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Biomedical subjects

N H Edelman

Publications and source records attributed to N H Edelman.

At least 19 recordsLinked to original sources
PubMed1992

Modulation of respiratory responses to carotid sinus nerve stimulation by brain hypoxia.

This study examines the effect of progressive isocapnic CO hypoxemia on respiratory afterdischarge and the phrenic neurogram response to supramaximal carotid sinus nerve (CSN) stimulation. Twelve anesthetized, vagotomized, peripherally chemodenervated, ventilated cats with blood pressure controlled were studied. During isocapnic hypoxemia, the amplitude of the phrenic neurogram was progressively depressed. In contrast, the increase in peak phrenic amplitude produced by CSN stimulation was unchanged, suggesting that the central respiratory response to CSN stimulation is unaffected by progressive hypoxemia. The time constant of respiratory afterdischarge (tau) was calculated from best-fit plots of phrenic amplitude vs. time after cessation of CSN stimulation. Under control conditions the value of tau was 57.7 +/- 3 (SE) s (n = 12). During progressive isocapnic hypoxemia, tau decreased as a linear function of arterial O2 content (CaO2) such that a 40% reduction of CaO2 resulted in a 48% reduction in tau. This reduction of respiratory afterdischarge may contribute to the genesis of periodic breathing during hypoxia.

Animals↗
PubMed1992

Central respiratory carbon dioxide chemosensitivity does not decrease during sleep.

The ventilatory response to CO2 decreases during slow-wave sleep (SWS) and rapid-eye-movement (REM) sleep compared with awake levels. However, it is not known to what extent this can be attributed to decreased sensitivity of the CO2 chemoreflex. Mechanical factors during sleep may decrease ventilatory output, or PCO2 at the central chemoreceptor may not increase to the same degree as PaCO2, particularly during REM sleep when brain blood flow (BBF) is increased. In 10 goats, we measured the ventilatory (VI), diaphragmatic electromyogram (EMGdI), and BBF responses to CO2 rebreathing during each sleep-wake state. delta VI/delta PaCO2 decreased from wakefulness to SWS (p less than 0.05) and REM sleep (p less than 0.05). In contrast, delta EMGdI/delta PaCO2 was decreased only during REM sleep (p less than 0.05). Concurrently, delta BBF/delta PaCO2 increased during REM sleep (p less than 0.05) compared with the awake state or SWS. A significant reciprocal correlation existed between delta EMGdI/delta PaCO2 and delta BBF/delta PaCO2 across sleep states (r = -0.786). When EMGdI was related to directly measured cerebral venous PCO2 (n = 4), a single linear function (r = 0.894) was found, independent of sleep-wake state. Similar results were obtained during quasi-steady-state hypercapnia. We conclude that central CO2 chemosensitivity is intact during sleep.

Animals↗
PubMed1979

Effects of graded reduction of brain blood flow on ventilation in unanesthetized goats.

The ventilatory effects of graded reductions in brain bloow flow (BBF) were studied in unanesthetized goats. At a BBF of 85% of control (PVO2 = 29.2 Torr, PVCO2 = 47.3 Torr) there were no clear ventilatory effects. At BBF of 70% of control (PVO2 = 25.2, PVCO2 = 50.5) and 50% of control (PVCO2 = 22.3, PVCO2 = 53.0) there was hyperpnea, due primarily to an increase of tidal volume. Further reduction of BBF (avg of 42% of control) first produced intense tachypnea and then (30--40% of control) caused apnea that was reversible. At 50% BBF there was a reduction of brain O2 consumption, (4.67--4.00 ml/min) and an increase in systemic O2 consumption. beta-Adrenergic blockade prevented the increase in systemic O2 consumption and reduced the hyperpnea by two-thirds at 50% BBF; the residual hyperpnea was associated with hypocapnia in contrast to the hyperpnea prior to beta-adrenergic blockade, which was virtually isocapnic. The data suggest that hyperpnea due to brain ischemia is a result of both brain acidosis and systemic hypermetabolism. The similarity of the pattern of responses to that previously reported for progressive carboxyhemoglobinemia suggests that brain hypoxia is a determinant of the ventilatory responses to brain ischemia.

Animals↗
PubMed1979

Effects of morphine on ventilatory response to exercise.

The effects of analgesic doses of morphine on ventilation, arterial blood gas tensions, chemical control of breathing, and the ventilatory response to exercise were studied in six normal subjects. After administration of 0.2 mg/kg morphine, resting ventilation decreased primarily because of a reduction of tidal volume. Ventilatory responses to carbon dioxide and hypoxia were significantly reduced to one-half and one-third of control, respectively. Ventilatory responses at any given level of exercise were significantly reduced after morphine. However, since oxygen consumption during exercise was similarly reduced after morphine, the relationship between ventilation and metabolic rate during steady-state exercise was not altered by the drug. In addition, morphine prolonged the attainment of steady-state ventilation in four of the six subjects, similar to that reported for chemodenervated subjects. The findings suggest that blunting of chemoreception for hypoxia and hypercapnia has no effect upon the link between metabolic rate and ventilation during steady-state exercise, but the hypoxia chemoreflex may be involved in determining the dynamic characteristics of the response.

Acid-Base Equilibrium↗
PubMed1979

Effects of graded reduction of brain blood flow on chemical control of breathing.

We measured ventilatory responses to CO2 (delta VI/delta PCO2) and transient hypoxia (delta VI/delta SaO2) during reductions of brain blood flow (BBF) to 70% and 50% of control in unanesthetized goats. Increase in inspiratory volume per change in CO2 tension (delta VI/delta PCO2) was measured during rebreathing with sampling of both arterial and cerebral venous blood; increase in inspiratory volume per fall in arterial oxygen saturation (delta VI/delta SaO2) was assessed by the transient N2 inhalation method. Delta VI/delta SaO2 did not significantly change at 70% BBF, but was depressed at 50% BBF. Delta VI/delta PCO2 increased (0.94 +/- 0.18 to 1.29 +/- 0.24 l . min-1 . Torr-1) at 70% BBF if arterial CO2 tension were used to represent the CO2 stimulus but was unchanged if venous CO2 tension were used. At 50% BBF, delta VI/delta PCO2 was depressed (0.38 +/- 0.13 l . min-1 . Torr-1) for both representations of the CO2 stimulus. Brain ischemia increased blood pressure and heart rate but blunted the increase in BBF caused by hypercapnia. We conclude that 1) moderate brain ischemia (70% BBF) does not affect chemosensitivity to hypoxia and CO2, 2) delta VI/delta PCO2 may not be accurately determined from PaCO2 during brain ischemia because cerebrovascular reactivity to CO2 is depressed, and 3) severe brain ischemia (50% BBF) blunts delta VI/delta SaO2 and delta VI/delta PCO2, probably as a consequence of hypoxic depression of the respiratory neurons.

Animals↗
PubMed1979

Enhanced responses to aerosolized bronchodilator therapy in asthma using respiratory maneuvers.

To determine if respiratory maneuvers may enhance the response to inhaled bronchodilator drugs, we evaluated the bronchodilator responses when isoproterenol was: inhaled as a bolus high (80 percent VC) compared to low (20 percent VC) lung volumes, and inhaled as a single 800 microgram dose compared to four 200 microgram doses given 20 min apart. Nine asthmatic subjects inhaled isoproterenol sequentially at high and low lung volumes on two separate days; 15 others inhaled single doses of 200, 400, 600, and 800 microgram isoproterenol on four separate days. FEV1, specific conductance (Gaw/VL), Vmax50%, and the slope of phase 3 of the single-breath nitrogen test (deltaN2/L) were measured 10 min after each dose. FEV1 and Gaw/VL increased and deltaN2/L decreased more following inhalation at high compared to low lung volume (P less than 0.05). Gaw/VL increased more in the group given 800 microgram in divided doses than the group given a single dose (P less than 0.05). These findings suggest that the bronchodilator response to isoproterenol may be enhanced by inhaling the drug in divided doses sequentially and by delivering the drug near maximal inspiration. An enhanced response after the latter maneuver may be due to more uniform distribution of the drug to airway receptor sites.

Adult↗
PubMed1978

A microcomputer-based data acquisition and analysis system for CO2 rebreathing studies.

A real-time microcomputer-based data acquisition and analysis system has been developed to automate the measurement of the ventilatory response to CO2 by the rebreathing method. Previous systems acquire the data on-line and then analyze and display the results off-line. The system described here performs all processing on-line and displays experimental results in real-time. The results of 5 min of data acquisition are available for display only 1.5 sec after completion of the experiment. Immediate interpretation of the results of each experiment enable a series of related studies to be performed on the same patient in a short time period. The microcomputer is Digital Equipment Corporation's LSI-11, a low cost 16 bit machine with the basic instruction set of a PDP-11/40. The system has 16 kbytes of memory, a CRT for data display, and a paper tape reader for program loading. Due to the time constraints of real-time processing and the memory constraints of a small system, the software is written entirely in assembler language. The software includes routines for numeric and character input, line and graphical output, linear curve fitting, start of rise detection and floating point computations.

Carbon Dioxide↗
PubMed1977

Blunted respiratory drive in congenital myopathy.

Two patients with clinically mild congenital myopathies presented with chronic respiratory failure. Muscle weakness alone could not account for the respiratory insufficiency since static respiratory pressures were not markedly impaired, ventilation during exercise was normal, and daytime ventilation was normal if ventilatory assistance was provided at night. The ventilatory responses to inhaled carbon dioxide were very low, suggesting that impairment of the central nervous respiratory chemoreceptor contributed to hypoventilation. These patients and others described in the literature suggest that central depression of ventilation may occur more frequently than previously recognized in patients with muscular disorders. Patients with chronic respiratory failure due to central depression of respiratory drive can be effectively managed by assisted ventilation at night.

Adult↗
PubMed1977

Control of breathing during methadone addiction.

Chemical control of breathing was studied before and after the administration of the daily dose of methadone in 14 former heroin addicts who were enrolled in a methadone maintenance program and taking 60 to 100 mg/day. Two major groups were identified: group 1 in which subjects (n=6) had taken the drug for less than two months, and group 2 in which the subjects (n=6) had taken the drug from eight to 43 months. Prior to the daily dose of methadone, the levels of arterial carbon dioxide tension were significantly higher and ventilatory response to hypoxia significantly lower in group 1 than in group 2. Ventilatory responses to carbon dioxide (CO2) were also lower in group 1, but the difference was not statistically significant. Following the daily dose of methadone, the subjects in group 1 manifested significant reductions of ventilation and arterial oxygen tension, significant increases in arterial carbon dioxide tension and significant depressions of ventilatory responses to both CO2 and hypoxia in comparison to values before the administration of methadone. In contrast, subjects in group 2 manifested only a significant decrease in ventilatory responsiveness to hypoxia with no change in ventilation, arterial blood gas tensions or ventilatory responsiveness to CO2 following the daily dose. Two intermediate subjects (five and seven months) behaved as long-term subjects with regard to arterial carbon dioxide tension and CO2 responses but as short-term subjects with regard to responsiveness to hypoxia. Thus, during the first two months of methadone maintence, there is continual alveolar hypoventilation due to depression o both central (CO2) and peripheral (hypoxia) chemoreception. After five months, alveolar hypoventilation is abolished as the CO2-sensitive chemoreflex acquires full tolerance to methadone at the maintenance dose level. In contrast, tolerance of the hypoxia-sensitive chemoreflex is developed more slowly and is never complete.

Adult↗
PubMed1977

Correlation between ventilatory and cerebrovascular responses to inhalation of CO.

To study the determinants of carbon monoxide (CO) induced hyperpnea simultaneous measurements were made of carboxyhemoglobin level in arterial blood (HbCO), ventilation (VE), cerebral blood flow (CBF), O2 delivery to the brain (CBF X O2 content of arterial blood), O2 consumption of the brain (CMRO2), and O2 tension in cerebral venous blood (PVO2) during inhalation of 1% CO in 40% O2 by six unanesthetized goats. HbCO increased to 65% in 10 min; VE remained constant until a HbCO level of approximately 50% was reached and then increased abruptly; CBF increased progressively; O2 delivery to the brain and CMRO2 decreased somewhat with CO inhalation; these decreases reached statistical significance at a HbCO level of 30-40% whereupon the rate of decline with respect to HbCO level increased substantially; and PVO2 decreased progressively from an average of from 31 to 14.6 Torr and averaged 19.2 Torr when hyperpnea was manifest. When considered in the light of previous studies which indicate that CO-induced hyperpnea is not caused by stimulation of the carotid bodies, these data suggest that this phenomenon is related to brain hypoxia. Calculations of brain tissue O2 tension with the Krogh equation support this contention.

Animals↗
PubMed1977

Ventilatory responses to hypercapnia and hypoxia during continuous aspirin ingestion.

Hypercapnic and hypoxic ventilatory responses were serially measured in nine normal subjects given 3.9 g aspirin (ASA) per day for 9 days. Minute ventilation (VE), end-tidal carbon dioxide tension (PETCO2), venous bicarbonate concentration [HCO3-], oxygen consumption (VO2), hypercapnic ventilatory response (deltaVE/deltaPCO2), and isocapnic hypoxic ventilatory response (A) were determined before, 2 h after the first dose, and at 72-h intervals during the next 14 days. Serum salicylate levels averaged 18.6 +/- 2.0 mg/dl. VE increased (P less than 0.05, PETCO2 decreased (P less than 0.05), and [HCO3-] did not change significantly during drug ingestion. deltaVE/deltaPCO2 increased gradually to a value 37% greater than control by day 3 and remained constant (P less 0.01). A increased by 251% and VO2 by 18% within 2 h and remained constant for the remainder of the ASA period (P less than 0.01). All values returned to base line within 24 h following cessation of ASA. We conclude that during continuous ASA ingestion there is a gradual increase of hypercapnic ventilatory response. This may reflect slow entrance of ASA into the central nervous system. In contrast, there is a rapid rise in hypoxic ventilatory response which may be mechanically linked to changes in metabolic rate.

Adult↗
PubMed1976

Complications of obesity-hypoventilation syndrome in childhood.

The obesity-hypoventilation syndrome is rare in children, but it leads to serious complications and is associated with a high mortality. We report a child with this syndrome whose condition improved after intestinal bypass surgery. Review of the literature indicates that vigorous treatment of this disorder is necessary to prevent fatalities.

Adolescent↗