Effect of expiratory loading on glottic dimensions in humans

1985 ◽  
Vol 58 (2) ◽  
pp. 605-611 ◽  
Author(s):  
T. P. Brancatisano ◽  
D. S. Dodd ◽  
P. W. Collett ◽  
L. A. Engel
Keyword(s):  
Inverse Relationship ◽  
Time Course ◽  
Normal Subjects ◽  
Positive End Expiratory Pressure ◽  
Expiratory Resistance ◽  
Mouth Pressure ◽  
Internal Impedance ◽  
Resistive Loads ◽  
Increased Activity ◽  
Medullary Neurons

We examined the effects of external mechanical loading on glottic dimensions in 13 normal subjects. When flow-resistive loads of 7, 27, and 48 cmH2O X l-1 X s, measured at 0.2 l/s, were applied during expiration, glottic width at the mid-tidal volume point in expiration (dge) was 2.3 +/- 12, 37.9 +/- 7.5, and 38.3 +/- 8.9% (means +/- SE) less than the control dge, respectively. Simultaneously, mouth pressure (Pm) increased by 2.5 +/- 4, 3.0 +/- 0.4, and 4.6 +/- 0.6 cmH2O, respectively. When subjects were switched from a resistance to a positive end-expiratory pressure at comparable values of Pm, both dge and expiratory flow returned to control values, whereas the level of hyperinflation remained constant. Glottic width during inspiration (unloaded) did not change on any of the resistive loads. There was a slight inverse relationship between the ratio of expiratory to inspiratory glottic width and the ratio of expiratory to inspiratory duration. Our results show noncompensatory glottic narrowing when subjects breathe against an expiratory resistance and suggest that the glottic dimensions are influenced by the time course of lung emptying during expiration. We speculate that the glottic constriction is related to the increased activity of expiratory medullary neurons during loaded expiration and, by increasing the internal impedance of the respiratory system, may have a stabilizing function.

Ventilatory and occlusion pressure responses to helium breathing

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Breathing Circuit ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Mouth Pressure ◽  
Partial Pressure Of Co2 ◽  
Lung Resistance ◽  
Balloon Technique ◽  
Resistive Loads ◽  
End Tidal ◽  
Airway Tone

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.

Effect of mechanical loading on displacements of chest wall during breathing in humans

1985 ◽  
Vol 58 (2) ◽  
pp. 477-484 ◽  
Author(s):  
P. M. Mengeot ◽  
J. H. Bates ◽  
J. G. Martin
Keyword(s):  
Mechanical Properties ◽  
Chest Wall ◽  
Time Course ◽  
Normal Subjects ◽  
Abdominal Muscle ◽  
Phase Lag ◽  
Breathing Frequency ◽  
Quiet Breathing ◽  
Rib Cage ◽  
Mouth Pressure

Using a respiratory inductive plethysmograph (Respitrace) we studied thoracoabdominal movements in eight normal subjects during inspiratory resistive (Res) and elastic (El) loading. The magnitude of loads was chosen so as to produce a fall in inspiratory mouth pressure of 20 cmH2O. The contribution of rib cage (RC) to tidal volume (VT) increased significantly from 68% during quiet breathing (QB) to 74% during El and 78% during Res. VT and breathing frequency did not change significantly. During loading a phase lag was present on inspiration so that the abdomen led the rib cage. However, outward movement of the abdomen ceased in the latter part of inspiration, and the RC became the sole contributor to VT. These observations suggest greater recruitment of the inspiratory musculature of the RC than the diaphragm during loading, although changes in the mechanical properties of the chest wall may also have contributed. Indeed, an increase in abdominal end-expiratory and end-inspiratory pressures was observed in five out of six subjects, indicating abdominal muscle recruitment which may account for part of the reduction in abdominal excursion. Both Res and El increased the rate of emptying of the respiratory system during the ensuing unloaded expiration as a result of a reduction in rib cage expiratory-braking mechanisms. The time course of abdominal displacements during expiration was unaffected by loading.

Fatigue of inspiratory muscles and their synergic behavior

1979 ◽  
Vol 46 (5) ◽  
pp. 897-904 ◽  
Author(s):  
C. Roussos ◽  
M. Fixley ◽  
D. Gross ◽  
P. T. Macklem
Keyword(s):  
Transpulmonary Pressure ◽  
Normal Subjects ◽  
Abdominal Pressure ◽  
Inspiratory Capacity ◽  
Inspiratory Muscles ◽  
Mouth Pressure ◽  
Residual Capacity ◽  
Resistive Loads ◽  
Accessory Muscles ◽  
Inspiratory Muscle Fatigue

The time (tlim) required to produce inspiratory muscle fatigue was measured in five normal subjects breathing at functional residual capacity (FRC) against a variety of high inspiratory resistive loads. In every breathing test the subjects generated with each inspiration a mouth pressure (Pm) that was a predetermined fraction of maximum Pm (Pmmax). They continued breathing until they were unable to generate this Pm. The Pm/Pmmax that could be generated indefinitely (Pmcrit) was around 60%. The inspiratory power output at that level of breathing was 6.6 kg.m/min (Wcrit). In three of those subjects the same experiment was conducted at an end-expiratory volume of FRC + one-half inspiratory capacity (1/2IC). The higher lung volume was actively maintained by the subjects watching end-expiratory transpulmonary pressure on an oscilloscope. For any fraction of the maximum mouth pressure at FRC + 1/2IC (Pm'max), tlim was shorter than FRC. Pmcrit decreased to 30% Pm'max and Wcrit to 2.6 kg.m/min. Monitoring the abdominal pressure revealed that the contribution of the diaphragm and intercostal accessory muscles alternated in time, possibly postponing the onset of fatigue.

Response of normal subjects to inspiratory resistive unloading

1989 ◽  
Vol 66 (3) ◽  
pp. 1113-1119 ◽  
Author(s):  
C. G. Gallagher ◽  
R. Sanii ◽  
M. Younes
Keyword(s):  
Average Rate ◽  
Minute Ventilation ◽  
Co2 Concentration ◽  
Normal Subjects ◽  
Resistive Load ◽  
Mouth Pressure ◽  
Inspiratory Resistance ◽  
Residual Capacity ◽  
Resistive Loads ◽  
End Tidal

The purpose of this study was to examine the role of the normal inspiratory resistive load in the regulation of respiratory motor output in resting conscious humans. We used a recently described device (J. Appl. Physiol. 62: 2491–2499, 1987) to make mouth pressure during inspiration positive and proportional to inspiratory flow, thus causing inspiratory resistive unloading (IRUL); the magnitude of IRUL (delta R = -3.0 cmH2O.1(-1).s) was set so as to unload most (approximately 86% of the normal inspiratory resistance. Six conscious normal humans were studied. Driving pressure (DP) was calculated according to the method of Younes et al. (J. Appl. Physiol. 51: 963–1001, 1981), which provides the equivalent of occlusion pressure at functional residual capacity throughout the breath. IRUL resulted in small but significant changes in minute ventilation (0.6 1/min) and in end-tidal CO2 concentration (-0.11%) with no significant change in tidal volume or respiratory frequency. There was a significant shortening of the duration (neural inspiratory time) of the rising phase of the DP waveform and the shape of the rising phase became more convex to the time axis. There was no change in the average rate of rise of DP or in the duration or shape of the declining phase. We conclude that 1) the normal inspiratory resistance is an important determinant of the duration and shape of the rising phase of DP and 2) the neural responses elicited by the normal inspiratory resistance are similar to those observed with added inspiratory resistive loads.

Desmopressin Stimulates Parallel Norepinephrine and Tissue Plasminogen Activator Release in Normal Subjects and Patients with Diabetes Mellitus

1988 ◽  
Vol 59 (02) ◽  
pp. 269-272 ◽  
Author(s):  
M B Grant ◽  
C Guay ◽  
R Lottenberg
Keyword(s):  
Diabetes Mellitus ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Time Course ◽  
Vascular Endothelial Cells ◽  
Normal Subjects ◽  
Plasma Norepinephrine ◽  
Endogenous Catecholamine ◽  
Tissue Plasminogen ◽  
Patients With Diabetes

SummaryDesmopressin acetate administration markedly stimulates release of tissue plasminogen activator (t-PA) from vascular endothelial cells. The mechanism for this effect is unknown. Because infusion of epinephrine has been shown to increase t-PA levels, we examined the role of endogenous catecholamine mediation of t-PA release by desmopressin. Intravenous desmopressin acetate (0.3 μg/kg) was infused over 30 min in 9 controls and 11 subjects with diabetes mellitus, a condition associated with abnormalities of the fibrinolytic system. Plasma was collected in the supine, overnight fasted state at 15 min intervals (0-60 min) for measurement of t-PA activity, t-PA antigen and fractionated catecholamines. t-PA activity peaked at 30-45 min and subsequently decreased. The norepinephrine levels paralleled the t-PA activity. t-PA activity increased 10-fold from 0.14 ± .12 to 1.49 ± 0.79 IU/ml (Mean ± SD) and plasma norepinephrine increased 2- fold from 426 ± 90 to 780 ± 292 pg/ml. However, epinephrine and dopamine levels did not change significantly. The response to desmopressin of control and diabetic subjects was not shown to differ and their data were combined. We conclude that desmopressin increases plasma norepinephrine in addition to t-PA and that the parallel time course of change suggests a possible role for norepinephrine in mediating endothelial cell t-PA release.

EARLY VARIATIONS OF PLASMA CORTISOL AFTER PULSE INTRAVENOUS INJECTION OF DIBUTYRYL CYCLIC ADENOSINE 3′,5′-MONOPHOSPHATE IN NORMAL SUBJECTS

1973 ◽  
Vol 72 (4) ◽  
pp. 753-761 ◽  
Author(s):  
Alberto Angeli ◽  
Giuseppe Boccuzzi ◽  
Roberto Frajria ◽  
Daniela Bisbocci ◽  
Franco Ceresa
Keyword(s):  
Intravenous Injection ◽  
Plasma Cortisol ◽  
Time Course ◽  
Healthy Adult ◽  
Normal Subjects ◽  
Adult Women ◽  
Healthy Women ◽  
Adrenal Steroidogenesis ◽  
The Mean ◽  
Zero Time

ABSTRACT 10 mg/kg of dibutyryl cyclic adenosine 3′,5′-monophosphate (Db-cAMP) was iv pulse injected into twelve healthy adult women. The plasma cortisol levels were determined as 11-OHCS at zero time and then at 2.5, 5, 7.5, 10, 15, 30, 60 and 180 min after the injection. The data were compared with those obtained at the corresponding times in two groups of eleven and seventeen healthy women after the injection of 250 ng and 250 μg of synthetic β-1-24 corticotrophin performed in the same manner as the injection of the nucleotide. The mean increments in plasma cortisol were significantly lower after Db-cAMP than after ACTH. Differences were noted by analyzing the time course of the responses. In the case of stimulation with Db-cAMP the 11-OHCS levels rose progressively to a maximum at 15–30 min. By contrast, a peak of plasma cortisol was evident in most cases within a few min after the injection of ACTH; after a fall, a later rise was then observed starting from 15 min. The differences in the plasma 11-OHCS responses after the two stimuli may also be of interest clinically for the investigation of some aspects of adrenal steroidogenesis.

Detection Latency of Added Loads to Breathing

1982 ◽  
Vol 63 (1) ◽  
pp. 11-15 ◽  
Author(s):  
J. G. W. Burdon ◽  
K. J. Killian ◽  
E. J. M. Campbell
Keyword(s):  
Peak Inspiratory Pressure ◽  
Normal Subjects ◽  
Reciprocal Relationship ◽  
Respiratory Cycle ◽  
Curvilinear Relationship ◽  
Similar Relationship ◽  
Detection Latency ◽  
Mechanical Information ◽  
Resistive Loads ◽  
Comparable Magnitude

1. Detection latency of a range of added elastic (0·95–4·50 kPa/l) and resistive (0·73–3·29 kPa l−1 s) loads to breathing were measured in five normal subjects. Detection latency was defined as the time from the onset of the breath to detection of the load. 2. Detection latency followed a curvilinear relationship when plotted as a function of the magnitude of the added loads. A similar relationship was found with both elastic and resistive loads although detection latencies to added elastances were longer than for added resistances. 3. When the added load was expressed in terms of comparable magnitude (peak inspiratory pressure) detection latencies for added elastances were found to be consistently longer than for added resistive loads. 4. These studies show that the detection latency to added inspiratory loads follows a reciprocal relationship, that detection latencies for elastic and resistive loads are clearly different and suggest that these loads are detected during the respiratory cycle at a time when the mechanical information regarding muscular pressure is greatest.

Sensation of dyspnea during hypercapnia, exercise, and voluntary hyperventilation

1990 ◽  
Vol 68 (5) ◽  
pp. 2100-2106 ◽  
Author(s):  
T. Chonan ◽  
M. B. Mulholland ◽  
J. Leitner ◽  
M. D. Altose ◽  
N. S. Cherniack
Keyword(s):  
Visual Analog Scale ◽  
Line Intensity ◽  
Time Course ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Base Line ◽  
Analog Scale ◽  
Voluntary Hyperventilation ◽  
The Difference ◽  
End Tidal

To determine whether the intensity of dyspnea at a given level of respiratory motor output depends on the nature of the stimulus to ventilation, we compared the sensation of difficulty in breathing during progressive hypercapnia (HC) induced by rebreathing, during incremental exercise (E) on a cycle ergometer, and during isocapnic voluntary hyperventilation (IVH) in 16 normal subjects. The sensation of difficulty in breathing was rated at 30-s intervals by use of a visual analog scale. There were no differences in the level of ventilation or the base-line intensity of dyspnea before any of the interventions. The intensity of dyspnea grew linearly with increases in ventilation during HC [r = 0.98 +/- 0.02 (SD)], E (0.95 +/- 0.03), and IVH (0.95 +/- 0.06). The change in intensity of dyspnea produced by a given change in ventilation was significantly greater during HC [0.27 +/- 0.04 (SE)] than during E (0.12 +/- 0.02, P less than 0.01) and during HC (0.30 +/- 0.04) than during IVH (0.16 +/- 0.03, P less than 0.01). The difference in intensity of dyspnea between HC and E or HC and IVH increased as the difference in end-tidal PCO2 widened, even though the time course of the increase in ventilation was similar. No significant differences were measured in the intensity of dyspnea that occurred with changes in ventilation between E and IVH. These results indicate that under nearisocapnic conditions the sensation of dyspnea produced by a given level of ventilation seems not to depend on the method used to produce that level of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory response to medroxyprogesterone acetate in normal subjects: time course and mechanism

1978 ◽  
Vol 44 (6) ◽  
pp. 939-944 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey ◽  
D. G. Kaiser
Keyword(s):  
Medroxyprogesterone Acetate ◽  
Time Course ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Maximum Effect ◽  
Adult Males ◽  
Stimulant Effect ◽  
Unbound Fraction ◽  
Arterial Pco2 ◽  
Lumbar Cerebrospinal Fluid

The time course of ventilatory adaptation to medroxyprogesterone acetate (MPA) and potential mediators of this response in plasma and lumbar CSF were determined in five healthy adult males. A significant decrease in arterial PCO2 (PACO2) at rest and exercise was noted within 48 h of drug administration with the maximum effect reached within 7 days and amounting to a 5-Torr decrement in PACO2. Blood and lumbar cerebrospinal fluid pH because significantly alkaline to control as soon as the ventilatory resporse was noted and remained alkaline during the treatment period. The ventilatory and dP/dt max response to exogenous CO2 was unchanged but their response to moderate exercise was increased after MPA. MPA-rlated materials were detected in both the plasma and CSF as soon as the ventilatory response was noted. The increase in CSF MPA-related materials approximated the unbound fraction determined in plasma. We conclude that [H+] in plasma and CSF is a function rather than a cause of ventilator acclimatization to MPA. MPA-related materials are capable of crossing the blood-brain barrier and could potentially exert their ventilatory stimulant effect by some central mechanism.

Respiratory and Laryngeal Function During Whispering

1991 ◽  
Vol 34 (4) ◽  
pp. 761-767 ◽  
Author(s):  
Elaine T. Stathopoulos ◽  
Jeannette D. Hoit ◽  
Thomas J. Hixon ◽  
Peter J. Watson ◽  
Nancy Pearl Solomon
Keyword(s):  
Young Adults ◽  
Chest Wall ◽  
Voice Disorders ◽  
Normal Subjects ◽  
High Rate ◽  
Lung Volumes ◽  
Laryngeal Function ◽  
Tracheal Pressure ◽  
Lower Lung ◽  
Resistive Loads

Established procedures for making chest wall kinematic observations (Hoit & Hixon, 1987) and pressure-flow observations (Smitheran & Hixon, 1981) were used to study respiratory and laryngeal function during whispering and speaking in 10 healthy young adults. Results indicate that whispering involves generally lower lung volumes, lower tracheal pressures, higher translaryngeal flows, lower laryngeal airway resistances, and fewer syllables per breath group when compared to speaking. The use of lower lung volumes during whispering than speaking may reflect a means of achieving different tracheal pressure targets. Reductions in the number of syllables produced per breath group may be an adjustment to the high rate of air expenditure accompanying whispering compared to speaking. Performance of the normal subjects studied in this investigation does not resemble that of individuals with speech and voice disorders characterized by low resistive loads.

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