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Biomedical subjects

N S Cherniack

Publications and source records attributed to N S Cherniack.

At least 181 records · Page 10Linked to original sources
PubMed1981

Role of carotid chemoreflex in respiratory acclimatization to hypoxemia in goat and sheep.

The role of the carotid body chemoreflex in the ventilatory acclimatization to chronic hypoxia was studied in the unanesthetized goat and sheep. The time-cours of changes in ventilation, PCO2, pH and PO2 of arterial blood and cisternal fluid (CF) were measured before and following exposure to a simulated altitude of 3660-5000 m, with and without intact carotid sinus nerves. At sea level, after section of carotid sinus nerves most animals hypoventilated chronically, and developed mild arterial hypoxemia and hypercapnia. Upon exposure to acute hypoxia, all of the intact animals hyperventilated and CF pH increased from 7.310 to 7.380 whereas after chemodenervation, the increase in ventilation was small and delayed, and CF pH decreased from 7.285 to 7.143. During exposure of the intact animals to chronic hypoxia, hyperventilation accompanied by decreases in arterial and CF P CO2 reached its peak in two days; these changes partially subsided during the next few days. Partial compensation of respiratory alkalosis occurred during the first day. In contrast, several chemodenervated animals died during chronic hypoxia; the survivors showed either a small decrease or an increase in Pa CO2. Thus, an intact peripheral chemoreflex drive during hypoxia is necessary for ventilatory acclimatization which raises the arterial and presumably tissue PO2 in spite of alkalosis. The new proposal is that a central tissue metabolic acidosis resulting from a direct effect of acute hypoxia is partly compensated as hypoxia is prolonged. This central compensation decreases ventilatory drive and hence opposes the ventilatory acclimatization during chronic hypoxia initiated by the peripheral chemoreflexes.

Acclimatization↗
PubMed1981

Characteristics and rate of occurrence of spontaneous and provoked augmented breaths.

The tidal volume and corresponding efferent phrenic activity of spontaneously occurring and provoked "augmented" breaths, AB, and the subsequent post-augmented breaths were studied in cats anesthetized with pentobarbitone during hypercapnia and hypoxia. The augmentation phase (phase II) begins at, or close to, the crest of what appears as a "normal" inspiration (phase I). The amplitude and duration of phase II remained fairly constant whereas the amplitude and the duration of phase I changed with chemical drive just as in control breaths. The smaller amplitude and shorter duration of post-augmented breaths as compared to control breaths seems to be due to both a lower-than-normal inspiratory "off-switch" threshold following the AB and an increased rate of rise of inspiratory activity. With increasing hypercapnia and hypoxia both the time interval between AB and the refractory period following an AB during which a new AB cannot be provoked were reduced. Following bilateral vagotomy AB was temporarily abolished but reappeared after 1-2 h. The relatively low rates of occurrence after vagotomy still showed the same type of dependence on chemical stimuli. The refractory period was not abolished although usually decreased by gallamine paralysis or high thoracic spinalization.

Animals↗
PubMed1981

Perception of changes in breathing in normal human subjects.

Respiratory sensation was evaluated in normal subjects from their ability to quantitate changes in tidal volume. Subjects attempted to duplicate or double tidal volumes of different sizes while breathing freely or against a resistive or elastic load. When the mechanical conditions during control and test breaths were constant, tidal volume duplication was accomplished with an error of approximately 100 ml, regardless of the control volume. The error in doubling, however, increased progressively with increasing control tidal volume. There was a greater error in both volume duplication and doubling when the mechanical conditions between control and test breaths were changed. When test breaths against a load followed unloaded control breaths, tidal volume failed to double, but intrathoracic pressure changes twice exceeded control values. Conversely, when unloaded test breaths followed loaded control breaths, pressure changes underwent less than a twofold increase while tidal volume more than doubled. The results indicate that tidal volume changes are normally sensed with considerable accuracy and suggest that both tidal volume per se, as well as the forces generated by the respiratory muscles, are used in the estimation of tidal volume changes.

Adult↗
PubMed1981

Effect of quiet sleep on resting and CO2-stimulated breathing in humans.

We examined the effects of different levels of inspired CO2 on ventilation and the pattern of breathing in healthy adults during the awake and the stage II quiet-sleep states. During both states, subjects were studied supine with their heads enclosed in a canopy. Tidal volume (VT) was determined from quantitative measurements of abdominal and rib cage excursions with magnetometers. Inspired CO2 was raised by blending CO2-enriched gas into the airflow, which continuously flushed the canopy. During sleep, while room air was breathed, VT decreased significantly from 410 to 360 ml, and respiratory rate also fell from 17 to 16 breaths/min. As a consequence, ventilation was significantly reduced from 6.5 to 5.8 l/min, and end-tidal CO2 partial pressure (PCO2) rose from 39.1 to 42.5 Torr. Ventilatory responses to CO2 were reduced, on the average, during sleep to 79% of waking levels. The change in average inspiratory flow produced by CO2 was also less during sleep. Waking and sleeping ventilatory responses to CO2 correlated inversely with the rise in end-tidal PCO2 when room air was breathed during sleep. At all levels of VT, the rib cage contribution to VT was greater during quiet sleep than during wakefulness. These findings suggest that quiet sleep, in addition to depressing ventilation and the response to CO2 alters the manner in which VT is attained by rib cage and abdominal displacements.

Abdomen↗
PubMed1981

Effect of aging on respiratory sensations produced by elastic loads.

We compared the effects of graded elastic loads on respiratory sensations in 19 healthy subjects greater than 60 yr of age to 21 healthy subjects less than 30 yr old. The magnitude of the respiratory sensation was quantitated by two well-established psychophysical techniques. In the magnitude-estimation method, subjects indicated the intensity of the sensation experienced with numbers; in the cross-modality method, the level of sensation was signaled with a dynamometer activated by thumb pressure. In addition, the effects of nonrespiratory stimuli were compared in the two groups. With both methods, the logarithm of the response to elastic loads was linearly related to the logarithms of the stimulus. The slope of the line relating the log of the response to the log of the stimulus (beta) was significantly greater in the younger group than in the older group using the magnitude-estimation method but not with the cross-modality matching test. There were no differences in the ability of the two groups to assign numbers to line length. However, the older group had a lower beta for magnitude estimation of thumb force than the younger group. The results suggest 1) that respiratory sensation follows Steven's law and grows exponentially with the stimulus; 2) that the growth of sensations produced by elastic loading is less in older than in younger individuals; and 3) differences in the perception of the mode used for matching in the cross-modality test may obscure significant differences in the sensations elicited by respiratory stimuli.

Adult↗
PubMed1981

Effects of hypercapnia and hypoxia on phrenic nerve activity and respiratory timing.

In the spontaneously breathing animal, respiratory responses to chemical stimuli are influenced by phasic proprioceptive inputs from the thorax. We have compared the effects of hypercapnia and hypoxia on the level and timing of phrenic nerve activity while these phasic afferent signals were absent. Progressive hyperoxic hypercapnia and isocapnic hypoxia were produced in anesthetized paralyzed dogs by allowing 3-5 min of apnea to follow mechanical ventilation with 100% O2 or 35% O2 in N2, respectively; during hypoxia, isocapnia was maintained by intravenous infusion of tris(hydroxymethyl)aminomethane buffer. The peak height (P) of nerve bursts, inspiratory time (TI), and expiratory time (TE) were measured from the phrenic neurogram. With the vagi intact or severed, hypoxia decreased TI, whereas hypercapnia did not; both stimuli decreased TE. At the same minute phrenic activity (P x frequency), P, TI, and TE were all less during hypoxia than during hypercapnia. The decreases in TI and TE with hypoxia were significantly less after carotid sinus denervation. The results indicate that the patterns of phrenic nerve activity in response to hypoxia and hypercapnia are different: hypoxia has a greater effect on respiratory timing, whereas hypercapnia has a greater effect on peak phrenic nerve activity. The effect of hypoxia on respiratory timing is largely mediated by the peripheral chemoreceptors.

Animals↗
PubMed1981

Respiratory responses in reversible diaphragm paralysis.

The effects of diaphragm paralysis on respiratory activity were assessed in 13 anesthetized, spontaneously breathing dogs studied in the supine position. Transient diaphragmatic paralysis was induced by bilateral phrenic nerve cooling. Respiratory activity was assessed from measurements of ventilation and from the moving time averages of electrical activity recorded from the intercostal muscles and the central end of the fifth cervical root of the phrenic nerve. The degree of diaphragm paralysis was evaluated from changes in transdiaphragmatic pressure and reflected in rib cage and abdominal displacements. Animals were studied both before and after vagotomy breathing O2, 3.5% CO2 in O2, or 7% CO2 in O2. In dogs with intact vagi, both peak and rate of rise of phrenic and inspiratory intercostal electrical activity increased progressively as transdiaphragmatic pressure fell. Tidal volume decreased and breathing frequency increased as a result of a shortening in expiratory time. Inspiratory time and ventilation were unchanged by diaphragm paralysis. These findings were the same whether O2 or CO2 in O2 was breathed. After vagotomy, no significant change in phrenic or inspiratory intercostal activity occurred with diaphragm paralysis in spite of increased arterial CO2 partial pressure. Ventilation and tidal volume decreased significantly, and respiratory timing was unchanged. These results suggest that mechanisms mediated by the vagus nerves account for the compensatory increase in respiratory electrical activity during transient diaphragm paralysis. That inspiratory time is unchanged by diaphragm paralysis whereas the rate or rise of phrenic nerve activity increases suggest that reflexes other than the Hering-Breuer reflex contribute to the increased respiratory response.

Animals↗
PubMed1981

Comparison of the respiratory responses to external resistive loading and bronchoconstriction.

The effects of resistive loads applied at the mouth were compared to the effects of bronchospasm on ventilation, respiratory muscle force (occlusion pressure), and respiratory sensations in 6 normal and 11 asthmatic subjects breathing 100% O2. External resistive loads ranging from 0.65 to 13.33 cm H2O/liter per s were applied during both inspiration and expiration. Bronchospasm was induced by inhalation of aerosolized methacholine. Bronchospasm increased ventilation, inspiratory airflow, respiratory rate, and lowered PACO2. External resistive loading, on the other hand, reduced respiratory rate and inspiratory flow, but left ventilation and PACO2 unaltered. FRC increased to a greater extent with bronchospasm than external flow resistive loads. With both bronchospasm and external loading, occlusion pressure increased in proportion to the rise in resistance to airflow. However, the change in occlusion pressure produced by a given change in resistance and the absolute level of occlusion pressure at comparable levels of airway resistance were greater during bronchospasm than during external loading. These differences in occlusion pressure responses to the two forms of obstruction were not explained by differences in chemical drive or respiratory muscle mechanical advantage. Although the subjects' perception of the effort involved in breathing was heightened during both forms of obstruction to airflow, at any given level of resistance the sense of effort was greater with bronchospasm than external loading. Inputs from mechanoreceptors in the lungs (e.g., irritant receptors) and/or greater stimulation of chest wall mechanoreceptors as a result of increases in lung elastance may explain the differing responses elicited by the two forms of resistive loading.

Adult↗
PubMed1980

Effects of expiratory loading on respiration in humans.

We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.

Adult↗