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Biomedical subjects

Y Jammes

Publications and source records attributed to Y Jammes.

At least 91 records · Page 5Linked to original sources

Changes in respiratory muscle activity in conscious cats during experimental dives at 101 ATA.

The rationale for the present study was to test the hypothesis that increased work of breathing during experimental deep diving may lead to respiratory muscle fatigue. For this purpose, electromyograms (EMGs) of respiratory and skeletal muscles, plus electrocardiogram and electroencephalogram (EEG) derivatives, were continuously recorded in conscious cats. In each muscle group, the ratio of power in a high (H) to that in a low (L) band of EMG frequencies was computed. Direct diaphragmatic stimulation in selected animals produced a mass action potential to obtain the muscle fiber conduction velocity (MFCV). The maximal pressure was 101 ATA (1,000 msw) with a maximal duration of 72 h. Four cats breathed an He-O2 mixture and five others a ternary mixture (10% N2 in He-O2). Inspired O2 partial pressure was 350 Torr. With the He-O2 mixture, all the animals died within 2-54 h during the study at maximal depth. EEG signs of high-pressure nervous syndrome (HPNS) were present in all cats, and low-frequency (11-14 Hz) hyperbaric tremor discontinuously contaminated all EMG tracings. The H/L ratio computed from diaphragmatic and intercostal muscle EMGs increased after 12 h at 101 ATA. With the He-N2-O2 mixture, the cats survived until the end of the sojourn at 101 ATA, during which no hyperbaric tremor was detected from EMG tracings, and EEG signs of HPNS were weak or absent. From 31 ATA, the H/L ratio decreased significantly in respiratory but not in skeletal muscles; this was associated with decreased MFCV in the diaphragm after several hours at maximal depth.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Changes in afferent and efferent phrenic activities with electrically induced diaphragmatic fatigue.

In anesthetized artificially ventilated cats, diaphragmatic fatigue was produced by direct muscle stimulation with trains of pulses for 30 min. Failure of contraction was assessed from decrease in the maximal relaxation rate of transdiaphragmatic pressure twitches. Motor activities (electromyogram and motor phrenic neurogram) were processed by fast-Fourier transform analysis, which provided the power spectrum density function (PSDF). The discharge frequency of diaphragmatic afferents was also measured. In control conditions (before fatigue), intra-arterial bolus injection of lactic acid enhanced tonically active diaphragmatic afferents, whereas it reduced the firing rate of afferent fibers activated in phase with diaphragmatic contraction or relaxation. The same sensory response pattern was observed with the development of diaphragmatic fatigue. Leftward shift in PSDFs of motor phrenic neurogram also occurred, but it preceded the failure of diaphragmatic contraction as well as the changes in the electromyogram's PSDF and afferent paths, which were closely associated with lengthening of both inspiratory and total breath durations. After section of the phrenic nerves, the motor phrenic response disappeared during the fatigue trial. This demonstrates the existence of complex reflex-induced changes in the ventilatory control during diaphragmatic fatigue. They seem to involve the participation of several types of phrenic afferents.

Action Potentials↗

T wave changes in humans and dogs during experimental dives.

Electrocardiogram (ECG) analysis was performed in three human divers studied at 21 and 23.5 ATA while they breathed various gas mixtures containing H2 and/or He (COMEX HYDRA IX experiment) and in five dogs exposed to 91 ATA of He-O2 or He-N2-O2. In all cases, the O2 partial pressure was slightly higher than its physiological value. These human and animal studies reveal that elevated pressure of different inert gases did not change the resting heart rate or its respiratory fluctuation. However, the T wave amplitude increased in proportion to the gas density in the three divers; this was also found in four of the five dogs studied. Changes in peak T wave configurations were also observed in the dog experiments. Positional changes in QRS or T vectors cannot explain these T wave changes.

Animals↗

Diaphragmatic fatigue produced by constant or modulated electric currents.

In anesthetized rabbits the efficiency of phrenic nerve stimulation with trains of electric current was studied either when ventilation was effected entirely by bilateral nerve stimulation (electrophrenic ventilation) or during unilateral nerve stimulation when animals were ventilated with a pump and open chest. Trains of rectangular electric pulses (RPT) with constant amplitude and frequency or sine waves, both the amplitude and frequency of which were modulated and controlled by a computer (MSWT), were used with each animal. MSWT closely reproduced the physiological shape of transdiaphragmatic pressure waves. Diaphragm fatigue, as determined from the decrease in the maximal relaxation rate of twitches, occurred after 20 minutes of bilateral or unilateral nerve stimulation with RPT, but only after 60 min (unilateral stimulation) or 98 min (bilateral stimulation) with MSWT. These data show the importance of the motor signal pattern in long-lasting nerve stimulation.

Animals↗

Quantitative EEG changes under various conditions of hyperventilation in the sensorimotor cortex of the anaesthetized cat.

The effects on the EEG rhythms recorded from the sensorimotor cortex (post-sigmoid gyrus) of anaesthetized cats were studied under 4 conditions of artificial mechanical hyperventilation (HV) before and after cervical bilateral vagotomy. In animals with intact vagus nerves, using visual examination, EEG changes were only observed within the 2nd min during HV produced by increased stroke volume (delta V) with associated hypocapnia. Quantitative EEG (qEEG) showed that, for the same increase in minute ventilation and the same degree of hypocapnia, delta V induced a greater and earlier relative decrease (2nd min) in the power density of delta, theta and alpha bands, than increased pump frequency (delta F). The delta F tests produced a fall only in the theta band and within the 3rd min. With constant paCO2, transient modifications occurred only with delta V and were limited to the first 30 sec. In bivagotomized cats, moderate EEG responses to delta V plus associated hypocapnia persisted partly in the alpha band. Finally, no changes appeared with delta V or delta F when the vagus nerves were cut and paCO2 was maintained constant. The present data suggest strongly that, in anaesthetized cats, peripheral vagal afferents from the respiratory system play a major role in the EEG changes caused by artificial hyperventilation.

Animals↗

Effects of breathing dense gas mixtures on cardiovascular function and EEG rhythms.

Gas mixtures containing oxygen and nitrogen or dense inert gases (sulfur hexafluoride, SF6, or argon, Ar) were inhaled by anaesthetized, artificially ventilated rabbits and cats. SF6 and Ar were compared to nitrous oxide (N2O), a dense inert gas well known for its anaesthetic properties. Concentrations in these gases were 50% (SF6) and 60% (Ar or N2O). In cats, there was a significant increase in total lung resistance with SF6 or Ar associated with a slight but significant drop in arterial blood pressure and heart rate (-5% and -10% with SF6 and Ar, respectively), with no change in electrocardiogram activity. N2O induced in some cats a slower electroencephalographic (EEG) pattern constituted by delta waves of higher amplitude, whereas neither SF6 nor Ar changed the EEG rhythms in this species. In the rabbits, the unsteadiness of the EEG rhythms did not make it possible to assess the cortical effects observed with SF6 or N2O.

Administration, Inhalation↗

Respiratory effects of cold-gas breathing in humans under hyperbaric environment.

Changes in total lung resistance (RL) during inhalation of cold gas mixtures were measured in 4 human volunteers during an experimental dive at 46 ATA. The subjects breathed helium-nitrogen-oxygen mixtures during the decompression schedule, and measurements were performed at 46, 36, 21, 12.5, 6 and 2 ATA (1 ATA = 100 kPa). RL was measured during eupneic ventilation when individuals inhaled either ambient gas at +30 to +33 degrees C (control condition), or cooled gas at +7 to +18 degrees C. RL values measured in control conditions increased with gas density. Thus, the changes in RL induced by cold gas breathing were expressed in percent of the corresponding control values. No cold-induced bronchospasm occurred at low ambient pressure, even at the lowest inspired temperature, +7 degrees C. However, the airway response was present at pressure up to 21 ATA and then occurred at higher level of inspired gas temperature. The convective respiratory heat loss (Cr), calculated at each pressure level and experimental condition, was linearly related to cold-induced changes in RL; the value of Cr inducing 20% increase in RL was around 1.4 kcal.min-1. The bronchomotor response was related to the increase in respiratory heat loss induced by the high thermal capacity of the gas mixture used in hyperbaric environment. The present observations confirm previous data obtained under hyperbaric conditions (25 ATA) as well some experiments performed at sea level in normal individuals breathing very cold air.

Adult↗

Pulmonary vagal sensory afferents and spontaneous EEG rhythms in the cat sensorimotor cortex.

Interactions between vagal afferent fibres and spontaneous electroencephalographic (EEG) activity, recorded on the sensorimotor cortex of the cat, were studied during the mechanical activation of pulmonary afferents. The interactions were compared to the cortical effects of the electrical stimulation of all vagal fibers or to the chemical activation of unmyelinated vagal afferents (C-fibers) by phenyldiguanide. The present study was performed on anesthetized cats, artificially ventilated with open chest. Over 60 locations were explored on the posterior sigmoid gyrus. Repetitive electrical stimulation (30 Hz, 0.8 ms shock duration) of the contralateral cervical vagus nerve or of both nerves induced within less than 5 s changes in the pattern and periodicity of EEG spindles, associated with depressed background rhythms or rhythmic EEG activities. Cortical responses were also observed after i.v. injection of phenyldiguanide. Changes in activity of pulmonary stretch receptors by lung hyperinflation or suppression of phasic lung inflations ('stop pump') had no effect on the EEG rhythms. On the other hand, expiratory threshold loading or passive hyperdeflation of the lungs elicited EEG changes similar to those obtained by electrical stimulation of all vagal fibers. After bilateral vagotomy, all these responses disappeared or were delayed. The present observations strongly suggest that sensory information carried by thin vagal fibers greatly influences cortical rhythms in the cat sensorimotor cortex.

Animals↗

Electromyographic study of respiratory muscles during human diving at 46 ATA.

Electromyographic (EMG) recordings of the 6th to 7th intercostal space (thoracic EMG) and abdominal muscles, ventilatory pattern, and the work of breathing were studied in 4 human subjects exposed for 12 days to 46 ATA of helium-oxygen (density = 8.7 g.liter-1) then of nitrogen-helium-oxygen gas mixture (ternary mixture) (density = 11.1 g.liter-1). We found that the respiratory muscle work necessary for eupneic ventilation was multiplied by 4 at 46 ATA. During quiet breathing as well as during forced inspiratory maneuvers, the power spectrum of thoracic EMG shifted to the left in three individuals during the sojourn at maximal pressure, whichever gas mixture was inhaled. This was corroborated by the decreased ratio of EMG power in a high to that in a low band of frequencies. These alterations disappeared at the end of the decompression period, suggesting the existence of inspiratory muscle fatigue at high pressure. Hyperbaric tremor was recorded on the thoracic EMG and was maximal with He-O2 inhalation. It disappeared at the end of the period at 46 ATA (He-N2-O2).

Adult↗

Tonic activity in inspiratory muscles and phrenic motoneurons by stimulation of vagal afferents.

In anesthetized rabbits, direct and integrated phrenic neurogram (Ephr) and electromyograms from the diaphragm (Edi) and intercostal (Eic) (2nd space) and transversus abdominis muscles (Etr) were simultaneously recorded in two protocols. 1) In animals breathing spontaneously, we used infinite inspiratory (RI) or expiratory (RE) resistive load and intravenous injections of carbachol, histamine, or phenyl diguanide (PDG). All circumstances except RE evoked tonic activities in Ephr, Edi, and Eic but never in Etr. Intravenous atropine abolished carbachol-induced bronchoconstriction and associated tonic inspiratory activities, but this effect persisted with RI, histamine, and PDG. Selective procaine block of conduction in thin vagal fibers (with persistence of the Breuer-Hering inflation reflex) reduced or suppressed the tonic response, which was abolished in all cases after vagotomy. 2) In rabbits artificially ventilated with open chest, passive deflation of the lung or intravenous injections of histamine or PDG also produced tonic discharge in Ephr and often in Eic. The present results demonstrate that 1) stimulation of vagal afferents and mostly thin sensory fibers elicits tonic inspiratory discharges, 2) bronchoconstriction is not necessary for the induction of the response, and 3) reflexes from the chest wall do not mediate this response in rabbits.

Animals↗

Vagal afferents and EEG rhythms in the Sl area in anesthetized cats: similarities between responses to electrical and chemical (phenyldiguanide) stimulations.

In anesthetized, artificially ventilated cats with open chest, bilateral stimulation of all afferent vagal fibres (pulse duration: 800 microseconds, 30 Hz, train duration 30 to 40 s) produced marked changes in the spontaneous EEG activities in the primary somatosensory cortex (Sl area). They were characterized by depressed background rhythms, with a tendency to desynchronization, decreased amplitude and number of spindles, with altered pattern, and/or evoked sustained fast rhythmic activities. These effects occurred within 1 to 5 sec during vagal stimulation. On the contrary, the EEG response was weaker or absent when only myelinated vagal afferents were stimulated (100 microseconds). I.v. injection of phenyldiguanide (PDG), used for stimulation of unmyelinated vagal sensory fibres and mainly of pulmonary afferents, induced EEG changes within the first 30 s, similar to those observed during electrical vagal stimulation. These EEG responses were unrelated to the induced hypotension. Cervical bivagotomy produced persistent changes in EEG activity, with enhancement of the magnitude, duration and number of spindles, which resembled the delayed effects induced by PDG. The present results obtained with three test agents (electrical or chemical vagal stimulation and bivagotomy) demonstrated that, in cats, vagal afferent information interacted with the spontaneous EEG rhythms in the Sl area.

Afferent Pathways↗

[Tracheobronchial muscle tonus and its reflex control].

Airway smooth muscle tone is reinforced during the inspiratory phase of the breathing cycle and depends largely from neurogenic motor drive carried by the vagus nerve. This muscle tone seems to be produced mostly by a vago-vagal reflex loop initiated by the tonic discharge of tracheo-bronchial and/or alveolar receptors connected to thin sensory vagal fibres (non-myelinated or C-fibres). Inhibitory influences carried by large myelinated vagal fibres connected to tracheobronchial stretch receptors and also numerous afferents from the upper airways, systemic and pulmonary circulation, digestive tract and skeletal and respiratory muscles participate to the modulation of airway tone. The identification of neurotransmitters specific of the motor or sensory pathways helps to understand the peripheral modulation of airway motor drive and also the central integration of some peripheral informations.

Animals↗

The effects of electrical stimulation of myelinated and non-myelinated vagal motor fibres on airway tone in the rabbit and the cat.

The bronchomotor effects of repetitive electrical stimulation of the peripheral end of the cervical vagus nerves were studied in anaesthetized and paralysed rabbits and cats. Stimulation of either myelinated or of all motor vagal fibres was obtained by varying the duration of electrical square pulses. In rabbits, selective stimulation of myelinated vagal fibres induced a bronchoconstriction, strongly potentiated by the recruitment of non-myelinated fibres. This potentiation was absent in cats. After ganglionic blockade with hexamethonium, the vagally mediated bronchoconstriction was abolished in rabbits, while a slight and transient effect persisted in cats. Propranolol did not modify the bronchoconstrictor response to vagal stimulation, which was abolished after further injection of atropine in both species. When propranolol plus atropine was administered and airway tone was increased by continuous i.v. injection of bronchoconstrictor agonists, the stimulation of vagal motor fibres was devoid of any bronchomotor effect in rabbits. However, in cats this resulted in a strong bronchodilation, which was doubled after recruitment of non-myelinated fibres. Thus, in the latter species preganglionic vagal motor fibres participate in the non-adrenergic-non-cholinergic vagal system. Amongst them, non-myelinated fibres play an important role.

Airway Resistance↗

Interaction between SO2 and cold-induced bronchospasm in anesthetized rabbits.

In anesthetized, paralyzed and artificially ventilated rabbits, reflex changes in lung resistance induced by cooling the inspired air from 38 to 15 degrees C were studied before and after 45 min periods of SO2 exposure at two different concentrations (0.5 or 5 ppm). Both concentrations of SO2 induced significant increase in RL in intact animals (+16% and +50%, respectively). The effect of 5 ppm SO2 persisted after vagotomy. The cold-induced bronchospasm was halved after exposure to 0.5 ppm SO2 and was no longer significant after exposure to 5 ppm SO2. In both cases, RL recovered to control values 40 min after the end of SO2 exposure and then, the magnitude of cold-induced bronchospasm also recovered. The reflex bronchoconstrictor response to phenyldiguanide (PDG) i.v. disappeared after exposure to 5 ppm SO2. However, the bronchomotor response to histamine i.v., which involved both reflex and direct actions on airway smooth muscle, was not altered. These results show that (1) prolonged increase in RL measured after SO2 exposure does not result from a vagal reflex; (2) the cold-induced bronchospasm, as well as the bronchomotor response to PDG, are reduced or suppressed during the period where the effect of SO2 persisted. This suggests that 45 min exposure to SO2 induces transient alterations in tracheobronchial wall, which reduce the accessibility to nervous receptors in the airways.

Administration, Inhalation↗

In vivo and in vitro studies on cold-induced airway response in normal and sensitized rabbits.

We measured the changes in lung resistance (RL) induced by cool inspired air under dry air conditions in anesthetized, paralyzed and artificially ventilated rabbits. We compared the airway response to cold air in non-sensitized (NS) animals with the response in rabbits sensitized (S) to bovine serum albumin. Using in vitro tracheal preparations from the same animals, we observed the effects of lowering the bath temperature on smooth muscle tension and also the response to acetylcholine (Ach). Dose-response curves to Ach were constructed and analyzed in terms of maximal contraction (delta Tmax) and pD2 coefficient (negative logarithm of the molar concentration of Ach producing 50% of maximum contraction). The magnitude of cold induced airway response tested in vivo was significantly greater in S (delta RL = +52% +/- 2) than in NS rabbits (+30% +/- 4; P less than 0.01). In vitro the decrease of temperature in the bathing medium induced a significant relaxation of tracheal spirals in both NS and S preparations (delta T = -2.42 +/- 0.34 g/mg wet tissue, -3.36 +/- 0.8 g/mg wet tissue, respectively). However, an adaptation of this response occurred after 8 min in NS rabbits whereas relaxation persisted in S rabbits. The tracheal contractile response to Ach was decreased by bath cooling in S ans NS animals (delta Tmax = 5.53 +/- 0.15 g/mg wet tissue and 5.03 +/- 0.27 g/mg wet tissue at 37 degrees C; 3.05 +/- 0.30 g/mg wet tissue and 1.93 +/- 0.35 g/mg wet tissue at 17 degrees C, respectively). Moreover, cooling also reduced the velocity of response. In all cases, S preparations displayed hyperresponsiveness to Ach and this was observed for maximal changes in tension as well as for pD2 values. Present observations show that cold induces different effects on airway smooth muscle with the production of a contractile response in in vivo preparations but relaxes isolated tracheal spirals. They also suggest that sensitization by foreign proteins may modify the intrinsic properties of tracheal smooth muscle.

Acetylcholine↗

Tonic sensory pathways of the respiratory system.

Both respiratory centres and the preganglionic vagal motoneurones, which control respiratory (striated) and airway (smooth) muscles respectively, receive information on the lungs, the circulation and the skeletal and respiratory muscles. Each of these nervous pathways has two components: one is phasic, i.e. in phase with biological rhythms, and comes from mechanoreceptors connected to large myelinated fibres; the second has a tonic low frequency firing rate and corresponds to the spontaneous activity of polymodal receptors connected to thin sensory fibres, which act mostly as sensors of changes in extracellular fluid composition (O2 and/or CO2 partial pressure, pH, release of algesic agents etc...). Some of them also detect large mechanical disturbances or local temperature changes. The influence of tonic background sensory activity is well known in animals concerning the role played by arterial chemoreceptors in the control of ventilation and of thin vagal afferents from the lungs (bronchopulmonary C-fibres and irritant receptors) in reflex facilitation of the bronchoconstrictor vagal tone. Moreover, the stimulation of thin sensory fibres in particular circumstances is responsible for hyperventilation (arterial chemoreceptors and muscle afferents), increased airway tone (arterial chemoreceptors and mostly thin vagal afferent fibres) or bronchodilation (muscle afferents). These peripheral inputs project centrally on different structures and also on brain stem neurones, which integrate simultaneously chemosensory, vagal and muscle information. This results in complex interactions between the different sensory pathways.

Animals↗

Bronchomotor response to cold air or helium-oxygen at normal and high ambient pressures.

Effects of inhalation of cold air or helium-oxygen mixture on lung resistance (RL) were studied in anesthetized and tracheotomized rabbits under normal ambient pressure and in human volunteers under normo- and hyperbaric conditions. In artificially ventilated rabbits, an increase in RL occurred when the tracheal temperature fell to 10 degrees C. This effect was more than double with helium breathing compared to air, despite a lower respiratory heat loss by convection (Hc) with helium. In 3 normal humans, inhalation of cold air (mouth temperature = 8 degrees C) at sea level had no effect on RL value. However, with a helium-nitrogen-oxygen mixture, a weak but significant increase in RL due to cold gas breathing was measured in 1 subject at 2 ATA and in 2 individuals at 3.5 ATA. The density of inhaled gas mixture (air or He-N2-O2) was near the same in the three circumstances (1, 2, and 3.5 ATA) but Hc value increased with helium. At 8 ATA a 30-55% increase in RL occurred in the 3 divers during inhalation of cold gas (Hc was multiplied by 6 compared to air at sea level) and at 25 ATA the cold-induced bronchospasm ranged between 38 and 95% (Hc multiplied by 27). Thus, in rabbits and humans helium breathing enhanced the cold-induced increase in RL at normal or elevated ambient pressure, and this effect was interpreted as resulting from different mechanisms in the two circumstances.

Adult↗

Role of vagal and spinal sensory pathways in diaphragmatic response to resistive loading.

The effects of severe inspiratory (I) or expiratory (E) resistive loads on diaphragmatic activity were studied in two groups of cats anaesthetized with sodium pentobarbital or ethylcarbamate-chloralose. In intact cats, I or E loading never changed the amplitude of integrated diaphragmatic electric myogram (EMG) measured at 1.0 s (Edi 1.0); only I loading, prolonged the duration of diaphragmatic activity (Tdi). After selective procaine block of non-volume related vagal sensory inputs, I or E loading markedly increased Edi 1.0 and changes in Tdi due to I loading persisted. After bivagotomy, which also suppressed volume related vagal feed back, Edi 1.0 increased during I or E loading but change in Tdi disappeared. Initial spinal section at C8 level only reduced changes in Tdi with inspiratory loading. Bivagotomy plus spinal section abolished all load induced changes in diaphragmatic activity. These results suggest that all vagal information from the lungs participate in the mechanism of load compensation but that spinal sensory pathways play a minor role in this response in anaesthetized cats.

Afferent Pathways↗