Activation of central adenosine A(2A) receptors enhances superior laryngeal nerve stimulation-induced apnea in piglets via a GABAergic pathway.

Activation of the laryngeal mucosa results in apnea that is mediated through, and can be elicited via electrical stimulation of, the superior laryngeal nerve (SLN). This potent inhibitory reflex has been suggested to play a role in the pathogenesis of apnea of prematurity and sudden infant death syndrome, and it is attenuated by theophylline and blockade of GABA(A) receptors. However, the interaction between GABA and adenosine in the production of SLN stimulation-induced apnea has not been previously examined. We hypothesized that activation of adenosine A(2A) receptors will enhance apnea induced by SLN stimulation while subsequent blockade of GABA(A) receptors will reverse the effect of A(2A) receptor activation. The phrenic nerve responses to increasing levels of SLN stimulation were measured before and after sequential intracisternal administration of the adenosine A(2A) receptor agonist CGS (n = 10) and GABA(A) receptor blocker bicuculline (n = 7) in ventilated, vagotomized, decerebrate, and paralyzed newborn piglets. Increasing levels of SLN stimulation caused progressive inhibition of phrenic activity and lead to apnea during higher levels of stimulation. CGS caused inhibition of baseline phrenic activity, hypotension, and enhancement of apnea induced by SLN stimulation. Subsequent bicuculline administration reversed the effects of CGS and prevented the production of apnea compared with control at higher SLN stimulation levels. We conclude that activation of adenosine A(2A) receptors enhances SLN stimulation-induced apnea probably via a GABAergic pathway. We speculate that SLN stimulation causes endogenous release of adenosine that activates A(2A) receptors on GABAergic neurons, resulting in the release of GABA at inspiratory neurons and subsequent respiratory inhibition.     

Maturational and anesthetic effects on apneic thresholds in lambs

Periods of apnea are relatively common in newborns but rare in older infants. Postnatal changes in the response of the central neural respiratory circuits to afferent inputs may have a role in the age-related incidence of apnea. Therefore we determined the central neural apneic threshold to CO2 and superior laryngeal nerve (SLN) stimulation in halothane-anesthetized newborn (4- to 7-day-old) and older (45- to 56-day-old) lambs. The animals were vagotomized, paralyzed, and mechanically ventilated with hyperoxic gas. Phrenic nerve activity served as a monitor of central respiratory output. The CO2 and SLN apneic thresholds were defined as the arterial PCO2 when phrenic activity began after hyperventilation, and the quantity of current applied to the SLN that abolished phrenic activity, respectively. At equivalent concentrations of halothane, newborn lambs had higher CO2 apneic thresholds (P less than 0.05) and lower SLN apneic thresholds (P less than 0.05) than did older lambs. Increasing concentrations of halothane decreased (P less than 0.05) the SLN apneic threshold and increased (P less than 0.05) the CO2 apneic threshold. Equal incremental changes in halothane concentration induced similar changes in the apneic thresholds of both ages of lambs. The data suggest that with maturation, the central neural respiratory circuits become more responsive to CO2 and less responsive to SLN afferents. Halothane alters central neural responsiveness to these inputs in both ages similarly.     

Influences from laryngeal afferents on expiratory bulbospinal neurons and motoneurons

The purpose of this study is to analyze the reflex effects of laryngeal afferent activation on respiratory patterns in anesthetized, vagotomized, paralyzed, ventilated cats. We recorded simultaneously from the phrenic nerve, T10 internal intercostal nerve, and single bulbospinal expiratory neurons of the caudal ventral respiratory group (VRG). Laryngeal afferents were activated by electrical stimulation of the superior laryngeal nerve (SLN) or by cold-water infusion into the larynx. Both types of stimuli caused inhibition of phrenic activity and facilitation of internal intercostal nerve activity, indicating expiratory effort. The activity of 46 bulbospinal expiratory cells was depressed during SLN electrical stimulation, and 13 of them were completely inhibited. In 44 of 56 neurons tested, mean firing frequency (FFmean) was decreased in response to cold-water infusion and 8 others responded with increased FFmean; in the remaining 4 neurons, FFmean was unchanged. Possible reasons for different neuronal responses to SLN electrical stimulation and water infusion are discussed. We conclude that bulbospinal expiratory neurons of VRG were not the source of the reflex motoneuronal expiratory-like activity produced by SLN stimulation. Other, not yet identified inputs to spinal expiratory motoneurons are activated during this experimental condition.     

Recovery from central apnea: effect of stimulus duration and end-tidal CO2 partial pressure

The present study was designed to investigate the effect of stimulus duration and chemosensory input on the recovery of central respiratory activity from apnea induced by superior laryngeal nerve (SLN) electrical stimulation. Newborn piglets less than 8 days of age were anesthetized, paralyzed, and mechanically ventilated at differing levels of end-tidal CO2 partial pressure (PCO2). The vagi were cut bilaterally in the neck. Integrated phrenic nerve activity was used as the index of respiratory activity. SLN stimulation caused apnea that persisted after stimulus cessation. The length of apnea following stimulus cessation was directly related to stimulus duration and inversely related to end-tidal PCO2. After apnea, respiratory activity returned gradually to the initial control level. The recovery pattern was well described by a linear regression function using the natural logarithm of time as the independent variable. Prolonging stimulus duration progressively inhibited the amount of initial respiratory activity following apnea. On the other hand, the rate of respiratory recovery was independent of stimulus duration and, except at low end-tidal PCO2 following long (30 s) stimuli, was independent of the end-tidal PCO2 level. These results demonstrate that a long-acting central mechanism regulates recovery from apnea induced by SLN stimulation.     

Fictive cough in the cat.

Experiments were performed to determine whether cough could be elicited in paralyzed cats ventilated on a respiratory cycle-triggered pump. Midcollicular decerebrate cats were paralyzed and artificially ventilated on a phrenic-triggered pump. Phrenic and cranial iliohypogastric nerve efferent activities were recorded. Cough was elicited by electrical stimulation of the superior laryngeal nerve (SLN) or probing the intrathoracic trachea. Fictive coughs induced by electrical stimulation of the SLN or mechanical stimulation of the intrathoracic trachea consisted of large-amplitude bursts in phrenic discharge immediately followed by large bursts in cranial iliohypogastric discharge. During fictive cough, phrenic postinspiratory discharge was reduced relative to control cycles. Codeine (0.03-1 mg/kg iv) decreased both SLN- and probe-induced fictive cough. I conclude that fictive cough can be produced in paralyzed cats ventilated on a phrenic-triggered pump. Furthermore, fictive cough can be produced in the absence of afferent feedback associated with active expiration.     

Some effects of superior laryngeal nerve stimulation on sympathetic preganglionic neuron firing

Repetitive electrical stimulation of afferent fibers in the superior laryngeal nerve (SLN) evoked depressant or excitatory effects on sympathetic preganglionic neurons of the cervical trunk in Nembutal-anesthetized, paralyzed, artifically ventilated cats. The depressant effect, which consisted of suppression of the inspiration-synchronous discharge of units with such firing pattern, was obtained at low strength and frequency of stimulation (e.g. 600 mV, 30 Hz) and was absent at end-tidal CO2 values below threshold for phrenic nerve activity. The excitatory effect required higher intensity and frequency of stimulation and was CO2 independent. The depressant effect on sympathetic preganglionic neurons with inspiratory firing pattern seemed a replica of the inspiration-inhibitory effect observed on phrenic motoneurons. Hence, it could be attributed to the known inhibition by the SLN of central inspiratory activity, if it is assumed that this is a common driver for phrenic motoneurons and some sympathetic preganglionic neurons. The excitatory effect, on the other hand, appears to be due to connections of SLN afferents with sympathetic preganglionic neurons, independent of the respiratory center.     

Antagonistic interaction of laryngeal and central chemoreceptor respiratory reflexes.

Stimulation of laryngeal afferent fibers evokes a profound reflex inhibition of central respiratory drive. The interaction of this airway reflex with chemoreceptive ventilatory control mechanisms is poorly understood. The present study was undertaken to determine whether there is significant interaction between the effects of central chemoreceptor and laryngeal afferent stimulation on central inspiratory activity and, if so, to also determine the nature of the interaction. The effect of electrical stimulation of the superior laryngeal nerve (SLN) on the timing and intensity of central inspiratory activity was determined from the rectified and filtered phrenic neurogram in 10 dogs. Each dogs was decerebrated, artificially ventilated, vagotomized, and had the carotid bodies denervated. In each case, stimulation of the right SLN at 3 and 10 Hz caused a frequency-dependent slowing or arrest of central inspiratory activity. Increases in arterial PCO2 (PaCO2) attenuated the absolute level of inhibition of central inspiratory activity recorded during both SLN stimulation and control periods. Tp clarify the nature of the interaction between chemoreceptor and laryngeal afferent stimulation, the relationship between PaCO2 and central inspiratory activity was investigated during stimulation of the SLN at 0, 3, and 10 Hz. Control central inspiratory activity increased as a sigmoidal function of PaCO2. This sigmoidal relationship was greatly depressed during SLN stimulation but did not appear to be shifted along the PaCO2 axis. The results of this study therefore suggest that the interaction between central chemoreceptor and laryngeal afferent stimulation is multiplicative: the inhibition of the central inspiratory activity is mediated by an attenuation and not a resetting of central chemoreflexes.     

Central inspiratory influence on abdominal expiratory nerve activity

Our purpose was to determine whether the intensity of abdominal expiratory nerve discharge is conditioned by the intensity of the preceding inspiratory phrenic discharge, independent of mechanical and chemical afferent influences. In decerebrate, paralyzed, vagotomized cats with bilateral pneumothoraxes, we recorded phrenic and abdominal (cranial iliohypogastric nerve, L1) nerve activities at hyperoxic normocapnia. We reduced the duration and intensity (i.e., integrated peak height) of phrenic nerve discharge for single cycles by stimulating the cut central end of the superior laryngeal nerve (SLN) during the central inspiratory phase (75 microA, 20-50 Hz, 0.2-ms pulse). Premature termination of inspiration consistently reduced expiratory duration (TE) and abdominal expiratory nerve activity (area of integrated neurogram), but the average reduction in TE was much less than the reduction in abdominal nerve activity (14 vs. 51%). Stimulation of the cut central end of the vagus nerve yielded similar results, as did spontaneous premature terminations of inspiration, which we observed in one cat. SLN stimulation during hyperoxic hypercapnia resulted in more variable responses, and higher stimulation frequencies were usually required to abort inspiration. SLN (or vagal) stimulation during expiration consistently increased abdominal expiratory nerve activity. We speculate that this facilitatory response is gated during inspiration, thereby allowing the inspiratory conditioning effect on the subsequent expiration to be expressed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Entrainment of respiratory rhythm to respiratory oscillations of arterial PCO2 in vagotomized dogs.

The aim of this study was to demonstrate that the medullary respiratory rhythm generator is capable of entraining to respiratory oscillations of arterial PCO2 (CO2 oscillations). We used 10 anesthetized, paralyzed, vagotomized, and mechanically ventilated dogs. First, rate of mechanical ventilation was manually adjusted so that it matched the dog's spontaneous respiratory rate, which established a constant phase relationship between the mechanical ventilation and the burst of phrenic neurogram (initial phase). Then this phase relationship was temporally disturbed by a brief electrical stimulation of the superior laryngeal nerve (SLN). In the control group, the initial phase and the steady-state phase relationship after SLN stimulation were randomly distributed within the phase plane, implying no interaction between the respiratory center and mechanical ventilation. In contrast, when CO2 output from the lung was increased 2.6-fold above the control level by venous CO2 loading, the initial phase and the steady-state phase after SLN stimulation were locked in such a way that the onset of the burst of phrenic neurogram coincided with the peak of CO2 oscillations. This was not demonstrated when the dog was made hyperoxic. We therefore conclude that the respiratory center could entrain to phasic chemical afferent inputs originating from CO2 oscillations, provided they are considerably amplified.     

Characterization of the postnatal development of superior laryngeal nerve fibers in the postnatal kitten

A combined electron microscopic and electrophysiological study of the superior laryngeal nerve (SLN) was undertaken in postnatal kittens ranging in age from 1–63 days. The superior laryngeal nerve is predominantly a sensory nerve innervating the upper respiratory tract, and could play a potential role in the modulation of respiration, particularly in the infant animal. Distribution of fibers in the developing SLN indicates that within the first postnatal month, 75% of the fibers are unmyelinated, and by 42 days, the myelinated fibers increase in number to approximately 50%. Of the myelinated fibers present in the one day old kitten, 3–4% of those exceeded 4 μm in total diameter, which is the minimum diameter for normal conduction velocity of action potentials. The distribution of the diameter sizes of the myelinated fibers is bell-shaped within the first 45 days after which the curve becomes skewed to the right (43–61 days; mean 2.6 μm, range 0.5–8.0 μm) to resemble the adult distribution of myelinated fibers (mean 4.2 μm, range 1.6–13.0 μm). Two variable plots of myelin width to axon diameter suggest a steeper slope for developing fibers as compared to that of the adult fibers. Electrical stimulation of the sectioned SLN indicates that evoked potentials could be recorded from the recurrent laryngeal nerve innervating the laryngeal intrinsic muscles and from the hypoglossal nerve to the tongue musculature in the youngest kittens tested (i.e., age 9 days). Stimulation at selected frequencies of 3 and 30/sec readily evoked apnea in the youngest kitten studied (i.e., age 5 days), while swallowing was more readily evoked at 28–30 days when using electrical stimulation.     

GABA antagonism reverses hypoxic respiratory depression in the cat

We assessed the role of gamma-aminobutyric acid (GABA) as a potential causative agent of hypoxic respiratory depression by monitoring the response of the phrenic neurogram to systemic infusion of the GABA antagonist bicuculline (0.01 mg.kg-1.min-1) under control conditions and during isocapnic brain hypoxia produced by CO inhalation in separate groups of anesthetized, glomectomized, vagotomized, paralyzed, and ventilated cats with blood pressure held constant. The maximum effect of bicuculline in subseizure doses in control cats was to increase minute phrenic activity to 151 +/- 14% of preinfusion values. Infusion was continued until seizure activity was seen in the electroencephalogram. A 53% decrease of arterial O2 content resulted in a marked reduction of both peak phrenic amplitude and phrenic firing frequency to 16 and 64% of control values, respectively. Infusion of bicuculline while the level of hypoxia was maintained constant restored both peak phrenic amplitude and phrenic firing frequency to prehypoxic levels. The maximum effect of bicuculline was to increase minute phrenic activity to 123 +/- 13% of the prehypoxic value. These results suggest that although GABA has only a modest role in determining the output of the control phrenic neurogram, a significant portion of the phrenic depression that occurs during hypoxia can be attributed to inhibition of respiratory neurons by GABA.     

Laryngeal apnea in rat pups: effects of age and body temperature.

In neonatal mammals of many species, including human infants, apnea and other reflex responses frequently arise from stimulation of laryngeal receptors by ingested or regurgitated liquids. These reflexes, mediated by afferents in the superior laryngeal nerves (SLNs), are collectively known as the laryngeal chemoreflex (LCR) and are suspected to be responsible for some cases of the sudden infant death syndrome (SIDS). The LCR is strongly enhanced by mild increases in body temperature in decerebrate piglets, a finding that is of interest because SIDS victims are often found in overheated environments. Because of the experimental advantages of studying reflex development and mechanisms in neonatal rodents, we have developed methods for eliciting laryngeal apnea in anesthetized rat pups and have examined the influence of mild hyperthermia in animals ranging in age from 3 to 21 days. We found that apnea and respiratory disruption, elicited either by intralaryngeal water or by electrical stimulation of the SLN, occurred at all ages studied. Raising body temperature by 2-3 degrees C prolonged the respiratory disturbance in response to either stimulus. This effect of hyperthermia was prominent in the youngest animals and diminished with age. We conclude that many studies of the LCR restricted to larger neonatal animals in the past can be performed in infant rodents using appropriate methods. Moreover, the developmental changes in the LCR and in the thermal modulation of the LCR seem to follow different temporal profiles, implying that distinct neurophysiological processes may mediate the LCR and thermal prolongation of the LCR.     

Association of Anemia with Reduced Central Respiratory Drive in the Piglet

Central respiratory drive was studied in 13 piglets of both sexes varying in age from 19 to 67 days. The distal trachea was cannulated and the maximum rate of isometric inspiratory pressure change (dP/dt)_max, was measured at the airway. Curves were constructed relating this measurement to changes in arterial PCO₂ during carbon dioxide rebreathing. Data were obtained at intervals corresponding to stepwise reductions in central respiratory drive produced by added chloralose anaesthesia. Laryngeal reflex activation was achieved by electrical stimulation of the superior laryngeal nerves (SLN). This caused permanent respiratory arrest at a critical level of central respiratory depression expressed as the slope of the curve relating (dP/dt)_max to arterial PCO₂. Severely anemic piglets showed markedly decreased central respiratory drive at a given dose of anesthesia compared to controls. This was consistent with the observed greater sensitivity to laryngeal nerve stimulation in these animals. It is concluded that anemia may be associated with impaired functional maturation of central respiratory mechanisms and consequent susceptibility to laryngeal reflex apnea and asphyxial death. These observations may pertain to factors associated with the sudden infant death syndrome.     

中缝核与阻塞性睡眠呼吸暂停关系的实验研究

本实验在６４只氨基甲酸乙酯麻醉、断双侧迷走神经、自主呼吸的健康家兔上进行,观察电、化学刺激中缝背核（ＮＲＤ）、中缝大核（ＮＲＭ）对颏舌肌和膈肌肌电、以及窒息增幅反应（ＡＡＲＡ）的作用。结果如下：１．长串电脉冲刺激ＮＲＤ,颏舌肌和膈肌肌电幅度明显升高,在刺激过程中呈持续性吸气相放电。长串电脉冲刺激ＮＲＭ,颏舌肌和膈肌肌电幅度显著抑制,呼吸节律减弱或消失;２．于ＮＲＤ微量注入谷氨酸钠,颏舌肌和膈肌肌电幅度升高,频率加快。在ＮＲＭ微量注射谷氨酸钠,ＡＡＲＡ降低。上述结果与电刺激ＮＲＤ、ＮＲＭ的效应基本一致;３．ＮＲＭ内微量注入吗啡,颏舌肌和膈肌的ＡＡＲＡ峰值被抑制,潜伏期延长,恢复期缩短。若注射吗啡后５ｍｉｎ再微量注入纳络酮,则吗啡的抑制效应减弱。结果提示：中缝核和阿片肽类物质对颏舌肌有重要的调制作用,可能与阻塞性睡眠呼吸暂停的发生有关     

Maturation of respiratory reflex responses in the piglet

Stimulation of chemo-, irritant, and pulmonary C-fiber receptors reflexly constricts airway smooth muscle and alters ventilation in mature animals. These reflex responses of airway smooth muscle have, however, not been clearly characterized during early development. In this study we compared the maturation of reflex pathways regulating airway smooth muscle tone and ventilation in anesthetized, paralyzed, and artificially ventilated 2- to 3- and 10-wk-old piglets. Tracheal smooth muscle tension was measured from an open tracheal segment by use of a force transducer, and phrenic nerve activity was measured from a proximal cut end of the phrenic nerve. Inhalation of 7% CO2 caused a transient increase in tracheal tension in both age groups, whereas hypoxia caused no airway smooth muscle response in either group. The phrenic responses to 7% CO2 and 12% O2 were comparable in both age groups. Lung deflation and capsaicin (20 micrograms/kg iv) administration did not alter tracheal tension in the younger piglets but caused tracheal tension to increase by 87 +/- 28 and 31 +/- 10%, respectively, in the older animals (both P less than 0.05). In contrast, phrenic response to both stimuli was comparable between ages: deflation increased phrenic activity while capsaicin induced neural apnea. Laryngeal stimulation did not increase tracheal tension but induced neural apnea in both age groups. These data demonstrate that between 2 and 10 wk of life, piglets exhibit developmental changes in the reflex responses of airway smooth muscle situated in the larger airways in response to irritant and C-fiber but not chemoreceptor stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of lung volume on activities of branches of the recurrent laryngeal nerve

To investigate the influence of inspiratory lung inflation on the respiratory activities of laryngeal motor nerves, vagally intact decerebrate paralyzed cats were ventilated by a servorespirator in accordance with their own phrenic nerve activity. Records were made of the activities of the phrenic nerve, the superior laryngeal nerve (SLN), the recurrent laryngeal nerve (RLN), and the intralaryngeal branches of the RLN serving the thyroarytenoid (TA) and posterior cricoarytenoid (PCA) muscles. Neural activities were assessed in the steady state at different end-tidal O2 and CO2 concentrations. Transient responses to withholding inspiratory lung inflation and to preventing expiratory lung emptying were also studied. Hypercapnia and hypoxia increased the inspiratory activities of the phrenic nerve, SLN, RLN, and its PCA branch. TA inspiratory activity was not changed. Expiratory activities of RLN, PCA, and TA were all increased in hypoxia. When lung inflation was withheld, neural inspiratory duration and the inspiratory activities of all nerves increased. The subsequent period of neural expiration was marked by an exaggerated burst of activity by the TA branch of the RLN. TA expiratory activity was also sharply increased after inspiratory efforts that were reflexly delayed by the prevention of lung emptying. TA activity in expiration was enhanced after vagotomy and was usually more prominent than when lung inflation was withheld before vagal section. The results demonstrate the importance and complexity of the influence of vagal afferents on laryngeal motor activity.     

Preliminary results on the splanchnico-laryngeal reflex in the cat]

Electrical stimulation of low threshold splanchnic afferent nerves in lightly anesthetized cat results in phrenic and recurrent laryngeal nerve responses. Both phrenic and recurrent laryngeal inspiratory nerve activities are inhibited, whereas expiratory recurrent nerve activity is triggered and even increased. The significance of this reflex is discussed in relation to laryngeal adductor muscle contractions and the abdominal pressure increase.     

Neural regulation of lysozyme secretion from tracheal submucosal glands of ferrets in vivo.

To investigate how central and peripheral nerves affect lysozyme secretion from tracheal submucosal glands in ferrets we injected substance P (20 nmol/kg in 200 microliters) intracisternally or intravenously into anesthetized artificially ventilated ferrets. We collected 3-ml samples from a perfused (3 ml/5 min) segment of trachea in situ during 15 min before and 45 min after injection of substance P. Content of lysozyme, a specific marker of tracheal submucosal gland serous cell secretion in ferrets, was measured spectrophotometrically in each sample. Intracisternal substance P increased peak lysozyme output threefold compared with baseline. This increase was abolished completely by cutting both superior laryngeal nerves (SLN) and was partially inhibited by atropine, phentolamine, or propranolol. Intravenous substance P increased peak lysozyme output 10-fold compared with baseline. This increase was partly abolished by cutting both SLN. We concluded that intracisternal substance P stimulated the central nervous system (CNS) and activated cholinergic, adrenergic, and nonadrenergic noncholinergic secretomotor nerves to tracheal glands and that intravenous substance P increased lysozyme secretion both by acting directly on tracheal glands and indirectly on the CNS to activate secretomotor nerves.     

Inspiratory rhythm in airway smooth muscle tone

In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.     

刺激兔丘脑不同核团和胼胝体引起的膈神经放电效应

实验在33例清醒、肌肉麻痹和切断双侧迷走神经的家兔上进行,观察了刺激丘脑不同核团(VIL,VL,VPM 和 MI)和胼胝体纤维以激活皮层时膈神经的放电效应。当在吸气相(膈神经放电时)给予上述核团及胼胝体纤维电脉冲刺激,可使膈神经放电短暂抑制,随后的呼气相缩短、吸气相提前出现。如果在呼气相刺激上述核团,也能使该呼气时相缩短,随后的吸气时相提前出现。当在皮层接受 VL 投射的局部区域给予回苏灵后,再刺激 VL,皮层诱发电位增大,除使原先的膈神经放电效应更为明显外,还可在呼气相刺激时引起膈神经即刻的短暂放电。以上实验结果提示,当用回苏灵使皮层活动加强后,刺激丘脑 VL 引起的膈神经放电效应明显增强。损毁红核或切断皮层下行传导束但保留皮层脊髓束后,刺激丘脑引起的膈神经放电效应均不受影响,表明传入冲动激活皮层后引起的膈神经放电效应可能主要经皮层脊髓束下传,而皮层红核脊髓束不起重要作用。