respiratory regulator. The forward part consists of the relation between the arterial level of carbon dioxide and ventilation when ventilation is controlled (the metabolic hyperbola). The forward and feedback parts of the respiratory regulator can be combined so as to predict resting ventilation and carbon dioxide levels under a number of circumstances. Methods of measurement of these chemoreflex ventilatory responses are also described so as to illustrate the physiological principles involved in the model.

Carbon Dioxide↗
PubMed1989

The effect of metabolic acid-base changes on the ventilatory changes at the end of heavy exercise.

The purpose of this study was to determine the effect of altered metabolic acid-base status on the changes in ventilation in the transition from heavy exercise above anaerobic threshold to rest. Seven subjects ingested, in a randomized and blind manner, either NaHCO3 or CaCO3 (placebo) at a dose of 300 mg.kg-1 body mass and ran on a treadmill for five minutes (90% VO2max and above anaerobic threshold) on ten different occasions. Changes in minute ventilation in the exercise transitions were studied by starting and stopping the treadmill abruptly with a remote switch. The fast increase in ventilation at the start of exercise was not accompanied by a corresponding fast drop in ventilation at the end of exercise (P less than or equal to 0.001) and the effects of chemicals on these changes were not significantly different (P greater than 0.05). A single-component exponential model, without a time delay, was used to determine the time constants of off-transitional decay in ventilation for the two chemicals in each subject. Parametric and non-parametric statistical tests revealed that the time constants were not as significantly different as the venous pH measurements which were significantly higher with NaHCO3 (P less than or equal to 0.001). The results indicate that the absence of fast change in ventilation at the end of heavy exercise is not due to lactic acidosis and the consequent slow ventilatory changes in the off-transition of heavy exercise are at least partly mediated by non-humoral factors such as a central neural reverberatory mechanism.

Acid-Base Equilibrium↗
PubMed1989

Changes in ventilation at the end of heavy exercise of different durations.

The purpose of this study was to examine the effects of duration and the concomitant ventilatory drift of heavy exercise on the changes in ventilation following the cessation of exercise. Seven male subjects ran on a motor-driven treadmill at a constant work-rate of 90% of VO2max for either 5 min or 7 min on 60 occasions. The exercise was terminated abruptly by stopping the treadmill with a remote switch while recording inspired minute ventilation (VI) breath by breath. The fast drop in VI at the end of exercise is significantly less than the corresponding increase at the onset of exercise (P less than 0.05) and this difference is greater with longer duration of exercise. The time constants of the slow ventilatory decline are significantly increased following 7 min of exercise (P less than 0.05). They are also positively related to the drift in VI that occurs with the continuation of heavy exercise beyond 3 min. This relationship is however not statistically significant (P greater than 0.05). These results indicate that the rate of ventilatory decline is slower after the end of a longer duration of exercise and this is caused by mechanism/s that also contribute/s to the ventilatory drift of heavy exercise. As, of the many different possibilities, only the respiratory after-discharge (central neural reverberatory) mechanism is likely to be more activated with a longer duration of exercise and on the basis of our previous observations (Jeyaranjan et al. 1988, 1989), the results suggest that the mechanism of after-discharge is an important mediator of ventilatory response during as well as after the cessation of heavy exercise.

Adult↗
PubMed1989

Projections from inspiratory neurons of the nucleus retroambigualis to phrenic motoneurons in the cat.

The connection between the inspiratory neurons of the nucleus retroambigualis and the phrenic motoneurons was examined using the techniques of antidromic mapping to discover collaterals and spike-triggered averaging to detect postsynaptic potentials. Axon collaterals within the region of the C5 phrenic nucleus were found for 17 of 26 (65%) inspiratory neurons and 6 of these 17 (35%) were shown to generate excitatory postsynaptic potentials in at least one phrenic motoneuron. It was concluded that these results demonstrate a strong connection for those inspiratory neurons of the nucleus retroambigualis with a collateral within the phrenic nucleus.

Animals↗
PubMed1989

Inhibition of inspiratory neurons of the nucleus retroambigualis by expiratory neurons of the Botzinger complex in the cat.

The connection between expiratory neurons of the Botzinger Complex and contralateral inspiratory neurons of the nucleus retroambigualis was examined using the technique of spike-triggered averaging of intracellular potentials. Out of a total of 34 expiratory neurons found in the Botzinger Complex, 25 (73%) could be antidromically activated from the inspiratory region of the contralateral nucleus retroambigualis. The spike activities of 15 of these antidromically activated expiratory neurons were used as triggers for the averaging of the intracellular potentials recorded from 39 inspiratory neurons in the region of the contralateral nucleus retroambigualis. Unitary, inhibitory, postsynaptic potentials were observed in 11 of the 39 (28%) averages, from 6 of the 15 (40%) trigger neurons. It was concluded that these experiments demonstrate a monosynaptic inhibitory connection from expiratory neurons in the Botzinger Complex to inspiratory neurons in the contralateral nucleus retroambigualis.

Action Potentials↗
PubMed1989

The connections from botzinger expiratory neurons to upper cervical inspiratory neurons in the cat.

These experiments examined possible inhibitory inputs to upper cervical inspiratory neurons from the expiratory neurons of the Botzinger complex. Eighty-one Botzinger neurons were tested with antidromic mapping for a projection to the C1 segment of the spinal cord; 44/81 (54%) were found to project, 27/79 (34%) contralaterally, 17/68 (25%) ipsilaterally, and 1/66 (2%) both contralaterally and ipsilaterally. Antidromic mapping in contralateral C1 demonstrated the presence of a collateral in 3/15 (20%) of the Botzinger neurons tested, while 3/9 (33%) had collateral arborizations in ipsilateral C1. The collaterals mapped were not localized to the region of the upper cervical inspiratory neurons. Microstimulation in C3 (12-17 microA, 0.2-ms duration) at locations which produced short-latency (2.7-3.5 ms) inhibition of phrenic nerve discharge resulted in the short latency (3.0 ms) inhibition of 1/27 (3.7%) upper cervical inspiratory neurons as demonstrated by cross-correlation. It was concluded that while some upper cervical inspiratory neurons may be inhibited during expiration by the Botzinger expiratory neurons, this connection is not a strong one.

Animals↗
PubMed1989

Role of lactic acidosis in the ventilatory response to heavy exercise.

The purpose of this study was to determine the role of lactic acidosis in the ventilatory response to heavy exercise above anaerobic threshold. Seven subjects ingested either NaHCO3 or CaCO3 at a dose of 300 mg/kg body weight and ran on a motor-driven treadmill at a work load corresponding to 90% of VO2max and above anaerobic threshold for a period of 5 min while minute ventilation and PETCO2 were recorded breath by breath. A total of 10 runs, 5 with CaCO3 and 5 with NaHCO3 in a randomized and blind order, were done in each subject. Statistical analyses of the effects of the chemicals on minute ventilation during the 15 s between min 4.75 and 5 of exercise showed that the differences in ventilation did not reach statistical significance (p greater than 0.05) in 5 of the 7 subjects. Venous pH measurements at the end of exercise revealed a significant increase with NaHCO3 (p much less than 0.05). It is concluded that lactic acidosis is not an essential determinant of ventilatory response to heavy exercise above anaerobic threshold in the majority of the subjects.

Acidosis, Lactic↗
PubMed1988

Changes in respiration in the transition from heavy exercise to rest.

Transitions from rest to exercise and vice versa are reported to be associated with instantaneous changes in minute ventilation and the changes in the off-transitions are thought to be the reverses of those in the on-transitions. Such changes have been observed mainly in mild-moderate exercise and their extrapolation to heavy exercise above anaerobic threshold is unwarranted. Hence, the purpose of this study was to determine the changes in ventilation in the transition from heavy exercise above anaerobic threshold to rest. Five healthy volunteers ran on a motor-driven treadmill at a constant work-load corresponding to 80% VO2max and above anaerobic threshold. Changes in minute ventilation and end-tidal PCO2 in the on- and off-transitions were determined breath by breath by starting and stopping the treadmill abruptly. The results indicate that, contrary to what is reported for mild-moderate exercise, an instantaneous drop in ventilation is absent in the off-transition of heavy exercise above anaerobic threshold. The gradual decline in minute ventilation may be due to a sustained respiratory drive from a central neural reverberatory mechanism, blood-borne respiratory stimuli and/or a peripheral neurogenic drive originating in the so-called metaboloreceptors.

Adult↗
PubMed1988

Projections from upper cervical inspiratory neurons to thoracic and lumbar expiratory motor nuclei in the cat.

Previous studies have demonstrated the existence of axonal projections from propriospinal respiratory neurons in the rostral cervical cord of the cat (upper cervical inspiratory neurons) to the vicinity of the phrenic and rostral thoracic inspiratory (external) intercostal motoneurons. However, no synaptic targets of the upper cervical inspiratory neurons have been identified. This study investigated the axonal projections to the caudal thoracic and upper lumbar cord and the possible existence of inhibitory connections to the expiratory intercostal and abdominal motoneurons. The connections from upper cervical inspiratory neurons to expiratory motoneurons in the lower thoracic cord were examined using the methods of antidromic mapping and the spike-triggered averaging of intracellular potentials. Of the 70 upper cervical inspiratory neurons examined, only four (5.7%) could not be antidromically activated from the T9 segment of the spinal cord. The axons of 66 upper cervical inspiratory antidromic activation at less than 5 microV, and the presence of collaterals was confirmed by antidromic mapping in 30 cases (49.2%). Of 21 axons tested for lumbar projections, 13 (61.9%) projected as far as T12, seven (33.3%) as far as L1, three (14.3%) as far as L2, and one (4.8%) was antidromically activated from L3. Spike-triggered averaging of the synaptic potentials recorded intracellularly from expiratory intercostal motoneurons in T9 and T10 spinal segments was done for 27 upper cervical inspiratory neurons, 17 of these with 4 or more motoneurons, for a total of 111 expiratory motoneurons. In 16 cases the motoneurons were injected with Cl- to reverse IPSPs and the spike-triggered averaging was repeated. No monosynaptic or disynaptic post-synaptic potentials were seen in any of the spike-triggered averages. We concluded that the upper cervical inspiratory neurons may provide inspiratory inhibition to expiratory motoneurons via a di- or oligosynaptic pathway involving segmental inhibitory interneurons and that either the spike-triggered averaging technique was not sensitive enough to detect the ipsilateral connections or the interneuron pathway was to the contralateral side of the spinal cord.

Animals↗
PubMed1988

The peripheral-chemoreceptor threshold to carbon dioxide in man.

1. The threshold of the ventilatory response to carbon dioxide mediated by the peripheral chemoreceptors was determined under mild hypoxic conditions during both rest and exercise in eight volunteers. 2. The method used was an adaptation of the Read rebreathing technique, modified for hypoxia and with prior hyperventilation. The method produced values of ventilation and carbon dioxide which, when plotted against each other, exhibited three straight-line segments of differing slopes. The break-points were interpreted as the resting peripheral- and central-chemoreceptor thresholds. 3. Similar plots of exercise ventilation and carbon dioxide were used to determine the peripheral-chemoreceptor threshold during exercise. However, the points for these plots were obtained from a number of separate rebreathing experiments in such a way as to avoid the divergence between the carbon dioxide levels as measured at the mouth and those at the site of the central chemoreceptors, which would normally occur during rebreathing in exercise. 4. During the course of rebreathing experiments similar to those done at rest, mild treadmill exercise was begun abruptly. The ventilation measured at the third breath of exercise was plotted against the level of carbon dioxide at which the exercise started. In this way, each such rebreathing experiment provided a single point for the plot of ventilation against carbon dioxide in exercise. 5. The results showed that the threshold of the ventilatory response to carbon dioxide mediated by the peripheral chemoreceptors was approximately 39 mmHg (5.2 kPa) while that for the central chemoreceptors was approximately 45 mmHg (6.0 kPa). Neither the peripheral-chemoreceptor threshold, nor the peripheral-chemoreceptor sensitivity to carbon dioxide was changed at the start of exercise.

Adult↗