PubMed Health⌕ Search

Biomedical subjects

N S Cherniack

Publications and source records attributed to N S Cherniack.

At least 145 records · Page 8Linked to original sources
PubMed1985

Effects of hypercapnia on inspiratory and expiratory muscle activity during expiration.

Persistence of inspiratory muscle activity during the early phase of expiratory airflow slows the rate of lung deflation, whereas heightened expiratory muscle activity produces the opposite effect. To examine the influence of increased chemoreceptor drive and the role of vagal afferent activity on these processes, the effects of progressive hypercapnia were evaluated in 12 anesthetized tracheotomized dogs before and after vagotomy. Postinspiratory activity of inspiratory muscles (PIIA) and the activity of expiratory muscles were studied. During resting breathing, the duration of PIIA correlated with the duration of inspiration but not with expiration. Parasternal intercostal PIIA was directly related to that of the diaphragm. Based on their PIIA, dogs could be divided into two groups: one with prolonged PIIA (mean 0.57 s) and the other with brief PIIA (mean 0.16 s). Hypercapnia caused progressive shortening of the PIIA in the dogs with prolonged PIIA during resting breathing. The electrical activity of the external oblique and internal intercostal muscles increased gradually during CO2 rebreathing in all dogs both pre- and postvagotomy. After vagotomy, abdominal activity continued to increase with hypercapnia but was less at all levels of PCO2. The internal intercostal response to hypercapnia was not affected by vagotomy. The combination of shorter PIIA and augmented expiratory activity with hypercapnia might, in addition to changes in lung recoil pressure and airway resistance, hasten exhalation.

Abdominal Muscles↗
PubMed1985

The effects of acute bronchoconstriction on respiratory activity in patients with chronic obstructive pulmonary disease.

Attacks of acute airway obstruction often complicate the course of chronic obstructive pulmonary disease (COPD). In asthmatic subjects, bronchospasm triggers an increase in respiratory drive, which results in hyperventilation and hypocapnia. In the present study, we assessed the effects of acute bronchoconstriction induced by aerosolized methacholine on breathing and lung mechanics in 12 patients with stable COPD. Even low doses of methacholine markedly increased airway resistance and caused hyperinflation and decreased inspiratory muscle performance in the patients. Increasing airway obstruction produced a progressive rise in PCO2 despite an increase in minute ventilation. Breathing frequency and average inspiratory flow were greater, but tidal volume decreased because of shortening of the inspiratory duration. The magnitude of CO2 retention during acute bronchoconstriction was inversely related to the changes in tidal volume and inspiratory time (p less than 0.01 for each). In subjects with COPD, the occlusion pressure response to progressive hypercapnia failed to increase during bronchoconstriction. These results show that patients with COPD retain CO2 during acutely increasing airway obstruction induced by bronchoconstriction partly because of a rapid shallow breathing pattern that reduces alveolar ventilation.

Aged↗
PubMed1985

Respiratory pressure sensation. Relationship to changes in breathing pattern and PCO2 during acute increase in airway resistance in patients with chronic obstructive pulmonary disease.

The intensity of sensations experienced during breathing by patients with chronic obstructive pulmonary disease (COPD) might influence their ventilatory response to altered lung mechanics. In 8 patients with COPD (mean FEV1, 1.6 +/- 0.6 L SD) the acuity with which changes in intrathoracic pressure were perceived was studied by a standard psychophysical technique, magnitude production of inspiratory pressure. Subjects voluntarily produced mouth pressures proportional to numbers randomly presented, and the sensory acuity to changes in pressure was assessed from the slope of log-log plots of numbers versus pressures. These slopes were then related to the ventilatory responses of the patients to external resistive loads of 10 cm H2O/L/s, applied during both inspiration and expiration, and methacholine-induced bronchoconstriction, which doubled baseline specific airway resistance. Both modes of increase in airway resistance caused an increase in end-tidal PCO2 in all patients (range, 0.5 to 11 mmHg). The magnitude of CO2 retention correlated significantly with the change in tidal volume during both external loading and bronchoconstriction (r = -0.77, p less than 0.01); decreases in tidal volume were associated with increases in PCO2. The slope for magnitude production of pressure was inversely related to changes in tidal volume during both modes of increases in airway resistance (r = 0.61, p less than 0.01 for both bronchoconstriction and external resistive loads). Patients with the highest exponents for pressure changes (highest slopes) demonstrated the greatest decreases in tidal volume. Consequently, a direct relationship was found between the magnitude of the exponent and the magnitude of CO2 retention during loaded breathing and bronchoconstriction (r = 0.81, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1985

Nicotine: a different approach to treatment of obstructive sleep apnea.

Reduced upper airway muscle activity may contribute to the occurrence of obstructive apneas during sleep. There is no uniformly successful treatment of these apneas, and it is possible that agents which increase upper airway muscle activity could reduce the occurrence of obstruction during sleep. Nicotine, a known stimulant of breathing, also increases the activity of muscles which dilate the upper airway proportionally more than it does ventilation. Hence, we evaluated the effect of nicotine on apneas during the first two hours of sleep in eight patients with sleep apnea syndrome. It was concluded that nicotine reduces apneas during the early hours of sleep, and this effect may be caused by its stimulating action on upper airway muscles.

Adolescent↗
PubMed1984

Comparison of the responses of the diaphragm and upper airway muscles to central stimulation of the sciatic nerve.

Electrical stimulation of the central end of the sciatic nerve was used to assess the effect of increased somatic sensory input on respiratory muscle electrical activity in anesthetized, spontaneously breathing dogs. Graded electrical stimulation of the sciatic nerve was associated with progressively greater activity of the upper airway dilating muscles (alae nasi, genioglossus, and posterior cricoarytenoid) as well as the diaphragm. Breathing frequency also increased because of a reduction in inspiratory and expiratory time. After cessation of stimulation of the sciatic nerve, increased activity of all the muscles studied persisted and only gradually returned to control levels. The responses to sciatic nerve stimulation were independent of the CO2 concentration of the inspired gas mixture. At any level of chemical drive electrical stimulation caused greater increases in the electrical activity of upper airway dilating muscles than that of diaphragm. Based on these results, it is concluded that stimulation of sciatic nerve activates upper airway muscles as well as the diaphragm, and the upper airway muscle activity is augmented to a greater degree than diaphragm activity. It seems possible that somatosensory afferent input produces unequal effects on different respiratory motoneurons.

Animals↗
PubMed1984

Action of nicotine on the respiratory activity of the diaphragm and genioglossus muscles and the nerves that innervate them.

Nicotine is known to alter respiration by stimulating peripheral chemoreceptors and receptors within the brain. In this study the sites of action and the effects of nicotine on hypoglossal nerve activity were compared to its effects on phrenic activity in paralyzed, vagotomized and chloralose-anesthetized cats. Since anesthesia is known to affect respiratory responses, we also compared the effects of intravenous nicotine given to conscious unsedated cats on genioglossus and diaphragm electrical activity. In eight conscious animals intravenous doses of nicotine ranging between 10 ng and 200 micrograms increased genioglossus activity significantly more than diaphragm activity. Studies in 26 anesthetized animals included injection of nicotine, intravenously, in the lateral ventricles, and application of nicotine to the ventrolateral surface of the medulla (the putative site of the central chemoreceptors) before and after section of the carotid sinus nerves. With all these interventions, changes in hypoglossal nerve activity were significantly greater than changes in phrenic nerve activity. The responses to nicotine could be blocked by application of hexamethonium to the ventrolateral medullary surface or by cooling the same area. The results indicate that: nicotine increases hypoglossal nerve activity by both its peripheral and central effects; nicotine has differential effects on different respiratory muscles and nerves; and the central action of nicotine may be mediated largely through receptors located near the ventral medullary surface.

Anesthesia↗
PubMed1984

Responses of upper airway, intercostal and diaphragm muscle activity to stimulation of oesophageal afferents in dogs.

The effects of oesophageal distension on respiratory patterns and the moving average electromyogram (e.m.g.) activity of three upper airway muscles--the alae nasi, the genioglossus, and the posterior cricoarytenoid--and four chest wall muscles--the costal and crural diaphragm and the inspiratory and expiratory intercostals--were examined in ten anaesthetized, tracheostomized, spontaneously breathing dogs. Distension was produced by inflations of a balloon placed in the middle part of the thoracic oesophagus with volumes of air ranging from 50 to 200 ml. Oesophageal distension increased respiratory frequency, mainly due to a significant shortening of the expiratory time. Activity of both the costal and crural parts of the diaphragm was inhibited with oesophageal distension, whereas that of the inspiratory intercostal muscles increased, tending to maintain a near-normal tidal volume and end-tidal CO2. Phasic inspiratory activity of all three upper airway muscles increased in response to oesophageal distension, as did the activity of the expiratory intercostal muscles. The changes in the breathing pattern and the electrical activity of all muscles in response to oesophageal distension were immediate, occurring during the first breath after the balloon was inflated. The responses were graded, so that increases in the volume of the oesophageal balloon progressively increased the activity of the upper airway and intercostal muscles, and decreased diaphragm activity. Bilateral vagotomy abolished the effects of oesophageal distension on upper airway and chest wall muscle activity, suggesting that vagal afferents constitute the major pathway for the reflex.

Animals↗
PubMed1984

Hypoglossal and phrenic responses to cholinergic agents applied to ventral medullary surface.

Application of cholinergic agents on the ventrolateral surface of the medulla in areas in which the "central chemoreceptors" are believed to be located stimulates breathing. It is also known that cranial nerves, such as the hypoglossal, have respiratory modulated activity (greater in inspiration than expiration) that responds to many of the same stimuli which affect breathing. In the present study we compared effects of cholinergic agents (acetylcholine, carbachol, methacholine, eserine) directly applied to chemoreceptive areas on the ventral medullary surface on phrenic and hypoglossal nerve activity. Studies were performed in paralyzed, anesthetized, and artificially ventilated cats after vagotomy. All cholinergic agents increased hypoglossal activity significantly more than phrenic activity in animals ventilated with O2 or 7% CO2 in O2 whether or not the carotid sinus nerves were intact. Atropine applied topically to the same medullary area blocked the respiratory effects of locally administered acetylcholine. The results suggest that cholinergic agents applied centrally can increase both phrenic and hypoglossal activity. Moreover the effects of the drugs are relatively greater on XII nerve activity than on phrenic discharge, suggesting that the drive from medullary cholinergic structures is distributed with unequal weight to different respiratory motoneurons.

Acetylcholine↗
PubMed1984

Responses to chemical stimulation of upper airway muscles diaphragm in awake cats.

The steady-state and transient effects of hyperoxic hypercapnia on the electromyographic activities of the genioglossus (GG), posterior cricoarytenoid (PCA), and diaphragm (D) were studied in conscious unsedated cats with chronically implanted electrodes. Hypercapnia (inhalation of 3.4 and 7.4% CO2 in O2) increased the phasic electrical activity occurring during inspiration in all three muscles and also increased tonic activity of the GG. The GG responded to steady-state CO2 inhalation alinearly and with larger increases in activity than the PCA and D. Phasic GG activity was present in only 4 of 10 cats breathing 100% O2, whereas phasic PCA and D activity could be observed in all animals studied. When gas mixtures containing CO2 were given, the GG reached its new steady-state level more slowly than the D or PCA, and when CO2 was rapidly removed from the inspired gas mixture, the GG attained its steady state sooner than either the PCA or D. These results suggest that in awake unsedated animals, chemical stimuli do not affect either transient or steady-state responses of the GG in the same way as the D. These differences seem to be explained mainly by different threshold characteristics of hypoglossal and phrenic neurons but also in part by dissimilarities in their steady-state responses.

Animals↗
PubMed1984

Phasic volume-related feedback on upper airway muscle activity.

The effects of vagally mediated volume-related feedback on the activity of upper airway muscles was assessed in nine pentobarbital-anesthetized, tracheostomized, spontaneously breathing dogs. Moving average electrical activity was recorded before and during single-breath airway occlusions from the genioglossus, posterior cricoarytenoid, and alae nasi muscles and compared with simultaneously recorded tidal volume and electrical activity of the phrenic nerve (6 dogs) or diaphragm (3 dogs). The normally early peak of upper airway muscle activity during unoccluded breaths was delayed to late or end inspiration during occluded breaths. Inspiratory depression started at a lower volume above end-expiratory volume and at an earlier time after inspiratory onset for the upper airway muscles than for the phrenic nerve and the diaphragm. The amount of depression at the end of inspiratory airflow was larger for all of the upper airway muscles than for the phrenic nerve and diaphragm. Depressive effects were most prominent in the genioglossus, followed by the posterior cricoarytenoid and the alae nasi. After vagotomy, depressive effects of volume-related feedback were no longer seen. These results suggest that activity of the upper airway muscles is modulated by vagally mediated feedback, apparently to a larger extent than that of the diaphragm and phrenic nerve.

Animals↗
PubMed1984

Effects of dopamine, isoproterenol, and lobeline on cranial and phrenic motoneurons.

Recent studies have suggested that the upper airway muscles receive a substantial portion of their excitatory input from the peripheral chemoreceptors. We examined the responses of the phrenic, hypoglossal, and recurrent laryngeal nerves to agents that are known to modify carotid body activity. Dopamine, an inhibitor, and isoproterenol and lobeline, two stimulators of carotid body activity, were administered into the lingual arteries of 14 anesthetized, paralyzed cats artificially ventilated with 100% O2. Dopamine decreased the activity of all three nerves (P less than 0.001) but inhibited the hypoglossal nerve more than the phrenic and recurrent laryngeal nerves (P less than 0.001). Isoproterenol and lobeline increased the activity of all three nerves (P less than 0.001) but stimulated the hypoglossal nerve more than the phrenic and recurrent laryngeal nerves (P less than 0.001). These relatively greater effects of all three agents on the hypoglossal nerve compared with the phrenic and the recurrent laryngeal nerves persisted under both hypoxic and hypercapnic conditions. After midcervical vagotomy, the responses of the hypoglossal to all three drugs remained larger than those of the phrenic nerve. After combined vagotomy and carotid sinus nerve section, the stimulatory effects of lobeline and the inhibitory effects of dopamine were no longer apparent. We conclude that it is possible to preferentially alter respiratory-related activity of the hypoglossal nerve compared with that of the phrenic nerve using agents that modify peripheral chemoreceptor activity.

Animals↗
PubMed1984

Nasal and laryngeal reflex responses to negative upper airway pressure.

The effects of negative pressure applied to just the upper airway on nasal and laryngeal muscle activity were studied in 14 spontaneously breathing anesthetized dogs. Moving average electromyograms were recorded from the alae nasi (AN) and posterior cricoarytenoid (PCA) muscles and compared with those of the genioglossus (GG) and diaphragm. The duration of inspiration and the length of inspiratory activity of all upper airway muscles was increased in a graded manner proportional to the amount of negative pressure applied. Phasic activation of upper airway muscles preceded inspiratory activity of the diaphragm under control conditions; upper airway negative pressure increased this amount of preactivation. Peak diaphragm activity was unchanged with negative pressure, although the rate of rise of muscle activity decreased. The average increases in peak upper airway muscle activity in response to all levels of negative pressure were 18 +/- 4% for the AN, 27 +/- 7% for the PCA, and 122 +/- 31% for the GG (P less than 0.001). Rates of rise of AN and PCA electrical activity increased at higher levels of negative pressure. Nasal negative pressure affected the AN more than the PCA, while laryngeal negative pressure had the opposite effect. The effects of nasal negative pressure could be abolished by topical anesthesia of the nasal passages, while the effects of laryngeal negative pressure could be abolished by either topical anesthesia of the larynx or section of the superior laryngeal nerve. Electrical stimulation of the superior laryngeal nerve caused depression of AN and PCA activity, and hence does not reproduce the effects of negative pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intranasal↗
PubMed1984

Respiratory response to partial paralysis in anesthetized dogs.

The ability to maintain alveolar ventilation is compromised by respiratory muscle weakness. To examine the independent role of reflexly mediated neural mechanisms to decreases in the strength of contraction of respiratory muscles, we studied the effects of partial paralysis on the level and pattern of phrenic motor activity in 22 anesthetized spontaneously breathing dogs. Graded weakness induced with succinylcholine decreased tidal volume and prolonged both inspiratory and expiratory time causing hypoventilation and hypercapnia. Phrenic peak activity as well as the rate of rise of the integrated phrenic neurogram increased. However, when studied under isocapnic conditions, increases in the severity of paralysis, as assessed from the ratio of peak diaphragm electromyogram to peak phrenic activity, produced progressive increases in inspiratory time and phrenic peak activity but did not affect its rate of rise. After vagotomy, partial paralysis induced in 11 dogs with succinylcholine also prolonged the inspiratory burst of phrenic activity, indicating that vagal reflexes were not solely responsible for the alterations in respiratory timing. Muscle paresis was also induced with gallamine or dantrolene, causing similar responses of phrenic activity and respiratory timing. Thus, at constant levels of arterial CO2 in anesthetized dogs, respiratory muscle partial paralysis results in a decrease in breathing rate without changing the rate of rise of respiratory motor activity. This is not dependent solely on vagally mediated reflexes and occurs regardless of the pharmacological agent used. These observations in the anesthetized state are qualitatively different from the response to respiratory muscle paralysis or weakness observed in awake subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1984

Respiratory function of hyoid muscles and hyoid arch.

The position of the hyoid arch suggests that it supports soft tissue surrounding the upper airway (UA) and can act to maintain UA patency. We also suspected that muscles inserting on the hyoid arch might show respiratory patterns of activity that could be affected by respiratory stimuli. To test these possibilities, we moved the hyoid arch ventrally in six anesthetized dogs either by traction on it or by stimulation of hyoid muscles. UA resistance was decreased 73 +/- (SE) 6% and 72 +/- 6% by traction and stimulation during expiration and 57 +/- 15% and 52 +/- 8% during inspiration. Moving averages of the geniohyoid (GH) and thyrohyoid (TH) obtained in six other dogs breathing 100% O2 showed phasic respiratory activity while the sternohyoid (SH) showed phasic respiratory activity in only two of these animals and no activity in four. With progressive hypercapnia, GH and TH increased as did SH when activity was already present. Airway occlusion at end expiration augmented and prolonged inspiratory activity in the hyoid muscles but did not elicit SH activity if not already present. Occlusion at end inspiration suppressed phasic activity in hyoid muscles for as long as in the diaphragm. After vagotomy activity increased and became almost exclusively inspiratory. Activity appeared in SH when not previously present. Duration and amplitude of hyoid muscle activity were increased with negative UA pressure and augmented breaths. We conclude that the hyoid arch and muscles can strongly affect UA flow resistance. Hyoid muscles show responses to chemical, vagal, and negative pressure stimuli similar to other UA muscles.

Airway Resistance↗
PubMed1984

Effects of CO2 and bronchoconstriction on costal and crural diaphragm electromyograms.

To determine if neural control of the crural diaphragm is similar to that of the costal diaphragm, electrical activity was recorded from these two parts of the diaphragm in 10 anesthetized dogs during resting O2 breathing and during progressive hyperoxic hypercapnia. Within a breath, the onset of crural diaphragm inspiratory activity started significantly earlier than that of the costal diaphragm under both resting and CO2 stimulated conditions, although the relative delay in costal diaphragm activity was smaller during hypercapnia than during resting O2 breathing. Following hyperventilation to apnea, both parts of the diaphragm resumed activity on the same breath. During CO2 rebreathing, the maximal increase in crural diaphragm peak electrical activity was significantly greater than that of the costal diaphragm. We also examined the effects of histamine-induced bronchoconstriction on diaphragm activity. Following administration of histamine aerosol there was a transient of irregular breathing during which in three animals costal diaphragm activity became nearly quiet, although there was continued activity of the crural diaphragm. Once breathing became more regular, there was a significantly greater stimulation of crural diaphragm than costal diaphragm activity; this difference persisted for 15 min after histamine inhalation. These results support the concept that electrical activity can be distributed nonuniformly to the costal and crural diaphragm and demonstrate that the crural diaphragm has a greater gain with hypercapnia and bronchoconstriction than does the costal diaphragm.

Aerosols↗
PubMed1984

Conditioning of the diaphragm with phrenic nerve stimulation after prolonged disuse.

We studied the effect of electrical stimulation of the phrenic nerve on the force frequency relationship of the disused diaphragm. A high quadriplegic who had been totally ventilator dependent for 6 months following a C2 fracture received bilateral phrenic nerve stimulators. During a 6-wk period of conditioning by electrical stimulation, the force of diaphragm contraction was assessed by measurement of transdiaphragmatic pressures during stimulation of each nerve over a range of frequencies. Tidal volume as well as rib cage and abdominal motion were studied. There was an upward shift of the force frequency relationship of the diaphragm over the 4-month period of phrenic nerve pacing using repetitive stimulus trains of 14 to 28 Hz. This improvement appeared to plateau at about 11 wk. The increase in contractility was accompanied by a progressive diminution in the stimulus frequency at which fusion of the contraction occurred. The disused diaphragm, like other skeletal muscle, may be conditioned with electrical stimulation.

Aminophylline↗
PubMed1983

Activity of upper airway muscles during augmented breaths.

The effect of augmented breaths on the electrical activity of upper airway (UAW) muscles was studied in fourteen spontaneously breathing anesthetized dogs. Moving average traces of the electrical activity recorded from the genioglossus (GG), the posterior cricoarytenoid (PCA), and the alar portion of the nasalis muscle (AN) were compared to tracings of diaphragm electrical activity. During augmented breaths the electrical activity of the diaphragm showed the characteristic biphasic pattern previously described: an initial phase following the contour of a normal breath (phase I) and an augmented phase arising near the crest of the initial phase (phase II). During all augmented breaths, the GG, PCA and AN showed the same biphasic pattern as the diaphragm. The normally rounded shape of UAW muscle EMG activity during control breaths changed to a more sharply peaked form during the second phase of the augmented breath. Onset of activity of all UAW muscles studied preceded that of the diaphragm; during control breaths, the average interval was 0.29 sec for the PCA, 0.25 sec for the GG and 0.14 sec for the AN (P less than 0.05). The amount of pre-activation was decreased to less than 0.10 sec during the second phase of the augmented breath. The slopes and amplitudes of phase I were similar to that of control breaths. The peak EMG activity of the augmented breath was 214% of the control breaths for the diaphragm, 247% for the GG, 168% for the AN and 161% for the PCA (P less than 0.005 for GG, P less than 0.001 for the others). During hyperoxic hypercapnia the slopes and amplitudes of phase II remained nearly constant for all four muscles, whereas the slopes and amplitudes of phase I changed with the chemical drive just as in control breaths. UAW resistance, recorded in five additional spontaneously breathing anesthetized dogs, was 32% less during inspiration than expiration during control breaths, and 31% less during phase I of augmented breaths; there was a further 18% decrease during phase II of augmented breaths (P less than 0.001). The results suggest that mechanisms responsible for augmented breaths act similarly on upper airway muscles and the diaphragm.

Airway Resistance↗