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Le choix des matériaux entrant dans la construction des structures se fait non seulement sur leurs caractéristiques mécaniques mais également en considérant l’aspect mise en œuvre.

Aciers, alliages spéciaux, titane, alliages légers, composites... les matériaux nous offrent une palette de plus en plus riche. En contrepartie, les choix deviennent plus subtils, moins évidents qu'il y a quelques lustres, mais surtout beaucoup plus importants dans leur finalité : sécurité qualité, coût.

La sécurité et la fiabilité largement démontrées par les aéronefs reposent non seulement sur la qualité des hommes, des matériels et des matériaux utilisés pour leur réalisation, mais aussi sur des principes constructifs généraux.

The neural mechanisms responsible for respiratory rhythmogenesis in mammals were studied first in vivo in adults and subsequently in vitro in neonates. In vitro data have suggested that the pacemaker neurons are the kernel of the respiratory network. These data are reviewed, and their relevance to adults is discussed.

1. Superfused brain stem‐spinal cord preparations of newborn rats, which continue to show a rhythmic respiratory activity in vitro, were used to analyse the mechanisms whereby the A5 noradrenergic area modulates the activity of the medullary respiratory rhythm generator in the newborn. 2. In preparations including the pons (ponto‐medullary preparations), noradrenaline (NA, 25‐100 microM) added to the bathing medium either increased (n = 29/50) or decreased (n = 21/50) the respiratory frequency and elicited a tonic discharge in the cervical ventral roots in 50% of the experiments. Double‐bath experiments showed that the increases in respiratory frequency were due to NA acting on the pons, whereas the decreases in respiratory frequency were due to NA acting on the medulla. The NA‐induced increases in respiratory frequency were attributed to inhibition of A5 neurons by NA and therefore to withdrawal of A5 inhibition on the medullary rhythm respiratory generator. The NA‐induced decreases in respiratory frequency seemed to mimic the effects of endogenous NA on the A5 medullary targets. 3. Noradrenaline‐induced tonic activity (i) could be induced after elimination of the pons but not on isolated spinal cord, (ii) could be elicited by alpha 1‐ but not alpha 2‐agonists, (iii) could be blocked by alpha 1‐ but not alpha 2‐antagonists. The tonic activity therefore originated from activation of alpha 1 receptors located in the medulla but its importance in respiratory function is doubtful. 4. In medullary preparations (elimination of the pons by transection), the effects of NA agonists and antagonists on respiratory frequency were analysed. Significant decreases in respiratory frequency were induced by NA, adrenaline, phenylephrine and alpha‐methyl‐NA, but not by the agonists classified as alpha 2 (clonidine and guanfacine), alpha 1 (6‐fluoro‐NA) and beta (isoprenaline). Since yohimbine, idazoxan and piperoxane (alpha 2 antagonists) blocked the NA‐induced decreases in respiratory frequency whereas prazosin (alpha 1‐antagonist) did not, it is postulated that alpha 2‐receptors may be involved in modulating respiratory frequency. 5. Stimulation, lesion and NA microejection experiments showed the complexity of the mechanisms mediating NA‐induced changes in respiratory activity but suggested that the main site of NA action is located in the rostral ventrolateral medulla, where electrical stimulations triggered inspiration prematurely, lesions suppressed the NA‐induced decrease in respiratory frequency, and localized application of NA led to an immediate decrease in the respiratory frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

1. Experiments were performed on anaesthetized newborn rats (aged 3‐10 days) to know whether an increase in central serotonin levels might favour the occurrence of obstructive apnoeas as previously suggested by in vitro results from our group. 2. The levels of serotonin (5‐HT), its precursor 5‐hydroxytryptophan (5‐HTP) and its metabolite, 5‐hydroxyindole‐acetic acid (5‐HIAA), were analysed in cerebrospinal fluid samples collected at the level of the obex prior to and after intraperitoneal injection of L‐tryptophan (50 mg kg‐1) in sixty‐eight anaesthetized newborn rats (control rats prior to injection and injected rats 15, 30 and 45 min after the injection). A significant increase in 5‐HT and 5‐HTP levels occurred 30 min after the injection, attesting to the activation of 5‐HT biosynthesis. 3. The EMG activity of both the genioglossus and the diaphragm was recorded before and after L‐tryptophan load (50 mg kg‐1) in twenty‐two newborn rats. After the injection of L‐tryptophan, the amplitude of the integrated genioglossus activity decreased, or was even abolished, either during a few respiratory cycles or for long periods in twenty‐one out of twenty‐two animals. Recovery of the genioglossus activity occurred within 45‐60 min. 4. The thoracic respiratory movements and the resulting upper airway pressure changes were recorded before and after L‐tryptophan injection (50 mg kg‐1) in sixty‐two animals. In some litters (n = 7), most of the animals (21/25) displayed, within 20‐40 min of the injection, recurrent episodes of obstructive apnoea often followed by central ones. These respiratory difficulties became severe and drastic, and led in two instances to respiratory distress and death. Lower doses of L‐tryptophan (10 mg kg‐1) did not induce any respiratory disorders unless these were potentiated by pargyline treatment (50 mg kg‐1, n = 7). The obstructive apnoeas liable to occur after an L‐tryptophan load (50 mg kg‐1) were prevented by blocking the 5‐HT receptor with methysergide (50 mg kg‐1, n = 5) or by blocking the 5‐HT biosynthesis by applying p‐chlorophenylalanine (PCPA) pretreatment at birth (300 mg kg‐1, n = 7). In other litters (n = 6), none of the eighteen newborn rats tested were affected by L‐tryptophan, however, In five young adult rats, L‐tryptophan again had no effect.4+ ĕ

Previous experiments performed in the in vitro newborn rat brainstem-spinal cord preparation reported that the addition of serotonin (5-HT, 30–50 µM) to the bathing medium induced increases in the respiratory frequency and a large tonic discharge on all the cervical ventral roots. The aim of the present work was to define whether the 5-HT-induced tonic discharge involved respiratory or non-respiratory motoneurones. Intracellular recordings demonstrated that cervical (C2) motoneurones (n = 27) were depolarized by 5-HT but that the 5-HT-induced tonic discharge was mainly due to recruitment of silent motoneurones (n = 18) which fired permanently (15/18; 17 ±3 Hz) under 5-HT. The respiratory motoneurones (n = 9) retained a phasic inspiratory discharge (5/9), even if some (4/9) occasionally exhibited a few spikes during expiration. Therefore, it is concluded that the 5-HT-induced tonic discharge is unlikely to have functional significance in respiration.

1. Intracellular recordings were made from 220 Phrenic Motoneurons (PM) in anaesthetized, spontaneously breathing cats, deafferented from C3 to C7, in order to look for somatic events related to the Recurrent Responses (RR) evoked in PM axons by repetitive stimulation of the phrenic nerve. RR appear sporadically at a constant latency, originate from a spinal nicotinic mechanism and can be evoked in a PM without the presence of an antidromic volley in its axon (Khatib et al. 1986). 2. Using stimuli effective for eliciting RR in axons, we failed to observe intracellularly somatic events corresponding to RR after the occurence of an antidromic action potential. RR were observed extracellularly in two cases, but in both cases the recording originated from axons. 3. We attempted to elicit somatic RR without a preceding antidromic action potential, using either parathreshold stimulation of the impaled PM, or suprathreshold stimulation of a phrenic strand which excluded the axon of the impaled PM. In both cases, RR-like events, with very stable latencies, appeared sporadically in 4/142 and 2/15 PMs respectively. 4. Parathreshold stimuli or stimulation of a strand were coupled with averaging of the synaptic noise in order to look for small events temporally related to the stimuli. Short latency small depolarizations, looking-like recurrent EPSPs, were revealed in 22/142 and 5/15 PMs respectively. 5. These results confirm the existence of interrelations between PMs, providing for re-excitation and coupling within the phrenic pool, in addition to centrally imposed synchronization.

The role of central respiratory drive, muscle spindles and tendon organs in producing respiratory movements has been studied in the cat by recording from motoneurones supplying a set of small axial muscles inserted between each rib and the vertebra immediately rostral, the levatores costae. The levator costae muscles are active during normal inspiration but activity is progressively stronger in the muscles located in more caudal thoracic segments. Intracellular recordings from levator costae motoneurons show a characteristic central respiratory drive potential (c.r.d.p.), comprising phases of depolarization during inspiration alternating with expiratory phased hyperpolarization due to post‐synaptic inhibition. Loading or unloading the levator costae muscles increases and decreases, respectively, their normal inspiratory activity. Electrophysiological and histological analysis of levator costae afferents reveals that each muscle contains three to five spindles and two to three tendon organs. By dissecting the levator costae nerve, afferent discharges from muscle spindle primary and secondary endings and those from tendon organs were recorded ‘in continuity’ and used to trigger an averager for analysing the synaptic potentials they evoke in levator costae motoneurones. Monosynaptic excitation and oligosynaptic inhibition originate from spindle (primary and secondary endings) and from tendon organ afferents respectively. Peculiarly a monosynaptic excitation has been evoked from a tendon organ. The action of the levator costae muscle on the respiratory movements of the ribs in the different thoracic spaces was analysed in relation to their anatomical properties and to the activity of the other respiratory muscles. The levator costae muscles, because of their relatively small size and well‐defined population of proprioceptors, appear to provide a favourable preparation for studying the integrative action of the motoneurone.

1. Experiments were performed on the brain stem‐spinal cord preparation of newborn rats, in which the phrenic and hypoglossal nerves continue to show rhythmic respiratory activity in vitro, in order to compare the effects of serotonin (5‐HT) on both activities and to analyse the mechanisms responsible for the depression by 5‐HT of the hypoglossal activity. 2. Under control conditions, simultaneous recordings of the inspiratory discharges of hypoglossal and cervical roots showed that the two bursts did not start simultaneously and had different patterns (time‐to‐peak and peak values); this suggests that both pools of motoneurons did not share the same central drive(s). 3. Adding 5‐HT and related agents to the bathing medium delayed and depressed the hypoglossal inspiratory discharge via activation of 5‐HT2 receptors since these effects were elicited by 5‐HT2 agonists (alpha‐methyl‐5‐HT and 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane‐HCl (DOI)) but not by 5‐HT1 agonists (RU 24969 and (+/‐)‐8‐hydroxy‐2‐(di‐N‐propylamino)tetralin hydrobromide (8‐OH‐DPAT)). The 5‐HT depression of the hypoglossal discharge was prevented by applying a pretreatment with a specific 5‐HT2 antagonist (ketanserin). Parallel to the hypoglossal discharge decrease, 5‐HT elicited a permanent cervical root discharge along with a persistent inspiratory bursting. Adding the 5‐HT precursor L‐tryptophan to the bathing medium depressed the hypoglossal (XII) discharge without affecting the cervical one. 4. Local application of 5‐HT within the hypoglossal motor nucleus decreased the hypoglossal output, revealing that the 5‐HT depression of the hypoglossal discharge was at least partly mediated by the 5‐HT effects at the level of the motoneurons. Local application of 5‐HT within the cervical motor nucleus elicited a permanent firing in the cervical root with a persistent inspiratory bursting. 5. Intracellular analysis confirmed the existence of differences in central respiratory drive between cervical and hypoglossal motoneurons under control conditions, as well as differences in response to 5‐HT. All the hypoglossal motoneurons became silent under 5‐HT bathing, and showed no change in the input membrane resistance, a moderate depolarization, and a delayed central respiratory drive with a decreased amplitude. The cervical motoneurons became more active during inspiration, despite a decrease in the amplitude of the central respiratory drive, which was compensated for by a large depolarization and an increased input membrane resistance. Some cervical motoneurons even fired at a low rate during expiration.(ABSTRACT TRUNCATED AT 400 WORDS)

Experiments were conducted on newborn rats in order to study the serotonergic modulation of the central respiratory activity during the neonatal period. In vitro experiments performed on isolated brainstem spinal cord preparations demonstrated that serotonin exerts a permanent excitatory modulation on the central respiratory rhythm generator but depresses the inspiratory motor output to the genioglossus muscle. In vivo experiments confirmed that increasing endogenous serotonin levels decreases the inspiratory activity of the genioglossus and elicits drastic obstructive apneas.

In anaesthetized cats (chloralose-urethan) the effects of brief tetanic electrical stimulation (50 to 100 ms) of the mesencephalic central gray matter and reticular formation on the inspiratory on-switch were studied during the expiratory (E) phase on the gross and unitary activities of phrenic, laryngeal inspiratory and laryngeal expiratory nerves. On the inspiratory laryngeal and phrenic nerves, stimulation elicited a short latency gross response concomitant with the train: the inspiratory Primary Response (Prim.R.) which is followed by an inspiratory Patterned Response (Patt.R.) of longer duration which corresponded to the inspiratory on-switch. The Patt.R. generally appeared from the Prim.R. within a latent period (Silent Phase: Sil.P.) as long as 100 ms. On the expiratory laryngeal nerve, stimulation elicited a brief activation (expiratory Prim.R.) concomitant with the beginning of the inspiratory laryngeal Prim.R. and which rapidly stopped as the latter continued during the stimulus train. The inspiratory Prim.R. corresponded to a simultaneous activation of both early and late (so defined during their spontaneous discharge) inspiratory motoneurones. The laryngeal motoneurones were more strongly activated than the phrenic ones. During the inspiratory Patt.R. all the phrenic motoneurones presented a recruitment delay earlier, compared with the spontaneous one, whereas the recruitment drastically changed from an inspiratory laryngeal motoneurone to another. Thus, the two pools of motoneurones presented different properties of activation. During the inspiratory Sil.P. no concomitant expiratory laryngeal activation was observed when most of the inspiratory motoneurones were inactive. As some inspiratory laryngeal motoneurones did not stop firing, the existence of some central respiratory neurones exhibiting a similar persistent activity and subserving the inspiratory on-switch mechanisms may be hypothesized.

1. Interactions between phrenic motoneurons have been analysed in anaesthetized, paralyzed cats after C3 to C7 deafferentation. Effects of electrical stimulation of the C5 phrenic axons have been studied on thin filaments dissected from the stimulated nerve. Repetitive stimulation could elicit, after the primary direct response of the stimulated axons, a secondary response named Recurrent Response, RR. 2. RRs have been obtained in 117/186 phrenic axons. They appear sporadically (mean occurrence: 3.75 RRs elicited by 100 shocks of stimulation) at a constant latency. They originate from a spinal mechanism since they persist after C2 transection and disappear after section of the ventral roots. 3. The mechanism responsible for RR shows spatial and temporal facilitation. The RR probability increases with the number of antidromically invaded motoneurons as revealed by changes either of stimulation intensity or of central respiratory drive. However, RR could be evoked in a motoneuron without an antidromic volley in its axon. 4. Systemic injections of nicotinic blocking drugs such as dihydro-ß-erytroidin or mecamylamine decrease or suppress the occurrence of RR; therefore, cholinergic synapses are involved in the RR generating process. 5. RR are assumed to be due to direct excitatory interactions between homonymous motoneurons. Recurrent axon collaterals impinging directly on neighbouring motoneurons would link together the different motoneurons of the phrenic pool. The functional significance of this phenomenon is discussed.

1. Respiratory activity was recorded on ventral cervical roots during in vitro experiments performed on superfused newborn rat brain stem‐cervical cord preparations. 2. Eliminating the pontine structures by performing a transection at the level of the ponto‐medullary junction resulted in a sustained increase in respiratory frequency, which suggests the existence of a pontine inhibitory drive impinging on the medullary rhythm generator. 3. Noradrenaline (NA) and drugs affecting NA efficiency were added to the bathing medium and the resulting changes in respiratory frequency were analysed. NA decreased the respiratory frequency, and this effect was potentiated by pargyline (an inhibitor of the NA degradation by monoamine oxidases) and blocked by yohimbine (an alpha 2‐antagonist). 4. Yohimbine or piperoxane (which blocks the alpha 2‐adrenoceptors) increased the resting respiratory frequency to the level reached after ponto‐medullary transection, whereas pargyline or desipramine (which potentiates NA efficiency) decreased the respiratory rate. Since these effects were no longer observed after elimination of the pons, it is suggested that a permanent release of endogenous NA by pontine areas may modulate the activity of the medullary respiratory rhythm generator. 5. When alpha‐methyltyrosine (an inhibitor of NA biosynthesis) was applied to the pons, the respiratory frequency was increased, whereas when tyrosine (a precursor of NA) was applied, the respiratory frequency decreased. This decrease was enhanced by pargyline, suppressed by alpha‐methyltyrosine and blocked by piperoxane. 6. To conclude, it is suggested that the mechanisms underlying NA biosynthesis (i) continue to function under these in vitro experimental conditions and (ii) are responsible for a permanent release of endogenous NA, which slows down the respiratory frequency. These results are discussed as regards the possibility that the medullary respiratory rhythm generator may be modulated via the noradrenergic area A5 in the newborn rat.