Phase locking of the respiratory rhythm in cats to a mechanical ventilator

Mechanical ventilation of paralyzed, pentobarbital-anesthetized adult cats was performed while recording phrenic nerve activity. The periodic changes in lung volume owing to mechanical ventilation affected the rhythm of central respiratory activity, resulting in a variety of regular and irregular patterns of coupling between respiratory system output, monitored by phrenic activity, and the mechanical ventilator. Phase-locked patterns, in which phrenic burst onset occurred at specific and repetitive phase(s) of the mechanical ventilator, with ratios of ventilator frequency: phrenic burst frequency of 1:2, 1:1, 3:2, 2:1, and 3:1 were observed. Regular and irregular patterns occurred over specific ranges of frequency and volume of the mechanical ventilator. A careful study was made of the 1:1 phase locking as the frequency and inflation volume of the mechanical ventilator were changed. The inspiratory time (TI) was defined as the interval between the time when phrenic activity began to rise and the onset of its rapid decline, and the expiratory time (TE) as the time between inspirations. In the 1:1 phase-locking region, as the frequency of the ventilator was increased both TI and TE decreased, and the phase of phrenic onset in the ventilator cycle changed. During ventilation with frequencies higher than the intrinsic phrenic frequency (initial burst frequency of phrenic activity with the ventilator turned off) inspiratory activity was prematurely terminated by lung inflation (Hering-Breuer inspiratory inhibitory reflex). During ventilation with frequencies lower than the intrinsic phrenic frequency, the onset of phrenic activity was delayed (TE was prolonged) by lung inflation (Hering-Breuer expiratory promoting reflex).     

反射性呼吸暂停中延髓各类呼吸性神经元的放电变化

在向家兔颈动脉窦区注入拘椽酸钠引起呼吸暂停期间,和在持续性肺充气引起延长的呼气相中,延髓大多数吸气神经元和膈神经停止放电;而大多数呼气性神经元呈连续性放电,放电频率持续地高于或接近于平静呼气时呼气神经元的高峰放电频率,并伴随肋间内肌电活动增强,直至呼气性神经元放电频率衰减或停止放电时,膈神经才恢复放电。这提示呼气性神经元的持续兴奋状态可能与呼气性呼吸暂停的维持或呼气相的延长有关。在延髓闩前部可以记录到少数放电频率渐增型的跨时相呼气-吸气神经元,在呼吸暂停期间,它们呈低频连续放电,逐渐增大放电频率,在其放电频率急剧增高时,膈神经恢复放电。这提示该类神经元可能与吸气的发动有关。本文尚就呼吸节律的发生机制做了讨论。     

家兔面神经后核内侧区在呼吸节律起源中的作用

从腹侧面暴露家兔延髓,脑内微量注射1%普鲁卡因阻滞面神经后核内侧区(mNRF),全部动物(n=20)一次注射(0.3—1.0μl)后即能可逆地消除呼吸节律。区域对照显示此区非常局限,范围约1.0×1.0×1.0mm。组织学检查表明为面神经后核内侧区。本文分析了 mNRF的呼吸相关神经元(RRNs)的放电形式。在 mNRF 有较多的呼气(E)神经元和呼气-吸气跨时相(E-IPS)神经元。在阻滞 mNRF 引起呼吸停止期间,观察到低位延髓背侧呼吸群(DRG)和腹侧呼吸群(VRG)尾端区 RRNs 放电的节律性消失,表现连续放电或停止放电。电刺激DRG,VRG 尾端区,只能诱发短串的膈神经放电,而不能产生节律性发放。说明这些区域的RRNs 无自动节律性活动的能力。结果表明,面神经后核内侧区与呼吸节律发生有关,它可能是呼吸节律发生器的一个重要的所在部位。     

兔孤束核腹外侧区微量注射谷氨酸钠及甘氨酸对膈神经放电的影响

实验在４０只麻醉、制动、断双侧颈迷走神经和人工通气的家兔上进行。在孤束核腹外侧区微量注射神经元胞体兴奋剂谷氨酸钠和抑制剂甘氨酸,探讨膈神经放电的变化。结果：微量注射谷氨酸钠,可使膈神经放电脉冲数明显增加,吸气时程延长,呼气时程缩短,呼吸频率变化不明显;微量注射甘氨酸,则膈神经放电脉冲数显著减少,甚至停止,吸气时程缩短,呼气时程不规则延长,呼吸频率降低。上述结果提示：孤束核腹外侧区对呼吸节律的形成具     

Inspiratory neuron activity in the ventrolateral medulla of the dog

The purpose of this study was to describe the distribution and activity pattern of respiratory neurons located in the ventrolateral medulla (VLM) of the dog. Spike activity of 129 respiratory neurons was recorded in 23 ketamine-anesthetized spontaneously breathing dogs. Pontamine blue dye was used to mark the location of each neuron. Most VLM neurons displaying respiratory related spike patterns were located in a column related closely to ambigual and retroambigual nuclei. Both inspiratory and expiratory neurons were present with inspiratory units being grouped more rostrally. The predominant inspiratory neuron firing pattern was "late" inspiratory, although eight "early" types were located. All expiratory firing patterns were the late expiratory variety. Each neuron burst pattern was characterized by determining burst duration (BD), spikes per burst (S/B), peak frequency (PF), time to peak frequency (TPF), rate of rise to peak frequency (PF/TPF), and mean frequency. CO2-induced minute ventilation increases were associated with decreases in BD and TPF and increases in PF, S/B, and PF/TPF. In 11 experiments the relative influences of vagotomy and tracheal occlusion on late inspiratory units were compared. Tracheal occlusion increased late inspiratory BD and S/B but did not alter PF/TPF. Vagotomy increased BD and S/B beyond those obtained by tracheal occlusion and, in some neurons, decreased the PF/TPF. We conclude that the location of respiratory units in the VLM of the dog is similar to that in other species, the discharge pattern of VLM respiratory units is similar to those in cat VLM, and vagotomy and tracheal occlusion affect discharge patterns differently.     

Existence of respiratory interneurons in the cervical spinal cord of the rabbit

A spinal "respiration" generator has been shown to fire phrenic motoneurones in rhythmic bursts. It is very likely driven through bulbo-spinal inspiratory neurones in intact preparations. Although no direct evidence for respiratory interneurones at the C4-C5 spinal levels has been obtained so far (except for Renshaw cells ), it is currently believed that only few inspiratory inputs to the phrenic motoneurones are transmitted monosynaptically from the medulla. We have tried here to record spinal interneuronal respiratory activities in decorticate, unanaesthetized, vagotomized and curarized rabbit preparations. Different functional categories of interneurones could be identified at the C4-C5 spinal levels: inspiratory and expiratory interneurons with various discharge patterns which rather well correspond to the functional categories of inspiratory and expiratory bulbo-spinal neurones described by Bianchi and Richter. In addition, multiunit inspiratory bursting could be followed over several 100 microns during each electrode penetration. The different categories of interneurones were encountered laterally from 700 to 1,000 microns, at depths ranging from 300 to 500 microns dorsally to the phrenic nucleus, down to the nucleus itself. These results indicate that part of the medullary inspiratory drive is channelled via spinal cord interneurones; they also suggest that an inhibition of phrenic motoneurones from the bulbo-spinal expiratory drive takes place via interneurones.     

Activity of bulbar respiratory neurones during cough and other respiratory tract reflexes in cats

Changes evoked by mechanical stimulation of the relevant parts of the respiratory tract in the activity of inspiratory and expiratory neurones in the ventral respiratory group of the medulla oblongata, and in pleural pressure and the diaphragmatic electromyogram, were determined during cough, sneeze and the aspiration and expiration reflexes in 17 anaesthetized (but not paralysed) cats. The results of 72 tests of elicitation of the given reflexes showed that: Compared with the control inspiration, both the mean and the maximum discharge frequency of spontaneously active inspiratory neurones rose during the inspiratory phase of cough, sneeze and the aspiration reflex. Regular recruitment of new inspiratory units was also observed in the inspiratory phase of cough and the aspiration reflex. Compared with the control expiration, both the mean and the maximum discharge frequency of spontaneously active expiratory neurones rose during the cough, sneeze and expiration reflex effort. Recruitment of latent expiratory neurones was always observed in the expulsive phase of the given respiratory processes. The recruitment of latent expiratory neurones was accompanied by reciprocal inhibition of the activity of inspiratory units and recruitment of latent inspiratory neurones by inhibition of the activity of expiratory units and recruitment of latent inspiratory neurones by inhibition of the activity of expiratory units. Regular recruitment of the same expiratory neurones in all expulsive respiratory processes, together with the similar incidence of inspiratory neurones in the inspiratory phase of sneeze and the aspiration reflex, indicates that they are "nonspecific" in character.     

Respiratory muscle control during vomiting

The changes in thoracic and abdominal pressure that generate vomiting are produced by coordinated action of the major respiratory muscles. During vomiting, the diaphragm and external intercostal (inspiratory) muscles co-contract with abdominal (expiratory) muscles in a series of bursts of activity that culminates in expulsion. Internal intercostal (expiratory) muscles contract out of phase with these muscles during retching and are inactive during expulsion. The periesophageal portion of the diaphragm relaxes during expulsion, presumably facilitating rostral movement of gastric contents. Recent studies have begun to examine to what extent medullary respiratory neurons are involved in the control of these muscles during vomiting. Bulbospinal expiratory neurons in the ventral respiratory group caudal to the obex discharge at the appropriate time during (fictive) vomiting to activate either abdominal or internal intercostal motoneurons. The pathways that drive phrenic and external intercostal motoneurons during vomiting have yet to be identified. Most bulbospinal inspiratory neurons in the dorsal and ventral respiratory groups do not have the appropriate response pattern to initiate activation of these motoneurons during (fictive) vomiting. Relaxation of the periesophageal diaphragm during vomiting could be brought about, at least in part, by reduced firing of bulbospinal inspiratory neurons.     

Spectral characteristics of electrical activity of the respiratory center in brain processes in fetus and newborn rats in vitro

Power spectral analysis of inspiratory discharges of C3-C5 ventral roots in brainstem-spinal cord preparation from foetal (18 and 20 gestation days) and newborn (0-1 and 2-3 postnatal days) rats was performed. The respiratory centre perinatal development manifests itself by decreasing of respiratory rhythm variability and increasing of inspiratory burst duration. In foetal inspiratory bursts, low-frequency oscillations (1-10 Hz) dominate. In early postnatal stage, the relative power of low-frequency oscillations begin to decrease, and medium frequency oscillations (10-50 Hz) start to dominate over the inspiratory discharge. The data obtained suggests, that perinatal maturation of respiratory centre is characterised by stabilisation of the respiratory rhythm generation and developmental alteration of inspiratory activity's spectral and temporary parameters.     

Bradykinin stimulates respiratory drive by activating pulmonary sympathetic afferents in the rabbit.

We recently identified a vagally mediated excitatory lung reflex by injecting hypertonic saline into the lung parenchyma (Yu J, Zhang JF, and Fletcher EC. J Appl Physiol 85: 1485-1492, 1998). This reflex increased amplitude and burst rate of phrenic (inspiratory) nerve activity and suppressed external oblique abdominal (expiratory) muscle activity. In the present study, we tested the hypothesis that bradykinin may activate extravagal pathways to stimulate breathing by assessing its reflex effects on respiratory drive. Bradykinin (1 microg/kg in 0.1 ml) was injected into the lung parenchyma of anesthetized, open-chest and artificially ventilated rabbits. In most cases, bradykinin increased phrenic amplitude, phrenic burst rate, and expiratory muscle activity. However, a variety of breathing patterns resulted, ranging from hyperpnea and tachypnea to rapid shallow breathing and apnea. Bradykinin acts like hypertonic saline in producing hyperpnea and tachypnea, yet the two agents clearly differ. Bradykinin produced a higher ratio of phrenic amplitude to inspiratory time and had longer latency than hypertonic saline. Although attenuated, bradykinin-induced respiratory responses persisted after vagotomy. We conclude that bradykinin activates multiple afferent pathways in the lung; portions of its respiratory reflexes are extravagal and arise from sympathetic afferents.     

延髓腹外侧Boetzinger复合体呼吸时相转换效应的研究

The effects of electrical stimulation of B?tzinger complex (Bot.C) on respiratory rhythm were investigated in 40 urethane anesthetized adult rabbits. The results were as follows. (1) A short train stimulation delivered in the early inspiratory phase produced a transient inhibition of phrenic discharge. The stimulus, when delivered in the mid or late inspiratory phase, could cause a premature termination of the inspiratory phase ("inspiratory off-switch") and a switching to the expiratory phase, which was accompanied with the reduced duration of the consecutive expiratory phase. There was a negative linear correlation between the threshold intensity of inspiratory off-switching and delivery time of stimulation. (2) A short train stimulation delivery in the expiratory phase elicited a transient phrenic discharge. The discharge in the late expiratory phase was followed by a premature onset inspiration. This effect was also dependent on the strength and delivery time of the stimulus. The results suggest that the Bot.C is involved in the central control of respiratory phase-switching.     

家兔孤束核区微量注射羟基马桑毒素对膈神经放电的影响

实验在44只乌拉坦麻醉、肌肉麻痹、切断双侧颈迷走神经的日本大耳白兔上进行。于一侧孤束核区微量注射不同浓度(0.1μg/μl,1μg/μl,5μg/μl,10μg/μl)的羟基马桑毒素1μl,可以引起膈神经放电活动产生可逆的吸气时程和呼气时程缩短,呼吸频率加快及膈神经放电积分的峰幅度降低。羟基马桑毒素0.1μg/μl组作用最弱,1μl/μl组作用最强。5μg/μl组,10μg/μl组还可使膈神经放电活动在呼气期出现短时的吸气性放电及呼气期间歇性不规则延长等呼吸节律紊乱现象。出现上述现象时血压、心率无明显变化,脑电图也未出现异常改变。结果提示:家兔孤束核区参与呼吸时相的转换,而羟基马桑毒素可能作用于孤束核区的呼吸时相转换机制,促进呼吸时相的转换。     

Opiate slowing of feline respiratory rhythm and effects on putative medullary phase-regulating neurons

Opiates have effects on respiratory neurons that depress tidal volume and air exchange, reduce chest wall compliance, and slow rhythm. The most dose-sensitive opioid effect is slowing of the respiratory rhythm through mechanisms that have not been thoroughly investigated. An in vivo dose-response analysis was performed on medullary respiratory neurons of adult cats to investigate two untested hypotheses related to mechanisms of opioid-mediated rhythm slowing: 1) Opiates suppress intrinsic conductances that limit discharge duration in medullary inspiratory and expiratory neurons, and 2) opiates delay the onset and lengthen the duration of discharges postsynaptically in phase-regulating postinspiratory and late-inspiratory neurons. In anesthetized and unanesthetized decerebrate cats, a threshold dose (3 microg/kg) of the mu-opioid receptor agonist fentanyl slowed respiratory rhythm by prolonging discharges of inspiratory and expiratory bulbospinal neurons. Additional doses (2-4 microg/kg) of fentanyl also lengthened the interburst silent periods in each type of neuron and delayed the rate of membrane depolarization to firing threshold without altering synaptic drive potential amplitude, input resistance, peak action potential frequency, action potential shape, or afterhyperpolarization. Fentanyl also prolonged discharges of postinspiratory and late-inspiratory neurons in doses that slowed the rhythm of inspiratory and expiratory neurons without altering peak membrane depolarization and hyperpolarization, input resistance, or action potential properties. The temporal changes evoked in the tested neurons can explain the slowing of network respiratory rhythm, but the lack of significant, direct opioid-mediated membrane effects suggests that actions emanating from other types of upstream bulbar respiratory neurons account for rhythm slowing.     

一氧化氮对呼吸节律性放电的调节作用

实验旨在探讨一氧化氮(nitric oxide,NO)在基本呼吸节律产生和调节中可能的作用。制作新生大鼠离体延髓脑片标本,主要包含面神经后核内侧区,前包钦格复合体、腹侧呼吸组以及背侧呼吸组的一部分。同时保留舌下神经根,用改良Kreb′s液灌流脑片并记录与之相连的舌下神经根呼吸节律性放电(respiratory rhythmical discharge activity,RRDA),在灌流液中分别给予不同浓度的NO供体硝普钠(sodium nitroprusside,SNP),NO合成前体L—精氨酸(L—Arginine,L-Arg)以及神经元型一氧化氮合酶(neuronal nitric oxide synthase,nNOS)特异性抑制剂7-nitro indazole (7-NI),观察其对RRDA的影响。结果显示,nNOS的特异性抑制剂7-NI对吸气时程和放电强度有明显抑制,而NO合成前体L—Arg,以及NO供体SNP对呼吸放电活动没有明显的影响。这提示,在哺乳动物基本呼吸节律的产生和调节中,NO可能对吸气中止和呼吸幅度具有调节作用。     

Parvalbumin in respiratory neurons of the ventrolateral medulla of the adult rat

A column of parvalbumin immunoreactive neurons is closely associated with the location of respiratory neurons in the ventrolateral medulla of the rat. The majority (66%) of bulbospinal neurons in the medullary ventral respiratory column (VRC) that were retrogradely labeled by tracer injections in the phrenic nucleus were also positive for parvalbumin. In contrast, only 18.8% of VRC neurons retrogradely labeled after a tracer injection in the VRC, also expressed parvalbumin. The average cross-sectional area of VRC neurons retrogradely labeled after VRC injections was 193.8 μm² ± 6.6 SE. These were significantly smaller than VRC parvalbumin neurons (271.9 μm² ± 12.3 SE). Parvalbumin neurons were found in the Bötzinger Complex, the rostral ventral respiratory group (VRG), and the caudal VRG, areas which all contribute to the bulbospinal projection. In contrast, parvalbumin neurons were sparse or absent in the preBötzinger Complex and in the vicinity of the retrotrapezoid nucleus, areas that have few bulbospinal projections. Parvalbumin was rarely colocalized within Neurokinin-1 receptor positive (NK1R) VRC neurons, which are found in the preBötzinger complex and in the anteroventral part of the rostral VRG. Parvalbumin neurons in the Bötzinger Complex and rostral VRG help define the rostrocaudal extent of these regions. The absence of parvalbumin neurons from the intervening preBötzinger complex also helps establish the boundaries of this region. Regional boundaries described in this manner are in good agreement with earlier physiological and anatomical studies. Taken together, the distributions of parvalbumin, NK1R and bulbospinal neurons suggest that the rostral VRG may be subdivided into distinct, anterodorsal, anteroventral, and posterior subdivisions.     

Comparative study of the activity of medullary respiratory neurones during polypnea triggered by hypothalamic electrical stimulation or by hypothalamic heating (author's transl)

We have compared in "encéphale isolé bas" cats the activity of medullary respiratory neurones during polypnea triggered by electrical stimulation (PSt) or by heating (PTh) of the hypothalamus. The medullary respiratory neurones are classified according to:--their anatomical localization (dorsal or ventral respiratory nucleus);--their axon destination (spinal : bulbo-spinal respiratory neurones; non spinal : propriobulbar neurones);--their discharge pattern;--the correlation coefficient between the number of spikes delivered in each burst and the duration of the corresponding respiratory phase (HILAIRE et MONTEAU, 1975). 1. During the two polypneas (PSt and PTh), we observe:--a reduction of activity that preferentially affects some groups of neurones (propriobulbar neurones) (fig. 3);--an inversion of the discharge firing rate, which increases during inspiration in normopnea and decreases in polypnea (fig. 1; fig. 6);--a decrease of the maximal discharge firing rate for the neurones of different groups (Table V). 2. However, two differences exist : during PSt, the maximal discharge firing rate increases for the inspiratory bulbo-spinal neurones of the dorsal nucleus and for the early-burster inspiratory propriobulbar neurones. The recruitment of the bulbo-spinal inspiratory neurones seems to be different; they are activated earlier during PSt than during PTh (Table VI). 3. Some of the observed differences are probably quantitative and we think that polypnea triggered by hypothalamic electrical stimulation is a good model for thermal polypnea.     

Differing activities of medullary respiratory neurons in eupnea and gasping

Our purpose was to compare further eupneic ventilatory activity with that of gasping. Decerebrate, paralyzed, and ventilated cats were used; the vagi were sectioned within the thorax caudal to the laryngeal branches. Activities of the phrenic nerve and medullary respiratory neurons were recorded. Antidromic invasion was used to define bulbospinal, laryngeal, or not antidromically activated units. The ventilatory pattern was reversibly altered to gasping by exposure to 1% carbon monoxide in air. In eupnea, activities of inspiratory neurons commenced at various times during inspiration, and for most the discharge frequency gradually increased. In gasping, the peak discharge frequency of inspiratory neurons was unaltered. However, all commenced activities at the start of the phrenic burst and reached peak discharge almost immediately. The discharge frequencies of all groups of expiratory neurons fell in gasping, with many neurons ceasing activity entirely. These data are consistent with the hypothesis that brain stem mechanisms controlling eupnea and gasping differ fundamentally.     

正常猫膈神经单纤维电活动特征

在麻醉猫和麻痹的切断迷走神经的清醒猫,观察了膈神经单纤维电活动特征。1.电活动类型:按膈神经单纤维放电与其总干放电的相位关系分为三种类型。(1)完全同步型,即单纤维放电与总干放电同时开始并同时停止,占76.9％。(2)部分同步型占15.4％,其中早期同步,即单纤维放电与总干放电同时开始,但提前终止,占1.9％,中期同步,即单纤维放电较总干放电开始晚,又提前终止,占5.8％,晚期同步,即单纤维放电较总干放电开始晚,但两者同时终止,占7.7％。(8)非同步型,即吸气相和呼气相都有放电,但呼气相时冲动频率较低,占7.7％。前两型为单纯的吸气性放电,共占92.3％。2.单纤维放电平均参数值:麻醉猫每次吸气发放11个冲动,其频率为21次/秒,清醒猫每次吸气发放18个冲动,其频率为34次/秒。结果表明:猫膈神经单纤维放电类型和文献上报导的直接记录膈神经运动神经元放电一致,即以单纯的吸气性放电为最多。     

Mu-opioid receptor agonist effects on medullary respiratory neurons in the cat: evidence for involvement in certain types of ventilatory disturbances

Mu-opioid receptor agonists depress tidal volume, decrease chest wall compliance, and increase upper airway resistance. In this study, potential neuronal sites and mechanisms responsible for the disturbances were investigated, dose-response relationships were established, and it was determined whether general anesthesia plays a role. Effects of micro-opioid agonists on membrane properties and discharges of respiratory bulbospinal, vagal, and propriobulbar neurons and phrenic nerve activity were measured in pentobarbital-anesthetized and unanesthetized decerebrate cats. In all types of respiratory neurons tested, threshold intravenous doses of the micro-opioid agonist fentanyl slowed discharge frequency and prolonged duration without altering peak discharge intensity. Larger doses postsynaptically depressed discharges of inspiratory bulbospinal and inspiratory propriobulbar neurons that might account for depression of tidal volume. Iontophoresis of the micro-opioid agonist DAMGO also depressed the intensity of inspiratory bulbospinal neuron discharges. Fentanyl given intravenously prolonged discharges leading to tonic firing of bulbospinal expiratory neurons in association with reduced hyperpolarizing synaptic drive potentials, perhaps explaining decreased inspiratory phase chest wall compliance. Lowest effective doses of fentanyl had similar effects on vagal postinspiratory (laryngeal adductor) motoneurons, whereas in vagal laryngeal abductor and pharyngeal constrictor motoneurons, depression of depolarizing synaptic drive potentials led to sparse, very-low-frequency discharges. Such effects on three types of vagal motoneurons might explain tonic vocal fold closure and pharyngeal obstruction of airflow. Measurements of membrane potential and input resistance suggest the effects on bulbospinal Aug-E neurons and vagal motoneurons are mediated presynaptically. Opioid effects on the respiratory neurons were similar in anesthetized and decerebrate preparations.     

Die rhythmogenese der atmung beschrieben mit hilfe des Lotka-Volterra-modells: Experimente und simulation

The aim of the present study was to simulate respiratory responses to vagal stimulation using theLotka-Volterra model, a system of two simultaneous non-linear differential equations. The experiments were carried out on vagotomized, artificially ventilated rabbits. Low-threshold, fast-conducting vagal afferent fibres were stimulated with relatively high frequencies (100–200 cps) at various stages of the respiratory cycle. The phrenic activity was recorded in order to analyze the latency and duration of exspiratory reactions with regard to the time relation between stimulatory and respiratory phase. The onset of the stimulatory phase was progressively delayed with regard to the onset of the inspiratory or expiratory phase, stimulation ceasing at the onset of the ensuing respiratory cycle. Real-time simulation was carried out on a hybrid computer. The vagal stimulation was imitated by altering the values of one of the system parameters. The onset of parameter changes was progressively delayed with regard to the onset of the inspiratory or expiratory phase of the model, and the parameters were reset to the initial values as soon as the following respiratory phase began. Comparison of experimental and model data revealed satisfactory agreement between the time-dependent system properties of both respiratory centre and model. The results are discussed with regard to the central nervous processes underlying the genesis of respiratory rhythm. Further light is also thrown on the central processing of afferent vagal input subserving inspiratory inhibitory reactions.

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