Biomedical subjects
Publications and source records attributed to G Benchetrit.
15 asthmatic children and 15 healthy children were trained to adjust their breathing pattern to a target pattern displayed on a video screen by using visual feedback. The error scores in the two groups were not significantly different. These data did not support the hypothesis that voluntary control of respiratory muscles is impaired in asthmatics.
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1. To assess whether voluntary control of breathing is impaired in patients with chronic obstructive pulmonary disease, a group of such patients performed a tracking task, requiring volitional control of respiratory muscles. 2. Eight patients (mean age 60 years; mean ratio of forced expiratory volume in 1 s to forced vital capacity = 31%) took part in the study. Five of the seven patients in whom blood gas measurements were made were mildly hypoxaemic (PaO2 = 53-71 mmHg), and one of these was hypercapnic (PaCO2 = 55 mmHg). Each subject performed a compensatory ventilatory tracking task using a tracking system which comprised a fixed target displayed on a monitor screen and a cursor moving in a line bisecting the target. The position of the cursor was perturbed by a forcing function and patients were required to keep the cursor on the target by breathing in and out of a spirometer. 3. To allow for any non-specific deficiency in motor control, patients performed a similar manual tracking task, using their dominant arm to move a joystick. As a control group, 11 healthy subjects (mean age 58 years; mean ratio of forced expiratory volume in 1 s to forced vital capacity = 77%) underwent an identical experimental protocol. 4. Motor control performances were measured in terms of the error between the target position and the subject's positioning of the cursor. Indices of performance were the root mean square of the error and the averages of the zero errors (i.e. end expiration/arm movement towards the trunk) and the peak errors (i.e. end inspiration/arm movement from the trunk).(ABSTRACT TRUNCATED AT 250 WORDS)
Fourteen subjects learned to adjust their breath pattern to two target breaths displayed on a video screen, by using visual feedback, during two sessions 24 h apart. These two targets were respectively the smallest and the largest breaths of a ten-breath sample previously recorded from each subject's resting spontaneous breathing. Performances were significantly better for the large than for the small target breath. This cannot be directly inferred from current knowledge related to the control of movement time and amplitude, but rather it may be inferred from the periodic character of breathing, to the higher mental load during the small breath task, or to the presumably different frequencies of target breaths in the whole span of spontaneous breathing. In the second session, performance on the two targets levelled out as a result of learning.
When we periodically perturbed the central respiratory oscillator with a controlled periodic stimulation provided by a mechanical ventilator, an entrainment phenomenon occurred: the actual rhythm of the respiratory centres was phase locked to the periodic stimulation. In some experiments, we observed an intermittence phenomenon: the respiratory rhythm successively seemed entrained, departed from this mode for few cycles, returned to the previous pseudo entrainment and so on. From intermittence data, we were able to plot a phase response curve. From literature data on the effects of a single stimulation applied at various moments in the respiratory cycle, we built up a mathematical model designed to simulate entrainment experiments. This model simulated entrainment phenomenon, but did not satisfactorily accommodate the experimental phase response curve. The section of the simulated phase response curve responsible for discrepancies was the result of the combination of an inspiratory shortening owing to a stimulation occurring during inspiration, and a positive relationship between inspiratory duration TI and expiratory duration TE. We changed the TE-TI relationship, assuming that the expiratory duration is determined not by the inspiratory duration but rather by the lung volume at the end of inspiration. The revised model was then able to exhibit almost all the qualitative properties previously noted in experiments. The significance in biological terms of the new TE-TI relationship, which is apparently incompatible with almost all previous experimental data, is discussed.
To better understand behavioural and genetic influences upon breathing, the breathing patterns of 8 pairs of monozygous (MZ) twins were measured under 4 behavioural conditions; relaxed without standardisation; eyes closed; eyes open; and reading. Breathing was quantified by inspiratory and expiratory durations (TI, TE), tidal volume (VT) and derived variables. Airflow shape was normalised and quantified using 8 dimensions. Reading caused breathing to increase by > 500 ml/min compared to the other four conditions. Differences in breathing between combinations of two conditions were compared by testing whether the differences within an individual were smaller than the differences between random pairs of individuals from the same 16 subjects. For almost all respiratory variables, and whatever the behavioural condition, there were highly significant similarities within an individual (p < 0.00025 on 32/80 comparisons). Under each condition, the differences within MZ twin-pairs were compared to the differences within random-pairs from the same subject population. There were highly significant similarities within twin-pairs for the airflow shape across all conditions. However, TI, TE and VT failed to consistently show significant similarities within twin pairs. Hence, an individual's airflow shape appears to be a fundamental characteristic which is conserved when behavioural condition and level of ventilation changes. Further, MZ twins have similar airflow shapes--whatever the behavioural situation. Hence, behavioural influences upon airflow shape act upon monozygous twin pairs in similar ways, or such influences were negligible under the conditions of the present study.
In anesthesized, paralyzed, and mechanically ventilated rabbits, the rate and duration of airflow were varied to investigate the effect on the central respiratory rhythm during 1:1 entrainment (1 phrenic nerve burst for 1 pump inflation). Our results showed that 1) the largest range of 1:1 entrainment was obtained with the longest inflation durations associated with the lowest flow rates and 2) both inspiratory (TI) and expiratory (TE) durations (as estimated by the period of phrenic nerve activity and phrenic nerve silence, respectively) increased when total respiratory duration (TT = TI+TE) increased. The phase relationships we studied were DI (the time elapsing between the onset of phrenic activity and the beginning of pump inflation) and DE (the time between the end of phrenic activity and the end of pump inflation). Both DI and DE increased when the total ventilatory period increased. However, for constant ventilatory period, DI changed with the rate and duration of airflow, whereas DE remained constant. In addition, under these conditions, TI, TE, and the integrated phrenic nerve activity remained constant independently of airflow rate and duration. The present results are discussed with regard to the pulmonary receptors (slowly and rapidly adapting receptors and C fibers) that are stimulated during mechanical ventilation, and hypotheses are drawn regarding their possible contribution to rhythm generation and the mechanism through which they may act.
Breathing was recorded via a pulsed ultrasonic flowmeter in 11 healthy subjects, at rest and during steady-state exercise (at 50% of their maximal O2 consumption) at both sea level (200 m) and simulated altitude (4,500 m in a hypobaric chamber). The pattern of breathing was quantified breath by breath in terms of classical respiratory variables (tidal volume and inspiratory and expiratory times), and the shape of the entire airflow profile was quantified by harmonic analysis. Statistical tests were used to compare the within-individual with the between-individual variations. In comparing the sea level vs. altitude rest (16% increase in ventilation) and sea level vs. altitude exercise (40% increase in ventilation) airflow profiles, we found a significantly greater resemblance within the individual than between individuals. Comparisons of sea level rest and exercise (295% increase in ventilation) and altitude rest and exercise (375% increase in ventilation) revealed no similarity within individuals. Despite airflow profile changes between rest and exercise, it is still possible to attest to a diversity of flow profile between individuals during exercise. Hypoxia at rest or during exercise does not alter the phenomenon of the individuality of breathing patterns.
INTRODUCTION: This work has been carried out to investigate in an animal model, the possibility of surgical selective reinnervation of the larynx following destruction of the laryngeal branch of the vagus nerve. MATERIAL AND METHODS: In ten dogs, on the right side of the neck only, the recurrent laryngeal nerve was identified, cut and section of the nerve removed. Following this the hemi-larynx on the operated side was reinnervated in the following manner. Using a microsurgical suture (described in the text) the motor nerves from extra-laryngeal muscles were anastomosed onto the nerves supplying the intrinsic abductors and adductors of the larynx. The nerve to sterno-thyroid was anastomosed onto the nerve supplying the posterior crico-arytenoid muscle (vocal cord abductor). Similarly the nerve supplying thyrohyoid was anastomosed onto the cut distal end of the adductor division of the recurrent laryngeal nerve. Clinical, electromyographical and histological evaluations have been used to prove the reinnervation. RESULTS: In the nine surviving animals successful re-innervations, as defined by the return of normal function, has been achieved for posterior crico-arytenoid and 7 adductor muscles. CONCLUSION: This study has demonstrated the feasibility of laryngeal reinnervation after surgical section of the recurrent laryngeal nerve, and give some cause for optimism for its ultimate application in man.
To determine the mechanism governing pulmonary edema induced by an organophosphorus compound, S-(2-diisopropylaminoethyl)-O-ethylmethyl phosphonothiolate (VX), lung lymph flow and lymph-to-plasma protein concentration ratio were measured in six anesthetized, open-chest, mechanically ventilated beagle dogs before and after intravenous injection of 6 micrograms/kg of VX. Systemic and pulmonary hemodynamic data (heart rate, aortic blood flow, and left atrial, systemic arterial, pulmonary arterial, and pulmonary capillary pressures) were continuously recorded. Arterial blood gases and pH were measured every 30 min. Histological examinations and lung water content measurements were also carried out. Following VX injection, lung lymph flow increased (from 109 +/- 38 to 179 +/- 66 microliters/min, p less than 0.05) while lymph-to-plasma protein concentration ratio remained unchanged (from 0.64 +/- 0.14 to 0.62 +/- 0.12, N.S.). Neither systemic nor pulmonary hemodynamics were changed. Lung water content expressed as blood-free wet-to-dry weight ratio increased from 4.31 +/- 0.23 to 5.35 +/- 0.26 (p less than 0.05). Histological examinations revealed in many cases diffuse congestion of lungs and interstitial edema. These results suggest that VX injection induces an increase in pulmonary capillary permeability which may lead to a high-permeability edema.
The characteristic pattern of breathing for an individual when awake at rest may be due to forebrain influences upon breathing. To examine this hypothesis we have studied the breathing pattern in 18 healthy subjects during relaxed wakefulness (W) and during Stage 4 sleep (S4), when forebrain influences upon breathing are absent or minimal. Inspiratory and expiratory times, respiratory frequency, tidal volume, and ventilation were quantified noninvasively by respiratory inductance plethysmography. The stability of respiratory variables between W and S4 sleep was tested within individuals. The results show that (i) individuals breathe differently from each other when awake and when in S4 sleep; the range between individuals during sleep being as large as it is when awake; (ii) differences in breathing pattern between two S4 periods within an individual are relatively small; (iii) the characteristic breathing pattern of an individual when awake tends to be maintained in S4 sleep. This persistence of a respiratory 'personality' into S4 sleep probably indicates that there are individual differences in respiratory rhythm generation in the absence of any forebrain influences upon breathing.
The aim of this study was to determine whether pulmonary receptors other than slowly adapting stretch receptors are capable of entraining the respiratory rhythm when periodically stimulated during artificial ventilation. Experiments were performed on anaesthetised (urethane, 1.5 g/kg) and paralysed (pancuronium bromide, 0.1 mg/kg) rabbits. Vagi were cooled in order to block conduction in the myelinated fibres innervating slowly adapting receptors. The effectiveness of this cooling was assimilated to the absence of the Hering-Breuer inflation reflex and the presence of the deflation reflex. Our results indicate that under such conditions: (1) harmonic entrainment (one phrenic burst for one pump period) can be observed, (2) the range of harmonic entrainment is more limited when the vagi are cooled, and (3) during harmonic entrainment the inspiratory duration and phrenic activity are similar to what is observed at the same period with intact vagi, whereas vagal cooling modifies the phase difference between the phrenic burst and the pump. We have concluded that periodic input from rapidly adapting receptors and/or vagal C-fibres can entrain the respiratory rhythm as does input from slowly adapting receptors but with different patterns as evidenced by phase relationship.
Sixteen healthy adult subjects underwent two studies separated by 4-5 years to test whether their resting pattern of breathing was reproducible over time. From breath-by-breath analysis of airflow, measured with a pneumotachometer, the pattern of breathing was quantified in terms of individual respiratory variables; inspiratory time (TI), expiratory time (TE), total breath duration (TTOT), tidal volume (VT), VT/TI, TI/TTOT, and by taking TI, TE and VT all together (TRIAD). Also, the shape of the entire airflow profile was quantified by harmonic analysis (ASTER). A statistical analysis was designed to compare differences between the 1st and the 2nd recording within individuals with those differences observed between random pairs of recordings from the two studies in the same 16 individuals. It was found that all variables were significantly more similar within-individuals than between-individuals; this is best demonstrated when considering the ASTER and/or the TRIAD. It was concluded that the individuality of breathing pattern is maintained over a long period despite changes in smoking habit, weight, mild respiratory diseases, and other changes which occurred between the two studies in our subjects.
The resting breathing patterns of healthy adult identical twins were compared to see if there was any possible genetic component in the determination of this pattern. From breath-by-breath analysis of airflow, measured with a pneumotachometer (9 pairs of twins), the pattern of breathing was quantified in terms of individual respiratory variables; inspiratory time (TI), expiratory time (TE), total breath duration (TTOT), VT/TI, TI/TTOT, and by taking TI, TE and VT all together (TRIAD). Also, the airflow shape was quantified by harmonic analysis (ASTER). A second study was performed under more strictly defined conditions of rest and where the respiratory variables were estimated with respiratory inductance plethysmography to eliminate the possible effect of a facemask (5 pairs of twins). In each study, for each variable, the differences within twin-pairs were compared to the differences within random-pairs from the same subject population. In both studies, there were highly significant similarities within twin-pairs in the pattern of breathing, being best demonstrated when the entire 'shape' of the pneumotachogram (ASTER) or the spirogram (TRIAD) was considered.
Changes in pulmonary capillary filtration induced by hyperoxia were investigated in 15 dogs. After 12 h of normobaric hyperoxic exposure, animals were anesthetized and artificially ventilated with 100% O2. A pulmonary lymphatic vessel was cannulated, and lymph flow and protein content were measured together with pulmonary and systemic hemodynamics. An increase in pulmonary capillary filtration was found when compared with reference data (normoxic dogs in similar conditions) gathered from available literature: lymph flow increased from 21.8 +/- 13.4 to 125.2 +/- 131.6 microliter/min, and the lymph-to-plasma protein concentration ratio increased from 0.67 +/- 0.08 to 0.78 +/- 0.08. To characterize the mechanisms involved, left atrial pressure was increased in two stages (approximately 10 and approximately 25 mmHg). The results clearly indicated an increase in pulmonary capillary permeability as evidenced by a decrease of the minimal estimate of the protein reflection coefficient from 0.62 +/- 0.05 to 0.42 +/- 0.05.
Experiments were performed to check the tolerance to severe hypoxia of the tissue layers (compact and spongy) of the tortoise heart. The animals were subjected to hypoxia (7% O2) at 18 degrees C, 28 degrees C and 38 degrees C for 30, 6 and 2 hr respectively, or to anoxia for 30 hr at 18 degrees C and 2 hr at 38 degrees C. At 18 degrees C the metabolic alterations caused by a 30 hr hypoxia were mild whereas at 28 degrees C and 38 degrees C the cardiac glycogen was depleted, lactate had accumulated and the phosphate creatine and ATP content had decreased. The extent of these metabolic changes was similar in the compact and in the spongy layers of the heart.
A computer program for cycle-by-cycle analysis and quantification of biological rhythms, written for an Apple II microcomputer with 48k RAM is described. The program comprises 4 steps: (1) file constitution suitable for biological data collecting; (2) signal digitalization at a sampling rate up to 1 kHz with storage in central memory; (3) determination of each cycle's limits (delimitation parameters being defined by the user; following delimitation, cycles may be dropped or saved for further analyses); (4) cycle-by-cycle harmonic analysis (fast Fourier Transform algorithm). The program is written in BASIC Applesoft, hardware-dependent functions (analog inputs, graphic display and random access disk storage) are implemented in subroutines (partly assembler) which may be easily modified. The program, consisting of 4 chained procedures is run interactively, although procedure (4) may be run automatically. Analysis of human ventilatory airflow signal with this program is given as an example of cycle-by-cycle shape analysis of a biological rhythm.
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