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Biomedical subjects

J A Dempsey

Publications and source records attributed to J A Dempsey.

At least 127 records · Page 7Linked to original sources
PubMed1990

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.

Adult↗
PubMed1990

Adaptations and limitations in the pulmonary system during exercise.

In most circumstances in health, efficient alveolar ventilation and alveolar-to-arterial exchange of O2 and CO2 are among the strongest of links in the gas-transport chain during maximal exercise. Indeed, in most instances, the metabolic cost of ventilation represents the only significant contribution of the pulmonary system to the limitation of O2 transport of locomotor muscles and thus to the limitation of maximum performance. Of the "weaknesses" inherent in the healthy pulmonary system response to exercise, the most serious one may well be its absence of structural adaptability to physical training or to the trained state. Thus, the lung's diffusion capacity and pulmonary capillary blood volume remain unaltered in the highly trained human or horse, while maximum pulmonary blood flow rises linearly with the enhanced max VO2. Similarly, ventilatory requirement rises markedly, with no alteration in the capability of the airways to produce higher flow rates or of the lung parenchyma to stretch to higher tidal volumes, and little or no change in the pressure-generating capability of inspiratory muscles. The case of the elderly athlete who remains capable of achieving high maximum pulmonary blood flows and ventilatory requirements and whose lung undergoes a normal aging process underscores the importance of deficits (from "normal") on the capacity end of this continuum of cost versus capacity in the pulmonary system. The asthmatic athlete may represent another such example of limited flow-generating capacity; and the healthy, young, highly fit athlete who shows marked reductions in SaO2 and in max VO2 at even moderately high altitudes demonstrates that, in many situations, precious little room can be added to the demand side or removed from the capacity side before signs of failure can be seen.

Adaptation, Physiological↗
PubMed1989

The effects of locomotion on respiratory muscle activity in the awake dog.

Using 6 chronically-instrumented awake dogs, we characterized the response of the respiratory muscles to mild and moderate treadmill exercise in terms of (1) the magnitude and timing of the EMGs of the costal and crural diaphragm, triangularis sterni and transverse abdominal muscles, and (2) the concomitant changes in esophageal (PE) and gastric (PG) pressures during treadmill exercise. Dogs wore a bivalved breathing mask which constrained breathing frequency and prevented some of the exercise-induced hypocapnia. Inspiratory and chest expiratory muscle EMGs increased linearly with a 1.5-fold tidal volume (VT) change during exercise. Abdominal muscle recruitment occurred during most exercise levels and exhibited (1) phasic activity coincident with footplant and (2) tonic activation evidenced by a baseline shift in PG and EMG activities. During control, inspiratory and expiratory flow preceded the onset of respiratory muscle EMG activity, but during exercise, electrical activation of these muscles coincided with the onset of mechanical flow. We conclude that phasic and tonic activation of expiratory muscles during exercise in the dog is significantly influenced by both respiratory and locomotory requirements. These patterns of expiratory muscle recruitment may assist inspiration by lengthening inspiratory muscles through decrements in end-expiratory lung volume and by passive recoil of the rib cage and abdominal compartments.

Animals↗
PubMed1989

The effects of chemical versus locomotory stimuli on respiratory muscle activity in the awake dog.

Using 6 chronically instrumented awake dogs, we contrasted the ventilatory and respiratory muscle EMG responses to steady-state normoxic hypercapnia with those occurring at similar levels of ventilation during steady-state treadmill exercise. During hypercapnia, increases in ventilatory output were primarily due to increments in VT whereas during exercise, increases in minute ventilation were due primarily to increases in frequency. With either hyperpnea, augmentation of both inspiratory and expiratory muscle EMG activity occurred but only diaphragmatic EMG activity was strongly correlated with tidal volume changes in both conditions. Using both EMGs and thoraco-abdominal pressures, we found that with increasing chemical or locomotory stimuli, during inspiration (1) diaphragmatic EMG activation occurred sooner relative to the onset of mechanical flow and (2) that respiratory muscles other than the diaphragm contributed significantly to the generation of inspiratory flow and VT either actively or passively through recoil. Post-inspiratory inspiratory activity of the crural diaphragm shortened relative to control in hypercapnia but did not change in exercise. Finally, during mild hyperpneas, end-expiratory lung volume did not change significantly in either hypercapnia or exercise but decreased at the higher levels of hyperpnea only during exercise. This may reflect differences not in the magnitude of phasic expiratory muscle activity, but rather in the degree of tonic abdominal muscle activation between the two conditions.

Animals↗
PubMed1989

Differential responses of expiratory muscles to chemical stimuli in awake dogs.

We assessed respiratory muscle response patterns to chemoreceptor stimuli (hypercapnia, hypoxia, normocapnic hypoxia, almitrine, and almitrine + CO2) in six awake dogs. Mean electromyogram (EMG) activities were measured in the crural (CR) diaphragm, triangularis sterni (TS), and transversus abdominis (TA). Hypercapnia and normocapnic hypoxia caused mild to marked hyperpnea [2-5 times control inspiratory flow (VI)] and increased activity in CR diaphragm, TS, and TA. When hypocapnia was permitted to develop during hypoxia and almitrine-induced moderate hyperpnea, CR diaphragm activity increased, whereas TS and TA activities usually did not change or were reduced below control. Over time in hypercapnia, CR diaphragm, TS, and TA were augmented and maintained at these levels over many minutes; with hypoxic hyperventilation CR diaphragm, TS, and TA were first augmented but then CR diaphragm remained augmented while TS and, less consistently, TA were inhibited over time. Marked hyperpnea (4-5 times control) due to carotid body stimulation increased TA and TS EMG activity despite an accompanying hypocapnia. We conclude that in the intact awake dog 1) carotid body stimulation augments the activity of both inspiratory and expiratory muscles; 2) hypocapnia overrides the augmenting effect of carotid body stimulation on expiratory muscles during moderate hyperpnea, usually resulting in either no change or inhibition; 3) at higher levels of hyperpnea both chemoreceptor stimulation and stimulatory effects secondary to a high ventilatory output favor expiratory muscle activation; these effects override any inhibitory effects of a coincident hypocapnia; and 4) expiratory muscles of the rib cage/abdomen may be augmented/inhibited independently of one another.

Animals↗
PubMed1989

Differential timing of respiratory muscles in response to chemical stimuli in awake dogs.

We assessed changes in respiratory muscle timing in response to hyperpnea and shortened inspiratory and expiratory times caused by chemoreceptor stimuli in six awake dogs. Durations of postinspiratory inspiratory activity of costal and crural diaphragm (PIIA), the delay in diaphragm electromyogram (EMG) after the initiation of inspiratory airflow, postexpiratory expiratory activity of the transversus abdominis (PEEA), and the delay of abdominal expiratory muscle activity after the initiation of expiratory airflow were measured. In control, four out of six dogs showed PIIA [8-10% of expiratory time (TE)]; all showed delay of diaphragm [19% of inspiratory time (TI)], delay of abdominal muscle activation (21% of TE), and PEEA (24% of TI). Hypercapnia decreased PIIA (4-9% of TE), maintained diaphragm delay at near control values (23% of TI), increased PEEA (36% of TI), eliminated delay of abdominal muscle activation (4% of TE), and decreased end-expiratory lung volume (EELV). Hypocapnic hypoxia increased PIIA (24-25% of TE), eliminated diaphragm delay (3% of TI), eliminated PEEA (3% of TI), reduced delay of abdominal muscle activation (14% of TE), and increased EELV. Most of these effects of hypoxic hypocapnia vs. hypercapnia on the within-breath EMG timing parameters corresponded to differences in the magnitude of expiratory muscle activation. These changes exerted significant influences on flow rates and EELV.

Abdominal Muscles↗
PubMed1989

Effects of incomplete pulmonary gas exchange on VO2 max.

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Exercise-induced hypercapnia in the horse.

The effects of exercise intensity and duration on blood gases in thoroughbred horses were studied to characterize the apparent exercise-induced failure in pulmonary gas exchange that occurs in these animals. In response to 2 min of exercise, arterial CO2 tension (PaCO2) decreased in mild and moderate exercise, returned to normocapnic levels in moderate to heavy exercise, and rose 5-10 Torr above resting values during very heavy exercise when CO2 production (VCO2) exceeded 20 times the resting value, and mixed venous CO2 tension approximated 140 Torr. Exercise-induced hypoxemia occurred at the onset of heavy exercise and was associated with the absence of a hyperventilatory response and an alveolar-arterial PO2 difference that increased four to six times above rest with very heavy exercise. PaCO2 was related to VCO2 but not fb, as changes in breathing frequency (fb) of 8-20 breaths/min at comparable VCO2 did not affect PaCO2. Prolonging very heavy exercise from 2 to 4 min caused a severe metabolic acidosis (arterial pH less than 7.15) and hypoxemia was maintained; however, CO2 was no longer retained, as PaCO2 gradually fell to below resting levels, due to an increased tidal volume at constant fb. We conclude that a truly compensatory hyperventilation to very heavy exercise in the horse is not achieved because of the excessive volumes and flow rates required by their extraordinarily high VCO2 and VO2. On the other hand, the frank CO2 retention during short-term high-intensity exercise occurs even though the horse is not apparently mechanically obligated to tolerate it.

Analysis of Variance↗
PubMed1989

Voluntary versus reflex regulation of maximal exercise flow: volume loops.

We determined the efficiency with which maximal exercise ventilatory output could be mimicked voluntarily. Five normal subjects exercised to maximal volitional effort and flow:volume and pressure:volume loops, and end-expiratory lung volume (EELV) and breathing pattern were measured. All subjects increased expiratory flow rate and reduced EELV sufficiently so that the forced vital capacity loop was approximated during at least some portion of expiration, but the generation of pleural pressure remained effective, i.e., equal to or only slightly in excess of that required to produce maximal expiratory flow (Pmax). Subsequently, while at rest, subjects used visual feedback and were able to closely mimic the flow:volume, EELV, and breath-timing achieved in maximal exercise; however: (1) expiratory pressures were excessive and usually exceeded average Pmax; (2) abdominal expiratory muscle activity was increased, as indicated by positive shifts in expiratory gastric pressure; and (3) total ventilatory work was increased 15 to 40% greater than that achieved in maximal exercise. Maximal voluntary efforts (MVV) caused EELV to increase and ventilatory work was increased 20 to 300% greater than during maximal exercise. We conclude that accurate determination of maximal effective ventilatory output available for maximal exercise or precise quantitation of the metabolic cost of producing maximal exercise ventilation requires replication of the pressure:volume, breath-timing, and EELV characteristics achieved in maximal exercise.

Adult↗
PubMed1988

Recombination among protein II genes of Neisseria gonorrhoeae generates new coding sequences and increases structural variability in the protein II family.

Expression of Neisseria gonorrhoeae Protein II (P.II) is subject to phase variation and antigenic variation. The P.II proteins made by one strain possess both unique and conserved antigenic determinants. To study the mechanism of antigenic variation, we cloned several P.II genes, using as probes a panel of monoclonal antibodies (MAbs) specific for unique determinants. The DNA sequences of three P.II genes showed that they shared a conserved framework, with two short hypervariable (HV) regions being responsible for most of the differences among them. We demonstrated that unique epitopes recognized by the MAbs were at least partially encoded by one of the HV regions. Moreover, we found that reassortment of the two HV regions among P.II genes occurs, generating increased structural and antigenic variability in the P.II protein family.

Antigens, Bacterial↗
PubMed1988

Regulation of end-expiratory lung volume during exercise.

We determined the effects of exercise on active expiration and end-expiratory lung volume (EELV) during steady-state exercise in 13 healthy subjects. We also addressed the questions of what affects active expiration during exercise. Exercise effects on EELV were determined by a He-dilution technique and verified by changes in end-expiratory esophageal pressure. We also used abdominal pressure-volume loops to determine active expiration. EELV was reduced with increasing exercise intensity. EELV was reduced significantly during even mild steady-state exercise and during heavy exercise decreased an average of 0.71 +/- 0.3 liter. Dynamic lung compliance was reduced 30-50%; EELV remained greater than closing volume. Changing the resistance to airflow (via SF6-O2 or He-O2 breathing) during steady-state exercise changed the peak gastric and esophageal pressure generation during expiration but did not alter EELV; breathing through the mouthpiece produced similar effects during exercise. EELV was significantly reduced in the supine position. With supine exercise active expiration was not elicited, and EELV remained the same as in supine rest. With CO2-driven hyperpnea (7-70 l/min), EELV remained unchanged from resting levels, whereas during exercise, at similar minute ventilation (VE) values EELV was consistently decreased. At the same VE, treadmill running caused an increase in tonic gastric pressure and greater reductions in EELV than either walking or cycling. We conclude that both the exercise stimulus and the resultant hyperpnea stimulate active expiration and a reduced FRC. This new EELV is preserved in the face of moderate changes in mechanical time constants of the lung. This reduced EELV during exercise aids inspiration by optimizing diaphragmatic length and permitting elastic recoil of the chest wall.

Adult↗
PubMed1988

Carotid body excision significantly changes ventilatory control in awake rats.

We determined the effects of carotid body excision (CBX) on eupneic ventilation and the ventilatory responses to acute hypoxia, hyperoxia, and chronic hypoxia in unanesthetized rats. Arterial PCO2 (PaCO2) and calculated minute alveolar ventilation to minute metabolic CO2 production (VA/VCO2) ratio were used to determine the ventilatory responses. The effects of CBX and sham operation were compared with intact controls (PaCO2 = 40.0 +/- 0.1 Torr, mean +/- 95% confidence limits, and VA/VCO2 = 21.6 +/- 0.1). CBX rats showed 1) chronic hypoventilation with respiratory acidosis, which was maintained for at least 75 days after surgery (PaCO2 = 48.4 +/- 1.1 Torr and VA/VCO2 = 17.9 +/- 0.4), 2) hyperventilation in response to acute hyperoxia vs. hypoventilation in intact rats, 3) an attenuated increase in VA/VCO2 in acute hypoxemia (arterial PO2 approximately equal to 49 Torr), which was 31% of the 8.7 +/- 0.3 increase in VA/VCO2 observed in control rats, 4) no ventilatory acclimatization between 1 and 24 h hypoxia, whereas intact rats had a further 7.5 +/- 1.5 increase in VA/VCO2, 5) a decreased PaCO2 upon acute restoration of normoxia after 24 h hypoxia in contrast to an increased PaCO2 in controls. We conclude that in rats carotid body chemoreceptors are essential to maintain normal eupneic ventilation and to the process of ventilatory acclimatization to chronic hypoxia.

Acute Disease↗
PubMed1988

Effects of altered CSF [H+] on ventilatory responses to exercise in the awake goat.

We investigated the effects of selective large changes in the acid-base environment of medullary chemoreceptors on the control of exercise hyperpnea in unanesthetized goats. Four intact and two carotid body-denervated goats underwent cisternal perfusion with mock cerebrospinal fluid (CSF) of markedly varying [HCO-3] (CSF [H+] = 21-95 neq/l; pH 7.68-7.02) until a new steady state of alveolar hypo- or hyperventilation was reached [arterial PCO2 (PaCO2) = 31-54 Torr]. Perfusion continued as the goats completed two levels of steady-state treadmill walking [2 to 4-fold increase in CO2 production (VCO2)]. With normal acid-base status in CSF, goats usually hyperventilated slightly from rest through exercise (-3 Torr PaCO2, rest to VCO2 = 1.1 l/min). Changing CSF perfusate [H+] changed the level of resting PaCO2 (+6 and -4 Torr), but with few exceptions, the regulation of PaCO2 during exercise (delta PaCO2/delta VCO2) remained similar regardless of the new ventilatory steady state imposed by changing CSF [H+]. Thus the gain (slope) of the ventilatory response to exercise (ratio of change in alveolar ventilation to change in VCO2) must have increased approximately 15% with decreased resting PaCO2 (acidic CSF) and decreased approximately 9% with increased resting PaCO2 (alkaline CSF). A similar effect of CSF [H+] on resting PaCO2 and on delta PaCO2/VCO2 during exercise also occurred in two carotid body-denervated goats. Our results show that alteration of the gain of the ventilatory response to exercise occurs on acute alterations in resting PaCO2 set point (via changing CSF [H+]) and that the primary stimuli to exercise hyperpnea can operate independently of central or peripheral chemoreception.

Acid-Base Equilibrium↗
PubMed1988

Effect of airway impedance on CO2 retention and respiratory muscle activity during NREM sleep.

We hypothesized that a sleep-induced increase in mechanical impedance contributes to CO2 retention and respiratory muscle recruitment during non-rapid-eye-movement (NREM) sleep. The effect NREM sleep on respiratory muscle activity and CO2 retention was measured in healthy subjects who increased maximum total pulmonary resistance (RLmax, 1-81 cmH2O.l-1.s) from awake to NREM sleep. We determined the effects of this sleep-induced increase in airway impedance by steady-state inhalation of a reduced-density gas mixture (79% He-21% O2, He-O2). Both arterialized blood PCO2 (PaCO2) and end-tidal PCO2 (PETCO2) were measured. Inspiratory (EMGinsp) and expiratory (EMGexp) respiratory muscle electromyogram activity was measured. NREM sleep caused 1) RLmax to increase (7 +/- 3 vs. 39 +/- 28 cmH2O.l-1.s), 2) PaCO2 and/or PETCO2 to increase in all subjects (40 +/- 2 vs. 44 +/- 3 Torr), and 3) EMGinsp to increase in 8 of 9 subjects and EMGexp to increase in 9 of 17 subjects. Compared with steady-state air breathing during NREM sleep, steady-state He-O2 breathing 1) reduced RLmax by 38%, 2) decreased PaCO2 and PETCO2 by 2 Torr, and 3) decreased both EMGinsp (-20%) and EMGexp (-54%). We concluded that the sleep-induced increase in upper airway resistance accompanied by the absence of immediate load compensation is an important determinant of CO2 retention, which, in turn, may cause augmentation of inspiratory and expiratory muscle activity above waking levels during NREM sleep.

Adult↗
PubMed1988

Inhibition of inspiratory muscle activity during sleep. Chemical and nonchemical influences.

The purpose of this study was twofold, namely, to determine (1) if phasic respiratory muscle activity can be inhibited during nocturnal mechanical ventilation, and (2) the mechanism by which this inhibition occurs. Twelve normal subjects were studied during non-rapid eye movement (NREM) sleep (Stages 2 to 4) while receiving negative (NPV, 8 subjects) or positive (PPV, 4 subjects) pressure ventilation and during spontaneous breathing. EMGdia (surface), end-tidal CO2 pressure (PETCO2), esophageal pressure (Pe), and ventilation were measured with a flow-through hood (NPV) or a mask (PPV). The following results were obtained during steady-state (3 to 22 min) mechanical ventilation. (1) A decrease in PETCO2 of 2 to 6 mm Hg resulted in elimination of phasic EMGdia in all subjects. Inhibition of respiratory muscle EMG (and a positive shift in Pe) occurred coincident with the breath-by-breath reduction in PETCO2, so that EMGdia was usually eliminated after the initial 4 to 6 breaths while using the ventilator. (2) Returning PETCO2 to the spontaneous sleeping level by adding CO2 to the inspired air (isocapnic mechanical ventilation) caused significant increases in EMGdia. During this isocapnic mechanical ventilation, however, EMGdia usually remained less than during eucapnic control. (3) Stopping the ventilator during hypocapnic ventilation caused a prolongation of expiratory time (TE) that was proportional to the degree of hypocapnia during the mechanical ventilation (100 to 1,200% increase over control). During isocapnic ventilation, cessation of mechanical ventilation caused no change in TE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗