Diaphragm Electromyogram Research Articles

Regulation of expiratory muscles during postnatal development in anesthetized piglets.

We compared maturation of the responses of the rib cage [triangularis sterni (TS)] and abdominal [transversus abdominis (TA)] expiratory muscles with each other and with the responses of the diaphragm (DIA) during hypercarbic and hypoxic stimulation. Studies were performed in anesthetized (urethan and chloralose) piglets of two age groups (< 6 days, n = 10; 14-21 days, n = 11) before and after bilateral cervical vagotomy. Hypercarbia (7% CO2-93% O2) was associated with comparable sustained increases in the minute electromyograms (EMGs) of both TS and TA, which were closely coupled to the DIA responses in both age groups. Hypoxia (12% O2-88% N2) caused a biphasic response of the minute EMG of both expiratory muscles and DIA; these biphasic responses were less prominent at 14-21 days than at < 6 days. Vagotomy caused an increase in the amplitude of both TS and TA (38 +/- 30 and 27 +/- 21%, respectively) as well as the DIA (45 +/- 16%) but did not affect their relative responses to chemostimulation. We conclude that during postnatal development 1) the rib cage and abdominal expiratory muscle responses to chemostimulation are coupled to each other and parallel those of the DIA and 2) the presence of vagal afferents attenuates the drive to both inspiratory and expiratory motoneurons under the current experimental conditions but does not influence the relative responses of expiratory muscles and DIA to hypercarbia or hypoxia. We speculate that comparable activation of inspiratory and expiratory pumping muscles serves to stabilize respiratory control in the face of altered chemosensory or vagal inputs during early postnatal life.

Anatomical relationship between crural diaphragm and lower oesophageal sphincter: an electrophysiological study

AbstractWe performed electrophysiological studies in 12 normal, healthy subjects to determine the relative locations of the lower oesophageal sphincter, crural diaphragm and squamocolumnar junction. Oesophagogastric junction pressure, crural diaphragm electromyogram and mucosal potential difference were measured using a specially designed catheter. This catheter had a side hole to measure pressure and electrodes placed around the side hole for crural diaphragm electromyogram recordings. Mucosal potential difference was measured at the side hole that measured pressure. Recordings were obtained using a motorized rapid pullthrough at a constant speed of 0.85 cm/sec. Rapid pullthroughs were performed under the following conditions: (a) end expiration (diaphragm relaxed), (b) during a sustained maximal contraction of the diaphragm, and (c) during 50% of maximal diaphragmatic contraction. Our results show that the lower oesophageal sphincter is 4.4 cm in length, 2 cm of which is located in the abdomen. The crural diaphragm is 1.7 cm in length and surrounds the proximal half of the lower oesophageal sphincter. The squamocolumnar junction is located in the upper half of the lower oesophageal sphincter in the majority of subjects. The relative location of the lower oesophageal sphincter to the crural diaphragm does not change during diaphragmatic contraction. We conclude that a part of the lower oesophageal sphincter is located in the abdomen. The intra‐abdominal location of the lower oesophageal sphincter may be important for its anti‐reflux barrier function.

Central and peripheral cardio-respiratory effects of saxitoxin (STX) in urethane-anesthetized guinea-pigs

F.-C. T. Chang, B. J. Benton, R. A. Lenz and B. R. Capacio. Central and peripheral cardio-respiratory effects of saxitoxin (STX) in urethane-anesthetized guinea-pigs. Toxicon 31, 645–664, 1993.—Effects of saxitoxin (STX; 10 μg/kg; i.p.) on cardio-respiratory activites were evaluated in urethane-anesthetized guinea-pigs. Concurrent recordings were made of electrocorticogram (ECoG), bulbar respiratory-related unit activities, diaphragmatic electromyogram (DEMG), electrocardiogram (Lead II ECG), blood pressure, heart rate, end-tidal CO 2, arterial O 2/CO 2 tensions, and arterial pH. The average time to STX-induced respiratory failure was about 10 min. The most striking effect prior to apnea was a state of progressive bradypnea which emerged 5–7 min after the toxin administration. Other noteworthy responses included (i) a time-dependent decrease in ECoG amplitudes which typically began before the development of a bradypneic profile; (ii) an increasing degree of diaphragm neuromuscular blockade; (iii) a state of combined hypercapnia and uncompensated acidemia; (iv) a declining blood pressure; (v) an incrementally dysfunctional myocardial performance; and (vi) an increasingly degenerative central respiratory activity profile which ultimately culminated in a complete loss of central respiratory drive. The therapeutic effect of intratracheally administered oxygen was equivocal in that the cardio-respiratory activities, be they of central of peripheral nature, remained conspicuously dysfunctional and precarious despite 100% oxygen ventilation. What can be inferred from this study is two-fold. First, STX-induced ventilatory insufficiency can be attributed to a loss of functional integrity of both central and peripheral respiratory system components. That is, although diaphragm blockade contributes significantly to STX-induced respiratory failure, analyses of single respiratory unit activity data reveale d that the central respiratory rhythmogenic mechanism also appeared to play a pivotal role in the development of a bradypneic profile which promotes, and directly causes, a complete loss of respiratory drive. Second, a state of unabating depression of central respiratory activities, which seemed to be refractory to the effect of O 2, suggests STX has a direct and persistent action on medullary rhythmogenic mechanisms. In conclusion, these findings indicate that both central and peripheral cardio-respiratory components are critically involved in STX-induced apnea, dysfunctional cardiovascular performance, and lethality.

Effects of acute sleep deprivation on control of the diaphragm during REM sleep in cats.

Recently, investigators demonstrated that acute sleep deprivation in healthy subjects results in significant periodic decrements in ventilation during recovery rapid-eye-movement (REM) sleep. The neural bases of such phenomena are unknown. The decrements in ventilation coincide with REM sleep-associated phasic activities, such as bursts of eye movements. The purpose of this study was to determine the effects of acute sleep deprivation on control of diaphragm activity during recovery REM sleep. In chronically implanted, naturally sleeping, unrestrained cats, we recorded the electroencephalogram, electrooculogram, pontogeniculooccipital waves, neck and diaphragmatic electromyograms, and the computed moving average of the diaphragm. Acute sleep deprivation resulted in an increase in REM sleep-associated phasic alterations in diaphragmatic control during recovery REM sleep. There was an increase in the percentage of bursts during recovery REM sleep with reduced inspiratory drive. Acute sleep deprivation resulted in a substantial increase in the number of brief pauses (fractionations) in diaphragmatic activity during recovery REM sleep. Respiratory timing was also affected by sleep deprivation, with a reduced expiratory time resulting in an increased duty cycle ratio. There was a significant increase in the percentage of bursts with decremented peak amplitude of the moving average of the diaphragm, a measure that correlates with tidal volume. Despite significant increases in respiratory-related phasic alterations, there were no parallel increases in excitatory phenomena, i.e., eye movements or pontogeniculooccipital waves. These results imply that respiratory control mechanisms in REM sleep are sensitive to the effects of prior sleep deprivation.

Response of upper airway and chest wall muscles to selective brain stem hypoxia in the newborn

In animals with intact peripheral chemosensory afferents, hypoxia differentially affects upper airway (UA) and chest wall muscles. To determine the contribution of brain stem (BS) hypoxia to the response of UA and chest wall muscles during early life, we perfused the BS through a vertebral artery intermittently with blood from an extracorporeal circuit in nine newborn piglets (age 1-5 days). BS perfusions were performed with hypoxemic blood (arterial PO2 32 +/- 6 to 38 +/- 8 Torr) with different levels of BS PCO2 (28 +/- 2, 37 +/- 4, and 56 +/- 5 Torr) while systemic normocapnic hyperoxia was maintained (arterial PCO2 36 +/- 3 to 40 +/- 6 Torr, arterial PO2 345 +/- 73 to 392 +/- 37 Torr). Electromyograms (EMGs) of alae nasi (AN), external intercostal (EI), and diaphragm (DIA) were recorded. Normocapnic hypoxia of the BS induced a sustained increase in AN EMG (P < 0.01, analysis of variance) and depression of EI and DIA EMGs without a transient increase. These contrasting responses were also observed during hypocapnic and hypercapnic hypoxia of the BS and were not affected by inputs from the peripheral chemoreceptors or rostral cerebral structures that were not exposed to hypoxia. We conclude that, despite eliciting the known central respiratory depression, BS hypoxia causes an increase in the respiratory drive to an UA airway muscle. Thus, BS hypoxia elicits a selective rather than a generalized respiratory muscle depression. The respiratory muscles with high energy expenditure (DIA and EI) are depressed while UA muscles are stimulated or disinhibited. This response is independent of the level of BS arterial PCO2.

Respiratory response to abdominal and rib cage muscle paralysis in dogs

To assess the respiratory response to abdominal and rib cage muscle paralysis, we measured tidal volume, esophageal and gastric pressures, arterial blood gases, and the electromyogram (EMG) of the diaphragm during progressive epidural anesthesia (lidocaine 2%) in 35 supine anesthetized dogs. The EMG activity of the diaphragm was measured with fine-wire electrodes; the abdominal cavity was thus left intact. Paralysis of the abdominal muscles alone did not produce any alterations. In contrast, when all rib cage muscles were also paralyzed, there were substantial increases in the peak height and the rate of rise of diaphragmatic EMG activity that were associated with a decrease in tidal volume and an increase in arterial PCO2 (PaCO2); swings in transdiaphragmatic pressure, however, were unchanged. The increased diaphragmatic activation due to rib cage muscle paralysis persisted after bilateral cervical vagotomy and was well explained by the increased PaCO2. These observations indicate that in the dog 1) the rib cage muscles contribute significantly to tidal volume, and their paralysis causes, through the increased hypercapnic drive, a compensatory increase in diaphragmatic activation; and 2) the rib cage inspiratory muscles enhance the diaphragm's ability to generate pressure during breathing.

Mu- vs. delta-opioid influence on respiratory and sleep behavior during development.

The role of mu- vs. delta-opioid receptors in modulating cardiorespiratory and sleep/wake behavior was studied in sixteen 4- to 11-, and 26- to 33-day-old chronically instrumented piglets. Each underwent 1.5-h recordings of sleep/wake state, diaphragmatic and posterior cricoarytenoid electromyogram (EMGdi, EMGpca), heart rate, and arterial pressure, pH, and gas tensions, before and after either naltrexone (2 mg/kg i.v.), a predominantly mu antagonist, or naltrindole (4 mg/kg i.v.), a specific delta antagonist. In younger piglets, 1) naltrindole, but not naltrexone, decreased percent of time spent in active and quite sleep and increased that in wakefulness, and 2) naltrexone, but not naltrindole, increased respiratory frequency, decreased the duration of EMGdi and EMGpca activity, and increased initial summed EMGdi activity, all independently of state. Older piglets exhibited 1) increased arousal with both drugs and 2) weaker stimulation of respiratory timing and no stimulation of EMGdi or EMGpca with naltrexone and enhanced EMGpca activity with naltrindole during transitional sleep only. Thus, in early neonatal life, delta-opioid systems modulate sleep/wake behavior, whereas mu systems modulate respiration. With age, these influences change and become less specific.

Optical imaging of the ventral medullary surface of cats: hypoxia-induced differences in neural activation

Large-array optical recording procedures provide the potential to examine simultaneous activity of large numbers of neurons. We applied this technique to examine regional neuronal activation on the ventral medullary surface (VMS) of cats during hypoxic challenges. VMS was exposed through a ventral surgical approach in eight adult cats under pentobarbital sodium anesthesia. Arterial pressure, end-tidal CO2, costal diaphragmatic electromyograms, and electrocardiograms were continuously monitored. A coherent image conduit with 12-microns-fiber resolution was attached to a charge-coupled device camera and positioned over the VMS. Reflected 700-nm light was digitized continuously at 2- to 3-s intervals during baseline period, hypoxic (6, 9, and 12% O2 in N2) exposure, and recovery. Forty images within each epoch were averaged and subtracted from baseline. Regional differences within the image were determined by analysis of variance procedures (alpha = 0.05). In caudal VMS, hypoxic challenges with 12% O2 consistently induced a regional diminution in reflected light (increased neural activity) that was rapid in onset and persisted for approximately 20 min after termination of exposure, well beyond the duration of discernible ventilatory alterations. In contrast, the same challenge resulted in decreased neural activity of similar duration in rostral VMS areas. Challenges with lower inspired concentrations of O2 reversed the pattern of diminished neural activity in rostral regions and led to a dose-dependent increase in neural activity, a dependency also observed in caudal VMS. We conclude that caudal VMS neurons demonstrate a unidirectional dose-dependent response pattern to hypoxic stimuli, whereas rostral VMS regions exhibit a bidirectional response to increasing hypoxic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Incidence and Natural History of Phrenic Neuropathy Occurring During Open Heart Surgery

To study the incidence of phrenic neuropathy following coronary artery bypass grafting and determine long-term outcome. Prospective observational. Surgical ICU in a university hospital, out-patient follow-up. Ninety-two consecutive patients undergoing open heart surgery. None. Chest radiographs (CXR) 48 to 72 h post-operatively, ultrasonography of diaphragm, phrenic nerve conduction studies, diaphragmatic electromyogram, each repeated every 1 to 3 months until normal. Seventy-eight of 92 (78 percent) patients had abnormal radiographs, 42 of 78 (54 percent) with abnormal CXRs had abnormal diaphragm motion, 24 of 42 (57 percent) with abnormal motion had phrenic neuropathy. Patients with normal diaphragm motion improved faster than those without; patients with normal nerve conduction (and abnormal motion) improved faster than those with abnormal nerve conduction. Phrenic neuropathy is relatively common if sensitive tests are utilized for diagnosis. Nerve conduction studies can predict duration of morbidity. Most patients have low morbidity and recover fully. Abnormal diaphragm motion alone is not diagnostic of phrenic nerve injury.

Costal and crural diaphragm function during CO2 rebreathing in awake dogs

If costal and crural diaphragm segments can perform as separate muscles, then CO2-stimulated ventilation may elicit differential segmental function. We studied diaphragm segmental length, shortening, and electromyogram (EMG) activity in 10 awake dogs chronically implanted with sonomicrometer transducers and EMG electrodes. During CO2 rebreathing, segmental shortening and EMG activity per whole tidal breath progressively increased, but segmental responses could not be differentiated at any level of CO2. With increasing CO2, resting end-expiratory length of both diaphragm segments increased. During the complete intrabreath inspiratory-expiratory cycle, costal and crural diaphragm revealed distinctive segmental function. At rest, crural shortening exceeded costal shortening in earliest inspiration, costal and especially crural shortening persisted into early expiration, and EMG activity of the crural segment was greater than that of the costal segment in earliest inspiration and showed more end-inspiratory/early expiratory [post-inspiratory inspiratory activity (PIIA)] activity. During CO2-stimulated breathing, neither segment shortened during the inspiratory flow of earliest inspiration. During CO2 rebreathing, shortening of the crural segment exceeded that of the costal segment during early inspiration and outlasted costal shortening during expiration; for both segments, shortening persisted after termination of inspiratory airflow. With increased CO2, EMG activity of the crural segment preceded that of the costal segment in earliest inspiration and was dominant into expiration, whereas costal EMG activity terminated abruptly with inspiratory flow. Thus, costal EMG PIIA was not evident during hypercapnia, whereas crural EMG PIIA was significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Regional diaphragmatic length and EMG activity during inspiratory pressure support and CPAP in awake sheep

We examined diaphragmatic mechanics in awake sheep during quiet breathing (QB) and the randomized application of 5, 10, and 15 cmH2O continuous positive airway pressure (CPAP), inspiratory pressure support (IPS), and equal combinations of IPS and CPAP (IPS/CPAP). We measured esophageal, gastric, and transdiaphragmatic (Pdi) pressures and regional length, shortening, and electromyogram (EMG) activity of both costal and crural diaphragmatic segments. Segmental resting length normalized to QB decreased during 15 cmH2O CPAP (costal, 19.2 +/- 3.3%; crural, 7.5 +/- 2.1%; P < 0.05) and during 15/15 cmH2O IPS/CPAP (costal 25.3 +/- 4.8%, crural 9.9 +/- 2.6%; P < 0.05). Only during 15 cmH2O IPS did costal shortening fraction increase (67% QB; P < 0.05). Compared with QB, during 15 cmH2O CPAP, end-tidal CO2 increased 6 Torr, regional EMG activity increased threefold, and Pdi increased 58%. During 15 cmH2O IPS these values decreased 3 Torr, threefold, and 44% respectively, but during IPS/CPAP they remained unchanged. Expiratory gastric pressure (Exp-Pga) reached 4.3 +/- 0.4 cmH2O at 15 cmH2O CPAP, but during IPS/CPAP Exp-Pga was less (maximum of 1.7 +/- 0.4 cmH2O) than at comparable CPAP (P < 0.05), despite the shorter diaphragmatic length. We conclude that: 1) IPS alters the actions of the diaphragm during CPAP, 2) Exp-Pga is poorly coupled to diaphragmatic end-expiratory length, and 3) both IPS and the release of Exp-Pga assist active diaphragmatic shortening.

Maternal marijuana smoking alters respiratory timing in the fetal lamb

The effect of single and repeated maternal marijuana smoke exposure on fetal breathing movements (FBMs) was investigated in 13 fetal lambs in the third trimester. These animals were surgically instrumented for long-term intrauterine recording of diaphragmatic electromyogram (EMG). Maternal inhalation of marijuana smoke [1.84% tetrahydrocannabinol (THC)] increased FBMs and resulted in a more continuous and regular breathing pattern. There was a significant increase in the number of breaths/h ( p < 0.01) and the incidence of FBMs ( p < 0.001) in the second hour. Breathing activity returned to presmoke level by the third hour. Duration of the longest breathing epoch was significantly increased from 16.8 ± 3.3 min to 31.9 ± 5.2 min( p < 0.005). Instantaneous breathing rate was much more stable in the second hour after marijuana exposure ( p < 0.01). Inhalation of placebo smoke did not result in any significant change in either overall breathing activity or continuity and stability of the breathing rate. The effects of marijuana smoke on fetal breathing were not observed after repeated smoke exposure. These results suggest that tolerance develops rapidly to the respiratory stimulating effect of marijuana smoke in the fetus.

Effect of methylxanthines on diaphragmatic fatigue in the piglet.

Studies in adult animal and human subjects have suggested that the methylxanthine drugs can delay the onset or attenuate the severity of diaphragmatic fatigue. We have investigated the effect of aminophylline and caffeine on the pressure-generating capacity of the fatigued diaphragm in 1-mo-old piglets. Measurements of ventilation, transdiaphragmatic pressure, blood gases and pH, diaphragmatic electromyogram, diaphragmatic pressure-frequency curve (PdiFC), diaphragmatic blood flow, and end-expiratory lung volume were obtained at baseline, after 90 min of inspiratory resistive loaded breathing (IRL), and again 30 min after methylxanthine infusion while still on IRL. IRL resulted in a significant decrease in minute ventilation secondary to a fall in tidal volume. Spontaneously generated transdiaphragmatic pressure increased 7-fold from baseline. EMG activity increased to both segments of the diaphragm. Abdominal expiratory muscle activity was noted after the onset of IRL and was accompanied by a fall in end-expiratory lung volume. The PdiFC was significantly decreased from baseline after 90 min of IRL, demonstrating diaphragmatic fatigue. Aminophylline did not alter the PdiFC of the diaphragm. Diaphragmatic electromyogram and tidal volume increased. No change in diaphragmatic blood flow was demonstrated after infusion of aminophylline. Serum theophylline levels averaged 117 +/- 11 mumol/L (21 +/- 2 micrograms/mL). Caffeine administration did not alter the PdiFC or the diaphragmatic electromyogram during IRL. Blood flow to both segments of the diaphragm decreased after caffeine infusion. Serum caffeine levels averaged 86 +/- 30 mumol/L (16.6 +/- 5.9 micrograms/mL).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of inspiratory resistive loaded breathing and hypoxemia on diaphragmatic function in the piglet.

The combined effects of inspiratory resistive loaded breathing (IRL) and hypoxemia on transdiaphragmatic pressure (Pdi) in nine 1-mo-old Yorkshire piglets were studied. IRL was adjusted to increase spontaneously generated Pdi five to six times above baseline but maintain arterial PCO2 < 70 Torr to prevent hypercapnic depression of diaphragmatic contractility. Measurements of ventilation, blood gases and pH, Pdi, diaphragmatic electromyogram, Pdi during phrenic nerve stimulation, diaphragmatic blood flow, and end-expiratory lung volume were obtained at baseline, after 2 h of IRL, and then after 1 h of hypoxemia (arterial PO2 approximately 40 Torr) combined with IRL. Diaphragmatic muscle samples were obtained after study completion and immediately frozen in liquid nitrogen for determination of tissue ATP, phosphocreatine, lactate, and glycogen levels. Ten 1-mo-old piglets were subjected to IRL alone and served as controls. IRL alone resulted in significant impairment of Pdi generation. The addition of hypoxemia for 1 h did not further compromise Pdi in comparison to control animals who were subjected to IRL alone. Blood flow to both the costal and crural segments of the diaphragm increased significantly during IRL; the addition of the hypoxemic stress resulted in further significant augmentation of blood flow to both segments of the diaphragm. No differences were noted in diaphragmatic muscle tissue ATP, phosphocreatine, or glycogen between control and IRL animals or between control and IRL plus hypoxemia animals. Muscle lactate levels increased significantly in the IRL plus hypoxemia animals only. The data from this study suggest that moderate hypoxemia during resistive-loaded breathing in the piglet does not accentuate diaphragmatic fatigue.

Blockade of NMDA receptor-channels by MK-801 alters breathing in adult rats

The role of N- methyl- d-aspartate (NMDA) receptor-channel activation in the production of respiratory pattern was studied by administration of the NMDA receptor-channel blocker (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801, 1–3 mg/kg, i.v.) to anesthetized adult rats. This dose of MK-801 blocked the excitatory effects of NMDA (applied iontophoretically) ob brainstem respiratory neurons. The predominant respiratory response to systemic MK-801 administration was an increase in inspiratory duration and a decrease in amplitude of diaphragm electromyogram and phrenic nerve discharge. Effects on inspiratory timing and amplitude were most pronounced when the rats were vagotomized. Significant changes in arterial blood gases and pH after systemic MK-801 administration in spontaneously breathing rats (vagi intact or cut) indicated that ventilation was depressed by NMDA receptor-channel antagonism. Respiratory timing changes in response to systemic MK-801 administration differed between two rat strains studied. Breathing patterns resembling apneusis, i.e., with irregular inspiratory durations prolonged 2- to 30-fold, occurred in 60% of the vagotomized, spontaneously breathing Sprague-Dawley rats and none of the Wistar rats. Thus, the breathing pattern in Sprague-Dawley rats is more sensitive to interference with NMDA-mediated mechanisms. We propose that respiratory pattern generation and transmission of rhythmic respiratory drive are mediated by synergistic activation of NMDA and non-NMDA receptors at brainstem and spinal cord sites.

Developmental changes in sequential activation of laryngeal abductor muscle and diaphragm in infants.

In animals and human adults, upper airway muscle activity usually precedes inspiratory diaphragm activity. We examined the interaction of the posterior cricoarytenoid muscle (PCA), which abducts the larynx, and the diaphragm (DIA) in the control of airflow in newborn infants to assess the effect of maturation on respiratory muscle sequence. We recorded tidal volume, airflow, and DIA and PCA electromyograms (EMG) in 12 full-term, 14 premature, and 10 premature infants with apnea treated with aminophylline. In most breaths, onset of PCA EMG activity preceded onset of DIA EMG activity (lead breaths). In all subjects, we also observed breaths (range 6-61%) in which PCA EMG onset followed DIA EMG onset (lag breaths). DIA neural inspiratory duration and the neuromechanical delay between DIA EMG onset and inspiratory flow were longer in lag than in lead breaths (P < 0.05 and P < 0.01, respectively). The frequency of lag breaths was greater in the premature infants [33 +/- 4% (SE)] than in either the full-term infants (21 +/- 3%, P < 0.03) or the premature infants with apnea treated with aminophylline (16 +/- 2%, P < 0.01). We conclude that the expected sequence of onset of PCA and DIA EMG activity is frequently disrupted in newborn infants. Both maturation and respiratory stimulation with aminophylline improve the coordination of the PCA and DIA.

Effect of bilateral vagotomy on oxygenation, arousal, and breathing movements in fetal sheep.

To investigate the effects of bilateral cervical vagotomy on arousal and breathing responses, we studied eight sham-operated and eight chronically instrumented unanesthetized vagotomized sheep fetuses between 136 and 144 days of gestation (term approximately 147 days). Each fetus was instrumented to record sleep states, diaphragmatic electromyogram, blood pressure, pH, and blood gas tensions. In a randomized order, fetal lungs were distended with four different O2 concentrations: 0 (100% N2), 21, 50, and 100% at a continuous positive airway pressure of 30 cmH2O via an in situ Y-endotracheal tube. Under control conditions, inspiratory time and the duration of the single longest breathing episode decreased from 598 +/- 99 (SD) ms and 24 +/- 10 min in sham group to 393 +/- 162 ms and 11.0 +/- 3.0 min in vagotomized group (P = 0.04 and 0.033), respectively. In response to lung distension with 100% N2, breathing time decreased from 44 +/- 17 to 20 +/- 18% (P = 0.045) in sham-operated fetuses, whereas it remained unchanged in the vagotomized group. In response to 100% O2, fetal arterial PO2 increased in five of eight fetuses sham-operated from 18.2 +/- 5.1 to 227 +/- 45 Torr (P = 0.0001) and in six of eight vagotomized fetuses from 18.5 +/- 4.4 to 172 +/- 39 Torr (P < 0.001). Although arousal was observed in all oxygenated fetuses at the onset of breathing, the duration of arousal was markedly attenuated in vagotomized fetuses (14 +/- 10 vs. 46 +/- 29 min in sham group; P = 0.024). Frequency and amplitude of breathing and respiratory output (frequency x amplitude) increased only in sham group (P = 0.02, 0.004, and 0.0002, respectively). We conclude that in response to lung distension and oxygenation, arousal and stimulation of breathing during active and quite sleep are critically dependent on intact vagal nerves.

Arterial oxygen tension threshold range for the onset of arousal and breathing in fetal sheep.

Mechanisms for the control of episodic fetal breathing movements or the onset of continuous breathing at birth remain unknown. Lung distension with 100% O2 at a continuous positive airway pressure of 30 cm H2O may induce arousal and continuous breathing. To investigate 1) the threshold range of arterial oxygen tension (PaO2) for the onset of arousal and breathing and 2) the graded response of breathing to various levels of PaO2, we studied 10 fetal sheep between 135 and 142 d of gestation (term = 147 +/- 2 d). Each fetus was instrumented to record sleep states, diaphragmatic electromyogram, arterial pH, and blood gas tensions. PaO2 threshold was determined through an indwelling O2 sensor catheter. Fetal lungs were distended at a continuous positive airway pressure of 40 cm H2O with 100% N2 or with O2 ranging from 40 to 100% via an in situ endotracheal tube. At the onset of arousal (n = 10), PaO2, arterial carbon dioxide tension, and Hb O2 saturation increased from control values of 21.7 +/- 0.75 torr (2.9 +/- 0.09 kPa), 41.8 +/- 1.1 torr (5.47 +/- 0.15 kPa), and 52.9 +/- 2.6% to 65.6 +/- 9.6 torr (8.74 +/- 1.28 kPa), 46.9 +/- 1.3 torr (6.25 +/- 0.17 kPa), and 92.9 +/- 2.06%, respectively, whereas the pH decreased from 7.31 +/- 0.006 to 7.27 +/- 0.009 (mean +/- SEM; p = 0.001, 0.04, 0.002, and 0.001, respectively). Seven of 10 fetuses breathed continuously. In these fetuses, PaO2 and arterial carbon dioxide tension further increased and pH decreased; however, no further significant increase in Hb O2 saturation was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

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

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

Immediate diaphragmatic electromyogram responses to imperceptible mechanical loads in conscious humans.

We used an esophageal electrode to measure the amplitude and neural inspiratory and expiratory (N TE) timing responses of crural diaphragmatic electrical activity in response to flow-resistive (R) and elastic (E) loads at or below the threshold for conscious detection, applied pseudorandomly to the oral airway of eight normal subjects. We observed a rapid first-breath neural reflex that modified respiratory timing such that N TE lengthened significantly in response to R loads in six of eight subjects and shortened in response to E loading in six of seven subjects. The prolongation of N TE with R loading resulted primarily from lengthening the portion of N TE during which phasic activity in the diaphragm is absent (TE NDIA), whereas E loading shortened N TE mainly by reducing TE NDIA. Most subjects responded to both types of loading by decreasing mean tonic diaphragmatic activity, the average level of muscle activity that exists when no phasic changes are occurring, as well as its variability. The observed timing responses are consistent in direction with optimally adaptive pattern regulation, whereas the modulation of tonic activity may be useful in neural regulation of end-expiratory lung volume.