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Biomedical subjects

N S Cherniack

Publications and source records attributed to N S Cherniack.

At least 217 records · Page 12Linked to original sources
PubMed1976

Airway occlusion pressures in awake and anesthetized goats.

The pressures generated by the inspiratory muscles as they contract isometrically during airway occlusion seem to be a measure of respiratory neuron efferent activity. The ventilatory and occlusion pressure responses to increasing levels of CO2 were studied in goats, awake and anesthetized, with and without inspiratory flow resistance. Hypercapnia was produced by rebreathing. Randomly, during rebreathing, inspiratory airflow was prevented on single breaths. Ventilation and pressures developed during the first 100, 200, 300 and 400 milliseconds of an inspiratory effort against a complete occlusion increased linearly with CO2 in both awake and anesthetized animals. Anesthesia reduced both the ventilatory and occlusion pressure responses to CO2. Inspiratory resistance increased occlusion pressure responses in awake goats but not in the same animals when anesthetized. Inspiratory airflow resistance seems to augment respiratory efferent activity as reflected in the pressure responses only in conscious goats. Thus the response to an inspiratory resistance seems to depend on the state of consciousness.

Airway Resistance↗
PubMed1976

Effect of liver failure on the cerebral circulatory and metabolic responses to hypoxia in the goat.

1. Six unanaesthetized goats were used to evaluate the effect of liver failure on the hypoxic responsiveness of cerebral blood flow. The animals breathed air and several different hypoxic gas mixtures enriched with sufficient CO2 to maintain an isocapnic state. The cerebral metabolic rate for O2 (CMRo2) was also measured in four of these goats. 2. In baseline studies there was a linear relationship between cerebral blood flow and arterial O2 saturation (Sa,o2) measured at different levels of isocapnic hypoxia. The slopes of the cerebral blood flow/Sa,o2 response lines were used to quantify the response of cerebral blood flow to hypoxia. In the healthy goat, CMRo2 was not depressed by hypoxia until the O2 tension (Po2) in arterial and cerebral venous blood had fallen below critical threshold values of approximately 3-2 and 2-2 kPa (24 and 16 mmHg) respectively. 3. Liver failure was accompanied by a fall in cerebral blood flow and CMRo2. There was also a depression in the response of cerebral blood flow to hypoxia and a disproportionate reduction of cerebral O2 delivery in hypoxia. CMRo2 was further reduced at arterial and cerebral venous Po2 values, which were much higher than the critical threshold values for producing hypoxic CMRo2 depression in health. 4. It is concluded that the brain becomes more vulnerable to the adverse effects of hypoxia during liver failure. This may be of practical importance in the management of patients with arterial hypoxaemia or other complications (e.g. anaemia or shock), which may reduce cerebral oxygen delivery.

Animals↗
PubMed1976

Effect of liver failure on the ventilatory response to hypoxia in man and the goat.

1. The ventilatory responses to transient and steady-state hypoxia were measured in ten patients with hepatic cirrhosis and in ten healthy control subjects. Successive measurements of these responses were also obtained in six goats before and after the experimental production of liver failure. Changes in the effect of steady-state hypoxia on the ventilatory response to hypercapnia were evaluated by successive studies in another goat. 2. In spite of a respiratory alkalosis during liver failure, the response to transient hypoxia was greater in the patients than in the control subjects. This response was increased after the onset of liver failure in all the goats. 3. In healthy humans and goats the responses to transient and steady-state hypoxia were similar in magnitude. During liver failure there was a disparity between the size of these responses, since the ventilatory increment evoked by steady-state hypoxia was unchanged in spite of the increase in response to transient hypoxia. Steady-state hypoxia consistently enhanced the ventilatory response to hypercapnia in a healthy goat, but frequently depressed the response to hypercapnia during liver failure. 4. The findings suggest that liver failure heightens the sensitivity of the peripheral chemoreceptors to the hypoxic stimulus, but may increase the tendency of the medullary centres to become depressed in hypoxia.

Adult↗
PubMed1976

Electromyographic response of respiratory muscles during elastic loading.

The response of respiratory motor neurons to graded elastic loading was assessed in anesthetized dogs by recording the electromyogram (EMG) from the diaphragm (ED) and the intercostal muscle (EIC). Elastic loads were applied for 1-20 breaths. The effects of changes in PCO2 on respiratory motor neuron output was assessed by applying loads during the course of CO2 rebreathing. On the first loaded breath, ED and EIC increased reflexly due chiefly to prolongation of inspiration. Vagotomy or vagal cooling to block the Hering-Breuer reflex eliminated the increase in ED and diminished the increase in EIC. During the second to fifth breath, the level of EMG activity was disproportionately high for the level of PCO2, suggesting an additional reflex component over and above the reflex activity present on the first loaded breath.

Animals↗
PubMed1976

Effects of hypercapnia on mouth pressure during airway occlusion in conscious man.

The effects of hypercapnia and inspiratory flow-resistive loading on mouth pressure during periods of arrested airflow were studied in conscious human subjects to determine the usefulness of inspiratory muscle force in the assessment of respiratory neural efferent activity. Hypercapnia increased the peak end-inspiratory mouth pressure (Ppeak) during complete airway occlusion and the pressures at 100, 200, and 300 ms after the onset of inspiration (P100, P200, P300). During rebreathing without added mechanical loads, P100 and Ppeak increased linearly with the electrical activity of the diaphragm and changes in P100 and Ppeak during hypercapnia correlated well with ventilatory responses to PCO2 (DELTA V/DELTA PCO2) suggesting that occluded mouth pressures are reliable measures of respiratory activity. In individuals with the greatest reduction in delta V/DELTA PCO2 during inspiratory flow-resistive loading, changes in P100 and Ppeak with PCO2 increased only minimally. In contrast, there was a much greater increase in occluded mouth pressures with hypercapnia in the presence of mechanical loading when inspiratory flow-resistive loading failed to depress delta V/DELTA PCO2. In all subjects, occluded mouth pressures were greater at any given PCO2 during mechanical loading than during free breathing. Mechanical loading resulted in augmented respiratory neural efferent activity unexplained by alterations in chemical stimulation.

Adult↗
PubMed1976

Effects of hypercapnia and flow-resistive loading on tracheal pressure during airway occlusion.

To determine whether the isometric force of concentration of the inspiratory muscles could be used to assess respiratory efferent neural activity, the tracheal pressure generated by the inspiratory muscles during airway occlusion (occluded tracheal pressure) was measured during progressive hypercapnia in anesthetized dogs breathing normally and breathing against added flow-resistive loads. Hypercapnia increased the peak end-inspiratory tracheal pressure and the occluded tracheal pressures generated 100, 200, and 300 ms after the onset of inspiration. The duration of the occluded inspiratory effort generally remained unchanged and the configuration of the pressure tracing was not affected. During normal breathing occluded tracheal pressures increased linearly with tidal volume and with the electrical activity of the diaphragm and the external intercostal muscles both before and after vagotomy. Inspiratory flow-resistive loading reduced the ventilatory response to CO2 but did not affect occluded tracheal pressures at any given PCO2 or the change in pressures with hypercapnia both before and after vagotomy. Similarly, expiratory flow-resistive loading failed to affect occluded tracheal pressures. These results suggest that occluded tracheal pressures measure respiratory efferent neural activity and can be used as indices of CO2 responsivity even during mechanical loading in anesthetized animals.

Airway Obstruction↗
PubMed1976

Effect of hypoxia on the pressure developed by inspiratory muscles during airway occlusion.

The effect of progressive isocapnic hypoxia on the pressure generated by the inspiratory muscle during airway occlusion was studied in 10 awake subjects during normal and obstructed breathing. Isocapnic hypoxia was produced by rebreathing a gas mixture of 6% CO2 in air while the expired gas was passed through a CO2 scrubber so as to maintain PACO2 constant (42.6 mmHg +/- 2.2 SE). Occlusion of the airway was performed randomly for a single breath at FRC. In all 10 subjects maximal pressure (Ppeak) and the pressures measured 100, 200, 300, and 400 ms after the onset of inspiration increased during hypoxia. Furthermore, good correlation was noted between the occlusion pressure response to hypoxia (delta P/DELTA[1/PO2-32]) and simultaneous changes in ventilatory response to hypoxia (delta VI/DELTA[1/PO2-32]). The occlusion pressure response to hypoxia therefore seems to be a reliable measure of respiratory center output. When rebreathing was repeated during inspiratory resistive loading, the occlusion pressure at any given PO2 and delta P/DELTA(1PO2-32) measured in the first 400 ms of inspiration increased in 9 of 10 subjects. Since PACO2 and PAO2 during both control and loaded experiments were the same, the increase in occlusion pressure in the presence of flow-resistive loading appeared to represent a neurally mediated increase in inspiratory motoneuron activity.

Adult↗
PubMed1975

The effect of variations in airflow pattern on gas exchange. A theoretical study.

It has been shown that gas exchange between the alveolar space and pulmonary capillary blood is affected by the pattern of airflow at the mouth in the non-homogeneous lung. The present theoretical study shows that even in the homogeneous lung, the pattern of airflow can affect gas exchange. When tidal volume, inspiratory and expiratory times remain constant, variations in the pattern of airflow result in significantly different values of steady state arterial PO2 and PCO2. This difference in steady state blood gases is exaggerated by low levels of minute ventilation and by long inspiratory times, but is unaffected by changes in the diffusion coefficient of the alveolar-capillary membrane.

Carbon Dioxide↗
PubMed1975

Abnormal breathing patterns.

In health, breathing is regular and the respiratory rate is sufficiency constant to be useful as a vital sign of health and disease. This regularity depends on a complex interplay of chemical and neural control systems that operate automatically to reset the rate and depth of breathing as changes occur in posture and activity, to adjust the level of ventilation so that changes in gas tensions and pH in the blood and in the brain intersitial fluid are exceedingly modest despite wide swings in metabolic rate and in environmental conditions, and to coordinate ventilation and circulation so that the requirements of individual tissues for O2 delivery and CO2 removal are satisfied. Two broad categories of disorders can result from malfunction of these systems (Table 1): (1) disproportionate ventilation (too high or too low) for the level of metabolic activity, thereby producing severe abnormalities in blood gas tensions or in acid-base balance, and (2) an irregular breathing pattern without eliciting gross changes in blood gas tensions or in acid-base balance. Because of the complexity of the control system, each of these categories represents a final common pathway that can be produced in different ways. In this presentation, we will attempt to describe the general features that characterize the operation of the control system and some new technics that make it possible to trouble-shoot the malfunctioning system in order to identify the mechanism(s) responsible for the abnormality in breathing pattern.

Animals↗
PubMed1975

Effect of liver failure on the response of ventilation and cerebral criculation to carbon dioxide in man and in the goat.

1. The acid-base state of arterial blood and cerebrospinal fluid, and the ventilatory response to CO2, were measured in twelve patients with liver disease. The CO2 response was also measured in eight goats before and after the experimental production of liver failure. Arterial PCO2 and pH, cerebral blood flow and the cerebral metabolic rate for oxygen were also measured in four of the goats while they breathed air and various CO2-enriched gas mixtures. 2. Liver failure was accompanied by a respiratory alkalosis in both the patients and in the goats. Decreased PCO2 and increased pH occurred in the cerebrospinal fluid and in the arterial blood of the patients. 3. The slope of the ventilatory response to CO2 was reduced when liver failure was severe, in patients and goats alike. In addition there was a reduction in the extrapolated PCO2 at zero ventilation, even when liver failure was mild. 4. Cerebral blood flow and metabolic rate were consistently reduced in the goats during liver failure. There was also less cerebral vasodilatation and a greater reduction in cerebral metabolism during experimental hypercapnia when these animals were in liver failure. 5. The decreases in the ventilatory and cerebral circulatory responsiveness to CO2 indicate that the brain is less well defended against hypercapnia in liver failure, and these changes are especially unfavourable as cerebral function deteriorates when the PCO2 is increased.

Adult↗
PubMed1975

Evaluation of breath holding in hypercapnia as a simple clinical test of respiratory chemosensitivity.

Breath holding was used as the basis of a simple test of respiratory chemosensitivity. Breath holding was begun at selected degrees of hypercapnia produced by CO2 rebreathing. In 16 healthy control subjects there was a linear regression of the log of breath-holding time on the PCO2 at the start of breath holding. Breath-holding time (BHT) and the slope of a log BHT/Pco2 plot were closely correlated with the ventilatory response to CO2. In five cases of the idiopathic hypoventilation syndrome, CO2 retention and reduced ventilatory response to CO2 were accompanied by prolonged breath-holding time and the regression of log BHT on Pco2 was abnormally flat. However, in 17 patients with chronic airways obstruction, breath-holding time was never prolonged and the log BHT/Pco2 relationship was normal, even though 13 had a diminished ventilatory response to CO2 and four had chronic CO2 retention. It is concluded that the BHT/Pco2 relationship provides a useful index of respiratory chemosensitivity which is not influenced by airways obstruction. This may be helpful in the detection of impaired chemosensitivity as a cause of CO2 retention even when the ventilation CO2 response is reduced non-specifically by coexisting airways obstruction.

Airway Obstruction↗
PubMed1975

Effect of fiberoptic bronchoscopy on respiratory performance in patients with chronic airways obstruction.

Lung volumes, airway resistance, expiratory flow rates, distribution of ventilation, and arterial blood gases were measured before and after fiberoptic bronchoscopy in 13 patients with moderately severe chronic airways obstruction and in 10 healthy non-smoking controls. Arterial blood gases were also monitored serially during the procedure. Arterial oxygen tension (Pao2) fell during fiberoptic bronchoscopy in both patients and controls whereas arterial carbon dioxide tension and pH remained unchanged. Control subjects had no change in lung mechanics after fiberoptic bronchoscopy. However, the patients consistently developed increased airway obstruction after fiberoptic bronchoscopy. Within 24 hours after bronchoscopy lung function in the patients returned to baseline values, except for the residual volume which remained abnormally high. The topical application of lignocaine (Lidocaine) for local anesthesia before fiberoptic bronchoscopy produced no effect on lung mechanics in nine patients and 10 controls, but Pao2 decreased in both the patient and control groups. These results indicate that fiberoptic bronchoscopy consistently inpairs lung mechanics and gas exchange in patients with chronic airways obstruction but that the impairment is mild and reversible. Lignocaine administration as well as the intubation procedure contribute to the fall in Pao2 which occurs both in the patients and in subjects without pre-existing lung disease.

Adult↗
PubMed1975

Effects of mechanical loading and hypercapnia on inspiratory muscle EMG.

The electromyograms of the diaphragm and an external intercostal muscle were analyzed to see if the effects of hypercapnia on inspiratory muscle electrical activity could be distinguished from those of mechanical loading and to determine whether changes in inspiratory muscle electrical activity were a sueful measure of CO2 response during mechanical loading. Anesthetized dogs were studied: 1) during progressive hypercapnia without mechanical loading, 2) during flow-resistive and elastic loading at constant PCO2, and 3) during progressive hypercapnia and mechanical loading. Both mechanical loading and hypercapnia increased total inspiratory diaphragmatic and intercostal muscle electrical activity. However, inspiratory duration was increased by mechanical loads but reduced by hypercapnia. Because of these changes in inspiratory duration, the average rate of diaphragmatic electrical activity remained unaffected by mechanical loading before and after vagotomy but was increased by hypercapnia. In contrast, both hypercapnia and mechanical loading increased the average rate of intercostal muscle electrical activity. There was a greater increase in both total and average rate of intercostal muscle electrical activity during hypercapnia in the presence of mechanical loading than during unloaded breathing. However, the change in total and average rate of diaphragmatic electrical activity with PCO2 was unaffected by added mechanical loads. These results suggest that diaphragmatic but not intercostal muscle electrical activity can be used as an index of CO2 response even during mechanical loading.

Airway Resistance↗
PubMed1975

Changes in strength of lung inflation reflex during prolonged inflation.

Recovery from respiratory inhibition produced by the lung inflation reflex was studied in anesthetized dogs, paralyzed and ventilated with a respiratory pump. During constant ventilation the lungs were periodically inflated using positive end-expiratory pressure, while the respiratory motor output was monitored in the phrenic nerve. Inhibition of the phrenic discharge was followed by gradual recovery throughout 8-min inflation periods despite constant blood gases. Recording afferent potentials in a vagus nerve indicated that adaptation of pulmonary stretch receptors contributed to the initial recovery of the phrenic discharge, but this recovery continued after the receptor discharge had stabilized. The phrenic discharge also recovered after initial inhibition in two situations which avoided stretch receptor adaptation: a) when the stretch receptor discharge from the separate lungs was alternated in an overlapping manner by asynchronous pulmonary ventilation, and b) during continuous electrical stimulation of a vagus nerve. Phrenic activity was temporarily increased above its control value after periods of lung inflation, asynchronous ventilation and vagal stimulation. It is concluded that the lung inflation reflex gradually attenuates during prolonged stimulation due to both stretch receptor adaptation and changes within the central pathways.

Adaptation, Physiological↗
PubMed1975

Changing effect of lung volume on respiratory drive in man.

Experiments were conducted on human subjects to study the effect of lung inflation during breath holding on respiratory drive. Two series of experiments were performed: the first to examine respiratory drive during a single breath hold, the second designed to examine the sustained effect of lung inflation on subsequent breath holds. The experiments involved breath holding begun either at the end of a normal expiration or after a maximum inspiration. When breath holding was repeated at 10-min intervals, the increase in BHT produced by lung inflation was greater in short breath holds (after CO2 rebreathing) than in long breath holds (after hyperventilation). If breath holds were made in rapid succession, the first breath hold was much longer when made at total lung capacity than at functional residual capacity, but this effect of lung inflation diminished in subsequent breath holds. It is concluded that the inhibitory effect of lung inflation decays during breath holding and is regained remarkably slowly during the period of breathing immediately after breath holding.

Adult↗
PubMed1975

Effects of a molecular change in collagen on lung structure and mechanical function.

Semicarbazide, a lathyrogen, was given to growing rats to elucidate the consequences of altering the molecular structure of fibrous proteins within the lung. Static pressure-volume (P-V) measurements during deflation of saline-filled lungs showed normal recoil pressure and compliance values within the physiological range of lung volume. Quasi-static P-V measurements were also normal during slow reinflation, even beyond physiological limits to a recoil pressure of 20 cm H20. However, the lungs of experimental rats ruptured at much lower recoil pressures than controls. Histology was normal in lungs fixed at 20 cm H20. In contrast, lungs showed dilation of terminal air spaces, rupture of alveolar walls, and an increase in mean linear intercept in experimental compared with control specimens, when fixed at 30 cm H20. Biochemical analyses revealed reduced cross-linking of lung collagen without change in its total content. There were no detectable changes in the quantity or quality of lung elastin. It is concluded that semicarbazide may selectively impair the maturation of lung collagen and that immaturity of lung collagen is associated with a reduction in the tensile strength of lung tissue, without changes in elasticity within physiological volume limits.

Animals↗