Effect of aerosolized histamine on occlusion pressure and ventilation in humans

1982 ◽  
Vol 53 (3) ◽  
pp. 690-697 ◽  
Author(s):  
R. P. Millman ◽  
D. A. Silage ◽  
D. D. Peterson ◽  
A. I. Pack
Keyword(s):  
Smooth Muscle ◽  
Neural Activity ◽  
Occlusion Pressure ◽  
Bronchial Smooth Muscle ◽  
Co2 Partial Pressure ◽  
Residual Capacity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Airway Conductance ◽  
Stimulation Of

To define further the mechanism by which inspiratory neural activity is increased in asthma, we studied the effect of aerosolized histamine on occlusion pressure (P100) and ventilation in conscious humans while end-tidal CO2 partial pressure was maintained at a constant, slightly hypercapnic level. The dose of histamine we employed varied from subject to subject but was such that it produced a 70% reduction in specific airway conductance in each subject. In 9 of the 13 subjects tested, inhaled histamine significantly increased P100. This increase was not due to changes in functional residual capacity, which was not affected by aerosolized histamine. Inhalation of isoproterenol abolished the effects of histamine on specific airway conductance and P100. Anesthesia of the airways by lidocaine eliminated the effect of histamine on P100 but did not alter the magnitude of the change in specific airway conductance produced by histamine. We conclude that the increase in occlusion pressure seen after the inhalation of histamine in humans depends on both contraction of bronchial smooth muscle and stimulation of airway receptors.

Inspiratory rhythm in airway smooth muscle tone

1985 ◽  
Vol 58 (3) ◽  
pp. 911-920 ◽  
Author(s):  
R. A. Mitchell ◽  
D. A. Herbert ◽  
D. G. Baker
Keyword(s):  
Smooth Muscle ◽  
Vagus Nerve ◽  
Airway Smooth Muscle ◽  
Phrenic Nerve ◽  
Nerve Activity ◽  
Lung Inflation ◽  
Phrenic Nerve Activity ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Stimulation Of

In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.

The effect of facial cold stimulation on airway conductance in healthy man

1969 ◽  
Vol 47 (5) ◽  
pp. 453-457 ◽  
Author(s):  
W. T. Josenhans ◽  
G. N. Melville ◽  
W. T. Ulmer
Keyword(s):  
Airway Resistance ◽  
Facial Skin ◽  
Air Trapping ◽  
Cold Stimulation ◽  
Resistance Increase ◽  
Cold Receptors ◽  
Residual Capacity ◽  
Young Subjects ◽  
Airway Conductance ◽  
Stimulation Of

The effect on airway conductance (Gaw) and functional residual capacity (FRC) of stimulation of cold receptors in facial skin was studied in 12 healthy young subjects, with a body plethysmograph. Mean Gaw decreased significantly, from 0.44 to 0.38 liter s−1 cm−1 H2O, in 10 subjects. FRC was only slightly affected, probably because the experiment was too brief to allow air-trapping. It is concluded that the Gaw decrease during exposure to cold results from bronchoconstriction due to (a) stimulation of trigeminal nerve cold receptors and to (b) pharyngeal and glottal airway resistance increase resulting from frequent involuntary 'dry' swallowing.

Interaction of sleep state and chemical stimuli in sustaining rhythmic ventilation

1983 ◽  
Vol 55 (3) ◽  
pp. 813-822 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Periodic Breathing ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Positive Pressure ◽  
Sleep State ◽  
Co2 Partial Pressure ◽  
Apnea Duration ◽  
O2 Concentration ◽  
End Tidal ◽  
End Tidal Co2

The effect of sleep state on ventilatory rhythmicity following graded hypocapnia was determined in two normal subjects and one patient with a chronic tracheostomy. Passive positive-pressure hyperventilation (PHV) was performed for 3 min awake and during nonrapid-eye-movement (NREM) sleep with hyperoxia [fractional inspired O2 concentration (FIO2) = 0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no immediate posthyperventilation apnea was noted following abrupt cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep levels and 1-2 Torr below the waking level. In hypoxia, PETCO2 increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr below NREM sleep levels and 1-2 Torr above awake levels. Apnea duration (5-45 s) was significantly correlated to the magnitude of hypocapnia (range 27-41 Torr). PHV caused no apnea when isocapnia was maintained via increased inspired CO2. Prolonged hypoxia caused periodic breathing, and the abrupt transition from short-term hypoxic-induced hyperventilation to acute hyperoxia caused apnea during NREM sleep when PETCO2 was lowered to or below the subject's apneic threshold as predetermined (passively) by PHV. We concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].

Diaphragm electrical activity during negative lower torso pressure in quadriplegic men

1981 ◽  
Vol 51 (3) ◽  
pp. 654-659 ◽  
Author(s):  
R. B. Banzett ◽  
G. F. Inbar ◽  
R. Brown ◽  
M. Goldman ◽  
A. Rossier ◽  
...  
Keyword(s):  
Partial Pressure ◽  
Tidal Volume ◽  
Respiratory System ◽  
Afferent Pathways ◽  
Co2 Partial Pressure ◽  
Inspiratory Muscles ◽  
Spinal Lesions ◽  
Diaphragm Electrical Activity ◽  
End Tidal ◽  
End Tidal Co2

We recorded the diaphragm electromyogram (EMG) of quadriplegic men before and during exposure of the lower torso to continuous negative pressure, which caused shortening of the inspiratory muscles by expanding the respiratory system by one tidal volume. The moving-time-averaged diaphragm EMG was larger during expansion of the respiratory system. When we repeated the experiment with subjects who breathed through a mouthpiece, we found qualitatively similar EMG changes and little or no change in tidal volume or end-tidal CO2 partial pressure. When the pressure was applied or removed rapidly, changes in EMG occurred within one or two breaths. Because end-tidal CO2 partial pressure did not increase, and because the response was rapid, we suggest that the response results from proprioceptive, rather than chemoreceptive, reflexes. As most of these men had complete spinal lesions at C6 or C7 the afferent pathways are likely to be vagal or phrenic.

Lung volume, closing volume, and gas exchange

1982 ◽  
Vol 52 (6) ◽  
pp. 1453-1457 ◽  
Author(s):  
S. C. Morrison ◽  
D. G. Stubbing ◽  
P. V. Zimmerman ◽  
E. J. Campbell
Keyword(s):  
Gas Exchange ◽  
Lung Volume ◽  
Normal Subjects ◽  
Close Correlation ◽  
Closing Volume ◽  
Tidal Breathing ◽  
Co2 Partial Pressure ◽  
Residual Capacity ◽  
End Tidal ◽  
Arterial O2 Saturation

The effect of a voluntary reduction in lung volume on arterial O2 saturation (SaO2) was studied in 10 normal subjects aged 19–63 yr. SaO2 was measured by ear oximetry first during tidal breathing at functional residual capacity, and then during tidal breathing at 380 ml above residual volume. Tidal volume and breathing frequency were kept constant, and end-tidal CO2 partial pressure remained stable or fell in 9 out of 10 subjects. When lung volume was reduced, SaO2 fell by a mean of 1.5% (range 0–3%). Closing volume (CV) was measured by the N2-washout method (mean 0.89 liter, range 0.41–1.44). There was a close correlation between CV and the fall in SaO2 (r = 0.867, P = 0.001). Arterial and mixed venous CO2 were measured in one subject; the results indicated some fall in cardiac output following the lung volume change, but this accounted for less than half of the fall in SaO2. The relationship between CV and the lung volume at which tidal breathing occurs is an important determinant of pulmonary gas exchange through its effect on the matching of ventilation to perfusion.

METABOREFLEX CHANGES RELATIONSHIP BETWEEN END-TIDAL CO2 PARTIAL PRESSURE AND VENTILATION

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S229
Author(s):  
N Hayashi ◽  
T Miyamoto ◽  
Y Fukuba ◽  
T Yoshida
Keyword(s):  
Partial Pressure ◽  
Co2 Partial Pressure ◽  
End Tidal ◽  
End Tidal Co2

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

1981 ◽  
Vol 50 (4) ◽  
pp. 724-730 ◽  
Author(s):  
B. Gothe ◽  
M. D. Altose ◽  
M. D. Goldman ◽  
N. S. Cherniack
Keyword(s):  
Partial Pressure ◽  
Tidal Volume ◽  
Quiet Sleep ◽  
Rib Cage ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Quantitative Measurements ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Different Levels

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.

Blood osmolality during in vivo changes of CO2 pressure

1983 ◽  
Vol 54 (1) ◽  
pp. 123-129 ◽  
Author(s):  
D. Boning ◽  
U. Vaas ◽  
K. M. Braumann
Keyword(s):  
Venous Blood ◽  
Hysteresis Loops ◽  
Whole Body ◽  
Co2 Partial Pressure ◽  
Rapid Restoration ◽  
Body Compartments ◽  
End Tidal ◽  
Buffer Capacities ◽  
End Tidal Co2

In 16 experiments male subjects, age 22.4 +/- 0.5 (SE) yr, inspired CO2 for 15 min (8% end-tidal CO2) or hyperventilated for 30 min (2.5% end-tidal CO2). Osmolality (Osm) and acid-base status of arterialized venous blood were determined at short intervals until 30 min after hypo- and hypercapnia, respectively. During hypocapnia [CO2 partial pressure (PCO2) -2.31 +/- 0.32 kPa (-17.4 Torr), pH + 0.19 units], Osm decreased by 3.9 +/- 0.3 mosmol/kg H2O; during hypercapnia [PCO2 + 2.10 +/- 0.28 kPa (+15.8 Torr), pH -0.12 units], Osm increased by 5.8 +/- 0.7 mosmol/kg H2O. Presentation of the data in Osm-PCO2 or Osm-pH diagrams yields hysteresis loops probably caused by exchange between blood and tissues. The dependence of Osm on PCO2 must result mainly from CO2 buffering and therefore from the formation of bicarbonate. In spite of the different buffer capacities in various body compartments, water exchange allows rapid restoration of osmotic equilibrium throughout the organism. Thus delta Osm/delta pH during a PCO2 jump largely depends on the mean buffer capacity of the whole body. The high estimated buffer value during hypercapnia (38 mmol/kg H2O) compared with hypocapnia (19 mmol/kg H2O) seems to result from very strong muscle buffering during moderate acidosis.

Accelerated decay of inspiratory pressure during hypercapnic endurance trials in humans

1988 ◽  
Vol 65 (2) ◽  
pp. 728-735 ◽  
Author(s):  
B. T. Ameredes ◽  
T. L. Clanton
Keyword(s):  
Breathing Pattern ◽  
Human Subjects ◽  
Constant Flow ◽  
Force Output ◽  
Mouth Pressure ◽  
Residual Capacity ◽  
Flow Generator ◽  
Normal Human ◽  
End Tidal ◽  
End Tidal Co2

Seven normal human subjects inspired a CO2-O2 mixture from a constant-flow generator while performing maximal inspiratory maneuvers from functional residual capacity. End-tidal CO2 (ETCO2) was maintained at either 5.5 (normocapnia), 3.5 (hypocapnia), or 7% (hypercapnia) on separate testing days. Subjects attained maximal mouth pressure (Pm) while breathing at either 1.25 or 1 l/s, utilizing a fixed breathing pattern (duty cycle 0.43) with an inspiratory time of 1.5 s. Maximal Pm was measured at rest and then during a 10-min endurance trial in which subjects repeated maximal voluntary inspirations with constant flow and breathing pattern. The endurance Pm data were fit to nonlinear exponential regression. The results indicated that 1) maximal Pm at rest was unaffected by changing ETCO2; 2) the rate of Pm decay over time was accelerated by hypercapnia, whereas hypocapnia showed no consistent effects; and 3) "sustainable" Pm, attained toward the end of the endurance trial, was not decreased; therefore sustainable force output was preserved in response to changing ETCO2.

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