Diaphragm Electromyogram Research Articles

Effects of increased end-expiratory lung volume on breathing in awake ponies

We studied the changes in breathing and respiratory muscle electromyograms (EMG) during passively induced increases in end-expiratory lung volume (EELV) in awake normal (N), hilar nerve-denervated (HND), carotid body-denervated (CBD), and HND + CBD ponies. EELV was increased by applying continuous negative pressure (-10 and -20 cmH2O) around the torso of the standing pony. In all groups, negative pressure produced sustained increases in EELV that were linearly related to the degree of negative pressure. Elevated EELV decreased breathing frequency (f) in N and CBD ponies but increased f in HND and HND + CBD ponies. When EELV was increased, tidal volume was unchanged or above control in N ponies but was below or near control in the other groups. In all groups during elevated EELV, arterial PCO2 initially decreased but then increased relative to control with isocapnia achieved after approximately 1.5 min. In all groups, the elevated EELV was accompanied by increased stimulation of the diaphragm as indicated by increased rate of rise of the integrated EMG (P less than 0.05). During elevated EELV, the duration of diaphragm EMG was reduced, but only in HND ponies was this reduction significant (P less than 0.05). In N ponies, the major effect of elevated EELV on the expiratory transversus abdominis (TA) muscle was an increase (P less than 0.05) in duration of activity and therefore total activity. The work of breathing was thus presumably shifted more to this muscle during elevated EELV. These changes in TA timing were not observed in HND and HND + CBD ponies during elevated EELV. We conclude that elevation of EELV, which presumably places the diaphragm on a less favorable portion of its length-tension relationship, results in compensatory increased stimulation of the diaphragm that is not critically dependent on hilar and carotid chemoreceptor afferents. However, hilar afferents do contribute to the changes in diaphragm and TA duration of activity during elevated EELV.

Effects of pentobarbital on respiratory functional dynamics in chronically instrumented guinea pigs

Respiratory effects of sodium pentobarbital (35 mg/kg; IP) were studied in guinea pigs chronically instrumented to permit concurrent recordings of bulbar respiratory-related units (RRUs), diaphragmatic electromyogram (DEMG), and electrocorticogram (ECoG). RRU activities were recorded from either the Bötzinger Complex (BOT; expiratory) or Nucleus para-Ambiguus (NpA; inspiratory). Pentobarbital-induced changes in respiratory-related activities were evaluated before, throughout the course of, and during recovery from, anesthesia. The most notable development following pentobarbital was a state of progressive bradypnea which was accompanied by a variety of complex changes in the amplitude and temporal attributes of RRU, DEMG and ECoG activities. As anesthetic effects progressed, the activity profiles of both BOT and NpA units underwent striking transformations from a behavioral and state-dependent wakefulness pattern to an activity profile characterized by i) a significantly augmented RRU cycle duration, burst duration and spike frequency; and, ii) an alteration to the pattern of within-burst spike frequency modulation. Along with changes in RRU activity, pentobarbital also produced a marked attenuation of the amplitudes of diaphragmatic activity as well as a discrete, time-dependent alteration in the amplitude and spectral characters of ECoG activities. Differences in BOT and NpA unit responses to alveolar CO 2 loading (ramp; 2% and 5%) across wakefulness and anesthesia states were also considerable. In addition to a depressed responsiveness to CO 2, the temporal attributes of BOT and NpA activity profiles also indicated an asymmetrical change under pentobarbital anesthesia. Taken together, these findings indicate that pentobarbital causes not only a fundamental alteration in bulbar rhythmogenic mechanisms, but also a differential influence on bulbar respiratory system components that are involved in the definition of the shape and the amplitude of central respiratory drive. In conclusion, this study offers, for the first time, direct evidence from physiologically and structurally intact preparations that the functional dynamics of respiratory system components are profoundly altered during pentobarbital anesthesia.

Effects of focal cooling of the ventral medullary surface on breathing pattern and blood pressure in dogs

We assessed the effect of focal graded cooling of the ventral medullary surface (VMS) on breathing pattern and blood pressure in 15 anesthetized, vagotomized and artificially ventilated dogs. Diaphragmatic electromyogram or phrenic neurogram, referred to as Ec, and blood pressure (BP) were obtained during localized (2 × 2 mm 2) cooling of the VMS. Greatest depression of both Ec and BP was obtained by cooling in the areas located 4–9 mm caudal to the foramen cecum (Fc) and lateral to the pyramids. Mild cooling in the e intermediate areas decreased both inspiratory duration (Ti) and the rate of rise of Ec (Ec/Ti), but respiratory rate was unchanged. Cooling of the rostal areas (0–3 mm from Fc) induced mild depression of Ec amplitude due to reduction in Ec/Ti without changing Ti, and prolonged expiratory duration (Te) significantly. Cooling of the caudal areas (12–18 mm from Fc) reduced Ec amplitude mildly due to reduction in Ti without affecting Ec/Ti, and shortened Te greatly. Cooling of the rostal areas produced mild fall in BP, but cooling of the caudal areas did not affect BP significantly. It is suggested that rostral and intermediate parts of the VMS participate in the shaping of inspiratory drive, whereas wide areas of the VMS including caudal part are involved in the determination of respiratory timing. It is also suggested that the rostal and intermediate parts, and not the caudal part, of the VMS are important in the regulation of vasomotor tone.

Bedside assessment of phrenic nerve function in infants and children

Phrenic nerve damage is widely recognized after cardiac operations and is associated with an increased morbidity and mortality. Retrospective studies in children have estimated a prevalence of phrenic damage of between 0.5% and 2.2%, but all these studies have limited their investigations to patients who have clinical problems postoperatively, and they have all used clinical or radiologic methods to diagnose the damage. These methods are indirect and hard to evaluate, making the accurate early diagnosis of phrenic nerve damage very difficult. Measurement of phrenic nerve conduction time (phrenic latency) allows direct evaluation of phrenic function and integrity, making it potentially much more specific than indirect methods. Using a simplified method of direct phrenic nerve stimulation, we have developed a method of measuring phrenic latency at the bedside in infants and children. A 1 Hz electrical stimulus is applied over the phrenic nerve in the neck and a diaphragmatic electromyogram from the seventh and eighth intercostal spaces is displayed on a storage oscilloscope. Phrenic latency can be measured directly from the screen. Using these methods we have now studied 37 children (aged 2 days to 15 years) before and after cardiac operations. Mean phrenic latency was 5.4 +/- 1.0 msec on the right and 5.4 +/- 1.0 msec on the left. Prolongation of phrenic latency by more than 2 msec was found in seven of 66 postoperative measurements (10.6%). These patients had a substantially worse postoperative course. We believe this technique to be an important contribution to the diagnosis of postoperative phrenic nerve damage, and one that can help in clinical practice to elucidate an important cause of postoperative morbidity and mortality.

Diaphragmatic force and substrate response to resistive loaded breathing in the piglet

Inspiratory resistive loaded (IRL) breathing results in hypoventilation and diaphragmatic fatigue in the piglet. We studied the effects of 6 h of IRL on ten 1-mo-old piglets. The load was adjusted to increase spontaneously generated transdiaphragmatic pressure five to six times baseline. Six 1-mo-old piglets acted as controls and were identically instrumented but were not subjected to IRL. Measurements of ventilation, blood gases and pH, diaphragmatic electromyogram, force-frequency curve, blood flow, and end-expiratory lung volume were obtained hourly. Diaphragmatic muscle samples were obtained after 6 h for determination of ATP, phosphocreatine, lactate, and glycogen levels. No changes occurred in the control animals. IRL resulted in a significant decrease in ventilation, an increase in diaphragmatic EMG, onset of abdominal expiratory muscle activity, and a fall in end-expiratory lung volume by 1 h. The force-frequency curve adjusted for lung volume change fell by 20% at all frequencies of stimulation at 1 h and by 40% at 6 h. Blood flow to the costal and crural diaphragm increased by 51 and 141%, respectively. No differences were noted in ATP, phosphocreatine, lactate, or glycogen between control and IRL animals. It is concluded that submaximal spontaneous contractions of the piglet diaphragm over a 6-h period cause a substantial decrease in its maximal force-generating capacity that is not related to substrate depletion.

Ovine Fetal Breathing and Swallowing Activity in Response to Plasma Glucose Changes

Fetal swallowing activity generally occurs simultaneously with fetal breathing movements (FBM) in sheep. The present study investigated the FBM and swallowing responses to altered fetal plasma glucose. Fetal lambs were chronically prepared with laryngeal, esophageal and diaphragm electromyogram (EMG) wires, an esophageal flow probe and vascular catheters. Beginning at 138 +/- 1 day, FBM and swallowing were monitored during control periods and in response to intravenous glucose infusions (14 mg/kg/min for 120 min) to fetuses of fed and fasted ewes. Glucose infusions to fetuses of fed ewes resulted in significant increases in fetal plasma glucose (21.2 +/- 0.7 to 40.5 +/- 1.9 mg/dl) and time breathing (46.2 +/- 6.3 to 60.0 +/- 9.5 min/2 h). In response to maternal fasting, fetal glucose levels (13.4 +/- 1.0 mg/dl) and time breathing (23.0 +/- 7.2 min/2 h) decreased significantly. Glucose infusion to fetuses of fasted ewes resulted in significant increases in time breathing (50.3 +/- 13.4 min/2 h) and diaphragmatic EMG activity (1,295 +/- 654 to 3,012 +/- 1,182 spikes/2 h). There was no change from basal levels of fetal EMG swallows (83.2 +/- 4.3 swallows/2 h) or esophageal flow (40.8 +/- 7.9 ml/2 h) in response to maternal fasting or fetal glucose infusions.

Breathing at birth and the associated blood gas an pH changes in the lamb

We examined the relationship between the initiation of breathing at birth and the timing of delivery of the chest in a group of 13 lambs undergoing spontaneous unassisted delivery at term. In 8 of 11 lambs with a diaphragm electromyogram or intrapleural pressure signal the first breath occured chest delivery. The first breath was always followed by a period of irregular and often powerful inspiratory effeorts. Some of these inspirations were followed by a forceful expiration. A regular respiratory rhythm never developed until the chest had delivered, suggesting that chest expansion is essential for the establishment of rhythm. Although Pa O 2 increased rapidly after birth, pHa declined and reached its lowest level approximately 20 minutes postnatally suggesting that considerable anaerobic metabolism occurs in the face of adequate arterial oxygenation. The level of respiratory activity in the first 30 min following birth did not appear to be related to arterial P O 2, P CO 2 or pH. Neither the appearance of the EMG activity of the first breath, nor blood samples taken from 2 lambs simultaneously with the first breath, suggested that the first breath was a gasp initiated by asphyxial blood gases. Our results therefore do not support the current hypothesis that the first breath is a gasp initiated by asphyxia accompanying delivery.

Electrical and mechanical inhibition of the crural diaphragm during transient relaxation of the lower esophageal sphincter

Electrical and mechanical correlates of crural diaphragm activity during swallow-induced and transient lower esophageal sphincter relaxation were monitored in 12 healthy subjects. Simultaneous esophageal manometric, pH, and crural diaphragm electromyogram recordings were performed for 1 hour in the postprandial period. Swallow-induced lower esophageal sphincter relaxation was associated with minimal inhibition of the crural diaphragm, but transient lower esophageal sphincter relaxation was accompanied by marked inhibition of the crural diaphragm. The degree of lower esophageal sphincter relaxation appeared to correlate with the degree of crural diaphragm inhibition during transient lower esophageal sphincter relaxation. Inhibition of crural diaphragm during transient lower esophageal sphincter relaxation may play an important role in facilitating flow across the gastroesophageal junction.

Influence of Carotid Denervation on the Arousal and Cardiopulmonary Responses to Upper Airway Obstruction in Lambs

Experiments were done on five lambs to determine if carotid denervation influences the arousal and cardiopulmonary responses to upper airway obstruction during sleep. Each lamb was anesthetized and instrumented for recordings of electrocorticogram, electro-oculogram, nuchal and diaphragm electromyograms, and measurements of arterial blood pressure and arterial Hb oxygen saturation. A tracheotomy was done and a fenestrated tracheotomy tube placed in the trachea. During the study, a 5 F balloon-tipped catheter was inserted into the tracheotomy tube so that air flow could be obstructed by inflating the balloon. No sooner than 3 d after surgery, measurements were made in quiet sleep and active sleep during control periods when the animal was breathing room air and during experimental periods of upper airway obstruction. Carotid denervation significantly affected the arousal response to upper airway obstruction. Arousal occurred during 14 of 14 epochs in quiet sleep and during 12 of 13 epochs in active sleep before the arterial Hb oxygen saturation decreased to 30%. However, the time to arousal was increased and the arterial Hb oxygen saturation at arousal was decreased in carotid-denervated lambs compared with what we have previously observed in carotid-intact lambs. These data provide evidence that the carotid chemoreceptors and/or carotid baroreceptors play a major role in causing arousal from sleep during upper airway obstruction in lambs. Our results may have implications for sudden infant death syndrome, because it is possible that alterations in the arousal response to respiratory stimuli play a role in sudden infant death.

Respiratory and cardiovascular effects of tetrodotoxin in urethane-anesthetized guinea pigs

Cardiorespiratory effects of tetrodotoxin (TTX) (15 μg/kg, i.p.) were investigated in urethane-anesthetized guinea pigs acutely instrumented for the recording of medullary respiratory-related units (RRUs), diaphragm electromyogram (DEMG), electrocorticogram (ECoG), electrocardiogram (ECG), blood pressure (BP), endtidal CO 2, and arterial O 2 and CO 2. Respiratory system responses showed a hyperventilatory profile during the initial stage of intoxication. This was followed by an abrupt onset of a progressive decrease in the respiratory frequency, and a respiratory rate depression-related respiratory failure. The average time to TTX-induced respiratory arrest and death was 10.3 ± 4.2 min. Concurrentlyecorded inspiratory and expiratory RRU activities indicated that respiration invariably failed in an end-expiratory. position as manifested by a sustained period of expiratory RRU discharge. The progressive rate depression prior to respiratory arrest was temporally correlated only to a concomitantly augmenting expiratory RRU discharge duration. Inspiratory RRU discharge duration, on the other hand, did not display any significant change throughout the course of intoxication. The asymmetry in RRU response patterns indicates either an expiratory network component's particular sensitivity to perturbation by TTX or a dissociative trend in some bulbar respiratory rhythmogenic mechanisms. Peripheral cardiorespiratory changes were also quite profound. These included a gradual and steadfast decline in BP, a steadily decreasing amplitude in DEMG oscillations, and a state of progressive hypercapnia and hypoxenia. Changes in heart rate and ECG waveform attributes prior to respiratory arrest were not appreciable. In conclusion, in addition to a variety of TTX-induced peripheral cardiorespiratory effects, findings from this study have revealed a central respiratory system component that appears to show an unusual sensitivity to perturbation by TTX. The significance of this unique phenomenon as it relates to the nature and extent of TTX-induced central respiratory depression is discussed.

Efficacy of Positive vs Negative Pressure Ventilation in Unloading the Respiratory Muscles

We compared the efficacy of positive pressure ventilation (PPV) vs negative pressure ventilation (NPV) in providing ventilatory muscle rest for five normal subjects and six patients with chronic obstructive pulmonary disease (COPD). All participants underwent measurement of transdiaphragmatic pressure (Pdi), pressure time integral of the diaphragm (PTI), integrated diaphragmatic electromyogram (iEMG), minute ventilation (Ve), tidal volume (Vt), and end-tidal CO2 (etCO2) during 15 minutes of PPV and NPV. For each subject, ventilator adjustments were made to obtain Ve similar to levels measured during quiet breathing (QB). We found that the iEMG, Pdi, PTI, and average coefficient of variation of the tidal volume (CV-Vt) were consistently lower during PPV as compared with NPV (p = 0.01). The iEMG normalized for Ve and Vt was also significantly lower during PPV (p = 0.01). During PPV, subjects were mildly hyperventilated (lower etCO2 and higher Ve) compared with QB and NPV, but no significant correlation was noted between the change in etCO2 and the change in iEMG. The change in PTI was significantly correlated with the change in iEMG (p less than 0.01). We conclude that in the short term, PPV is more effective than NPV in reducing diaphragmatic activity. Positive pressure ventilation may be the preferred method of assisted ventilation in future studies of ventilatory muscle rest therapy.

Endogenous opioid effects on abdominal muscle activity during inspiratory loading

In a previous study in unanesthetized goats, we demonstrated that continuous naloxone (NLX) administration during inspiratory flow-resistive loading (IRL) significantly increased tidal volume (VT) but not diaphragm electromyogram (EMGdi). End-expiratory gastric pressure did increase with NLX, implying that increased abdominal muscle activity may have accounted for the NLX effect. In the current study we directly tested the hypothesis that endogenous opioid elaboration depresses the abdominal muscle response to a continuous inspiratory flow-resistive load. In seven unanesthetized goats, VT, arterial blood gases, EMGdi, and EMG activity of external oblique (EMGeo), transversus abdominis (EMGta), and external intercostal (EMGei) muscles were monitored. IRL (50 cmH2O.l-1.s) was continued for 3 h, after which NLX (0.1 mg/kg) or saline was given. Our results showed that VT decreased from 323 +/- 32 (SE) ml at baseline to 260 +/- 16 ml 5 min after the load was imposed (P less than 0.05) and further decreased to 229 +/- 18 and 217 +/- 15 ml by 120 and 180 min, respectively (180 vs. 5 min, P less than 0.05). EMGdi increased from 62 +/- 5 to 83 +/- 4% max at 5 min (P less than 0.05) but was unchanged thereafter. In contrast, for this same time period EMGeo increased from 35 +/- 5 to 58 +/- 11% max but decreased from 67 +/- 11% max at 120 min to 37 +/- 5% max at 180 min (P less than 0.05). NLX administration resulted in significant increases in EMGeo (91% above 180-min value). In contrast, EMGdi increased minimally after NLX (15% above 180-min value).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Intraesophageal Electrode Position on Signal Amplitude of the Crural Diaphragm Electromyogram

We studied the effect of electrode position relative to the lower esophageal sphincter (LES) on the crural diaphragm electromyogram (EMG) recording in 15 healthy human subjects. Three coil electrodes, each 1 cm in axial length and spaced 1 cm apart, were positioned on the distal 5 cm of a 6‐cm‐long Dent sleeve device. Bipolar EMG signals were recorded simultaneously from proximal and distal pairs of electrodes during spontaneous respiration, maximum inspiration with open airway, and maximum inspiration with closed airway. The catheter was positioned so that the side hole at the proximal margin of the sleeve recorded esophageal pressure just above the upper end of the LES. During spontaneous inspiration, the amplitude of the proximal diaphragm EMG signal was significantly higher than the distal. There was a significant difference in the amplitude of the two diaphragm EMG signals during maximum inspiration with open airway, and nearly significant differences in the two EMG signals during maximum inspiration with closed airway. We found that electrode position strongly influences the amplitude of the crural diaphragm EMG signals as measured by intraesophageal electrodes. Assessment of the crural diaphragm EMG with only one pair of electrodes may underestimate the signal amplitude.

Chemical activation of thin-fiber phrenic afferents: respiratory responses

In supine chloralose-anesthetized and mechanically ventilated dogs, we assessed the effects of group III and IV thin-fiber phrenic afferents on cardiorespiratory control by injecting capsaicin into the phrenic artery of an in situ isolated and innervated left diaphragm. Inspiratory motor drive was assessed by measuring the electromyogram of left and right diaphragm, left parasternal, and mylohyoid muscles in five protocols. 1) Three boluses (2 ml) of capsaicin (1, 10, and 50 micrograms/ml) were injected 30 min apart. Only the 50-micrograms/ml injection elicited a significant increase in arterial pressure, heart rate, and inspiratory motor drive. 2) Repeated doses of capsaicin were tested. The pressor and hyperpneic responses were weakened. 3) High doses of capsaicin (100 and 500 micrograms/ml) were given. Hyperpneic and pressor responses were similar to those elicited by the 50-micrograms/ml dose. 4) When the left phrenic nerve was sectioned, the pressor and hyperpneic responses to the 50-micrograms/ml injection were abolished. 5) Capsaicin (50 micrograms/ml) was infused into the arterial supply of the in situ vascularly isolated and innervated gastrocnemius. Arterial pressure, breathing frequency, and inspiratory motor drive to all inspiratory muscles increased significantly and to a greater degree than in the diaphragm. In conclusion, diaphragmatic thin-fiber afferents have an excitatory effect on the inspiratory motor drive and arterial pressure that is similar to that seen in limb muscles.

Effects of focal cooling in the ventrolateral medulla on chemoresponsiveness in dogs

Studies in cats and dogs have shown that the ventrolateral region of the medulla participates significantly in the shaping of the respiratory rhythm. The purpose of this study was to examine the effects of unilateral focal cooling (15–20°C) in the ventrolateral medullary region on respiratory responses to hypercapnia and hypoxia in dogs. A cryoprobe was used to cool selected locations in the ventrolateral medulla in 9 anesthetized and vagotomized dogs. Diaphragmatic electromyogram (EMG) was measured with implanted electrodes. The animals were ventilated artificially at a constant rate with 100% O 2 and the inspired gas was switched to 7% CO 2 in O 2 or 10% O 2 in N 2 to determine the response to hypercapnia or hypoxia. The sites cooled ranged 4.0–8.0 mm rostral to obex, 3.0–5.5 mm lateral to midline, and within 1.5 mm deep from the ventral surface of the medulla. Unilateral focal cooling in this region significantly decreased the responses of both the amplitude and the rate of rise of diaphragmatic EMG to hypercapnia and hypoxia. These results support the hypothesis that neural structures in the ventrolateral medulla are important in the respiratory responses to hypoxia and hypercapnia as well as for the setting of respiratory drive and timing.

Effect of dorsolateral pontine lesions on diaphragmatic activity during REMS

Muscle atonia is a feature of normal rapid-eye-movement sleep (REMS). The suppression of accessory respiratory muscle activity has been investigated and a role for sleep-disordered breathing hypothesized, but the suppression of diaphragmatic activity has rarely been considered. We hypothesized that the activity of the diaphragm was suppressed by an area of the dorsolateral pons during REMS. Lesions in this region have previously been shown to abolish the atonia of REMS. The diaphragmatic electromyogram (EMG) activity was analyzed in five naturally sleeping cats before and after pontine lesions leading to REMS without atonia. Although respiratory timing parameters were not altered by the lesion, the inspiratory rate of rise was significantly increased in all cats, and the brief pauses (40-100 ms) in the diaphragmatic EMG normally seen in REMS were virtually abolished. We conclude that the dorsolateral pons has a role in suppressing diaphragmatic activation during REMS. This suppression affects the average rate of rise of diaphragmatic activity and also leads to brief intermittent complete cessation of ongoing muscle activity. These decrements in diaphragm activity could jeopardize ventilation during REMS.

Ontogeny of sleep/wake and cardiorespiratory behavior in unanesthetized piglets

Young and older piglets (2–15, 25–35 days old) underwent chronic recording of electrocorticogram, vertical and horizontal electrooculograms, electromyograms of submental muscles, diaphragm (EMG di) and posterior cricoarytenoid (EMG pca), and heart rate, arterial pressure, pH and gas tensions. With age, (1) the distribution of percent time spent in various sleep-wake states differed; (2) heart rate decreased in all S/W, arterial pressure increased in wakefulness (W), transitional sleep (TS) and quiet sleep (QS); (3) respiratory frequency decreased, EMG di and EMG pca duration and EMG pca amplitude increased in all S/W, EMG di amplitude decreased in TS and QS and rate of rise of EMG di and EMG pca decreased in W, TS and QS. Active sleep was characterized by smaller normalized EMG pca amplitudes in the young, short EMG pca to EMG di intervals in both ages and predominance of prolonged diminished muscle activity (DMA) of either muscle. Discoordination between EMG pca and EMG di activation and the occurrence of DMA were influenced by youth and male gender. These results provide insight into subtle expressions of gender and sleep influences on developmental respiratory control.

Effect of Lung Inflation on Pulmonary Resistance during NREM Sleep

Previous investigations have demonstrated an inverse relationship between lung volume and airway resistance in awake humans. We wished to examine this relationship in the absence of conscious influences. We therefore studied eight healthy subjects who slept in a tank respirator. Hyperinflation was induced by continuous negative tank pressure while the subjects breathed spontaneously. Ventilation, pulmonary resistance (total pulmonary resistance, seven subjects; upper airway resistance, one subject), diaphragm and genioglossus electromyograms (EMGs), and sleep state were measured. During control NREM sleep, group mean maximal pulmonary resistance was 42.5 cm H2O/L/s (range, 17.4 to 106.4 cm H2O/L/s). During steady-state hyperinflation (mean increase in lung volume = 0.53 L), pulmonary resistance decreased 40% (range, -3 to -90%). Ventilation, sleep state, and end-tidal CO2 were unchanged. Inspiratory muscle EMG was increased in two of two subjects during hyperinflation. Genioglossus EMG was characterized by phasic and tonic activity during the control period in two of two subjects. Both components were decreased during steady-state hyperinflation. When lung volume was returned to baseline, pulmonary resistance and genioglossus EMG increased to baseline levels. We conclude that alteration in lung volume within the tidal volume range significantly alters pulmonary resistance during NREM sleep. This influence occurs independent of chemical stimuli or genioglossal muscle activity, and may be related to traction on neck structures caused by descent of mediastinal structures.

Human lower esophageal sphincter pressure response to increased intra-abdominal pressure

We studied the effects of increased intra-abdominal pressure on the lower esophageal sphincter (LES) pressure in 15 healthy subjects. The role of the diaphragm in the genesis of LES pressure during increased intra-abdominal pressure was determined by measuring diaphragm electromyogram (EMG). The latter was recorded using bipolar intraesophageal platinum electrodes that were placed on the nonpressure sensing surface of the sleeve device. We also measured the LES pressure response to increased intra-abdominal pressure during inhibition of the smooth muscles of the LES by intravenous atropine (12 micrograms/kg). Straight-leg raising and abdominal compression were used to increase intra-abdominal pressure. Our results show that the increase in LES pressure during straight-leg raising is greater than the increase in gastric pressure. During abdominal compression, the rate of LES pressure increase is faster than that of the gastric pressure, suggesting an active contraction at the esophagogastric junction. The increase in LES pressure during periods of increased intra-abdominal pressure is associated with a tonic contraction of the crural diaphragm as demonstrated by EMG recording. Atropine inhibited the resting LES pressure by 50-70% in each subject but had no effect either on the peak LES pressure attained during increased intra-abdominal pressure or tonic crural diaphragm EMG. We conclude that 1) there is an active contraction at the esophagogastric junction during periods of increased intra-abdominal pressure and 2) tonic contraction of the crural diaphragm is a mechanism for this LES pressure response.

Inspiratory and expiratory muscle function during continuous positive airway pressure in dogs

Continuous positive airway pressure (CPAP) is known to produce activation of the expiratory muscles. Several factors may determine whether this activation can assist inspiration. In this study we asked how and to what extent expiratory muscle contraction can assist inspiration during CPAP. Respiratory muscle response to CPAP was studied in eight supine anesthetized dogs. Lung volume and diaphragmatic initial length were defended by recruitment of the expiratory muscles. At the maximum CPAP of 18 cmH2O, diaphragmatic initial lengths were longer than predicted by the passive relationship by 52 and 46% in the costal and crural diaphragmatic segments, respectively. During tidal breathing after cessation of expiratory muscle activity, a component of passive inspiration occurred before the onset of inspiratory diaphragmatic electromyogram (EMG). At CPAP of 18 cmH2O, passive inspiration represented 24% of the tidal volume (VT) and tidal breathing was within the relaxation characteristic. Diaphragmatic EMG decreased at CPAP of 18 cmH2O; however, VT and tidal shortening were unchanged. We identified passive and active components of inspiration. Passive inspiration was limited by the time between the cessation of expiratory activity and the onset of inspiratory activity. We conclude that increased expiratory activity during CPAP defends diaphragmatic initial length, assists inspiration, and preserves VT. Even though breathing appeared to be an expiratory act, there remained a significant component of active inspiratory diaphragmatic shortening, and the major portion of VT was produced during active inspiration.