scholarly journals Time course evolution of ventilatory response to inspiratory unloading in patients

Critical Care ◽  
10.1186/cc210 ◽  
1998 ◽  
Vol 2 (Suppl 1) ◽  
pp. P080
Author(s):  
G Annat ◽  
P Mahul ◽  
S Duperret ◽  
B Delafosse ◽  
D Weismann ◽  
...  
Keyword(s):  
Time Course ◽  
Ventilatory Response

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.

Time course of augmentation and depression of hypoxic ventilatory responses at altitude

1994 ◽  
Vol 77 (1) ◽  
pp. 313-316 ◽  
Author(s):  
M. Sato ◽  
J. W. Severinghaus ◽  
P. Bickler
Keyword(s):  
Pulse Oximetry ◽  
Sea Level ◽  
Time Course ◽  
Ventilatory Response ◽  
Barometric Pressure ◽  
Hypoxic Ventilatory Response ◽  
Set Point ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Arterial O2 Saturation

Hypoxic ventilatory response (HVR) and hypoxic ventilatory depression (HVD) were measured in six subjects before, during, and after 12 days at 3,810-m altitude (barometric pressure approximately 488 Torr) with and without 15 min of preoxygenation. HVR was tested by 5-min isocapnic steps to 75% arterial O2 saturation measured by pulse oximetry (Spo2) at an isocapnic PCO2 (P*CO2) chosen to set hyperoxic resting ventilation to 140 ml.kg-1.min-1. Hypercapnic ventilatory response (HCVR, 1.min-1.Torr-1) was tested at ambient and high SPO2 6–8 min after a 6- to 10-Torr step increase of end-tidal PCO2 (PETCO2) above P*CO2. HCVR was independent of preoxygenation and was not significantly increased at altitude (when corrected to delta logPCO2). Preoxygenated HVR rose from -1.13 +/- 0.23 (SE) l.min-1.%SPO2(-1) at sea level to -2.17 +/- 0.13 by altitude day 12, without reaching a plateau, and returned to control after return to sea level for 4 days. Ambient HVR was measured at P*CO2 by step reduction of SPO2 from its ambient value (86–91%) to approximately 75%. Ambient HVR slope was not significantly less, but ventilation at equal levels of SPO2 and PCO2 was lower by 13.3 +/- 2.4 l/min on day 2 (SPO2 = 86.2 +/- 2.3) and by 5.9 +/- 3.5 l/min on day 12 (SPO2 = 91.0 +/- 1.5; P < 0.05). This lower ventilation was estimated (from HCVR) to be equivalent to an elevation of the central chemoreceptor PCO2 set point of 9.2 +/- 2.1 Torr on day 2 and 4.5 +/- 1.3 on day 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Women at altitude: ventilatory acclimatization at 4,300 m

2001 ◽  
Vol 91 (4) ◽  
pp. 1791-1799 ◽  
Author(s):  
Stephen R. Muza ◽  
Paul B. Rock ◽  
Charles S. Fulco ◽  
Stacy Zamudio ◽  
Barry Braun ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Time Course ◽  
Ventilatory Response ◽  
Alveolar Ventilation ◽  
Cycle Phase ◽  
Hypoxic Ventilatory Response ◽  
Menstrual Cycle Phase ◽  
Response Parameter ◽  
Effective Ventilation ◽  
End Tidal

Women living at low altitudes or acclimatized to high altitudes have greater effective ventilation in the luteal (L) compared with follicular (F) menstrual cycle phase and compared with men. We hypothesized that ventilatory acclimatization to high altitude would occur more quickly and to a greater degree in 1) women in their L compared with women in their F menstrual cycle phase, and 2) in women compared with men. Studies were conducted on 22 eumenorrheic, unacclimatized, sea-level (SL) residents. Indexes of ventilatory acclimatization [resting ventilatory parameters, hypoxic ventilatory response, hypercapnic ventilatory response (HCVR)] were measured in 14 women in the F phase and in 8 other women in the L phase of their menstrual cycle, both at SL and again during a 12-day residence at 4,300 m. At SL only, ventilatory studies were also completed in both menstrual cycle phases in 12 subjects (i.e., within-subject comparison). In these subjects, SL alveolar ventilation (expressed as end-tidal Pco 2) was greater in the L vs. F phase. Yet the comparison between L- and F-phase groups found similar levels of resting end-tidal Pco 2, hypoxic ventilatory response parameter A, HCVR slope, and HCVR parameter B, both at SL and 4,300 m. Moreover, these indexes of ventilatory acclimatization were not significantly different from those previously measured in men. Thus female lowlanders rapidly ascending to 4,300 m in either the L or F menstrual cycle phase have similar levels of alveolar ventilation and a time course for ventilatory acclimatization that is nearly identical to that reported in male lowlanders.

Ventilatory responses to static handgrip exercise

1983 ◽  
Vol 54 (6) ◽  
pp. 1457-1462 ◽  
Author(s):  
S. R. Muza ◽  
L. Y. Lee ◽  
R. L. Wiley ◽  
S. McDonald ◽  
F. W. Zechman
Keyword(s):  
Time Course ◽  
Ventilatory Response ◽  
Maximum Voluntary Contraction ◽  
Muscle Afferents ◽  
Voluntary Contraction ◽  
Static Exercise ◽  
Handgrip Exercise ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
End Tidal

Previous research indicates that fatiguing static exercise causes hyperventilation and a decrease of end-tidal CO2 partial pressure PETCO2. The objectives of this study were 1) to examine the changes in pattern of breathing during static exercise, and 2) to define the isocapnic ventilatory response. Six healthy males were studied once a week at one of three levels of static handgrip exercise: 15, 25, or 30% maximum voluntary contraction (MVC) was sustained for 5 min while holding PETCO2 constant or allowing it to run free. During 25 and 30% MVC, we observed 1) progressive increases in mean tidal volume (VT), inspiratory ventilation (VI), VT/TI, heart rate (HR), and arterial BP, 2) increased breath-to-breath variability of VT, 3) no significant changes in respiratory frequency (f), and 4) progressive decreases in PETCO2. Keeping PETCO2 constant at preexercise levels did not change the pattern or magnitude of the ventilatory response to exercise. The time course and magnitude of the subjects' perceived effort resembled the time course and magnitude of the ventilatory response. The variability of VT during the response to static exercise suggests an element of control instability. The identical ventilatory responses during hypocapnic and isocapnic conditions may result from the slow response of the central chemoreceptors; an overriding influence of muscle afferents; and/or increased central command arising with fatigue.

scholarly journals The prefrontal oxygenation and ventilatory responses at start of one-legged cycling exercise have relation to central command

2016 ◽  
Vol 121 (5) ◽  
pp. 1115-1126 ◽  
Author(s):  
Ryota Asahara ◽  
Kanji Matsukawa ◽  
Kei Ishii ◽  
Nan Liang ◽  
Kana Endo
Keyword(s):  
Time Course ◽  
Perceived Exertion ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Hemoglobin Concentration ◽  
Carbon Dioxide Tension ◽  
Rating Of Perceived Exertion ◽  
Subjective Rating ◽  
Central Command ◽  
Cycling Exercise

When performing exercise arbitrarily, activation of central command should start before the onset of exercise, but when exercise is forced to start with cue, activation of central command should be delayed. We examined whether the in-advance activation of central command influenced the ventilatory response and reflected in the prefrontal oxygenation, by comparing the responses during exercise with arbitrary and cued start. The breath-by-breath respiratory variables and the prefrontal oxygenated-hemoglobin concentration (Oxy-Hb) were measured during one-legged cycling. Minute ventilation (V̇e) at the onset of arbitrary one-legged cycling was augmented to a greater extent than cued cycling, while end-tidal carbon dioxide tension (ETco2) decreased irrespective of arbitrary or cued start. Symmetric increase in the bilateral prefrontal Oxy-Hb occurred before and at the onset of arbitrary one-legged cycling, whereas such an increase was absent with cued start. The time course and magnitude of the increased prefrontal oxygenation were not influenced by the extent of subjective rating of perceived exertion and were the same as those of the prefrontal oxygenation during two-legged cycling previously reported. Mental imagery or passive performance of the one-legged cycling increased V̇e and decreased ETco2. Neither intervention, however, augmented the prefrontal Oxy-Hb. The changes in ETco2 could not explain the prefrontal oxygenation response during voluntary or passive one-legged cycling. Taken together, it is likely that the in-advance activation of central command influenced the ventilatory response by enhancing minute ventilation at the onset of one-legged cycling exercise and reflected in the preexercise increase in the prefrontal oxygenation.

The Pharmacodynamic Effect of a Remifentanil Bolus on Ventilatory Control

2000 ◽  
Vol 92 (2) ◽  
pp. 393-393 ◽  
Author(s):  
H. Daniel Babenco ◽  
Pattilyn F. Conard ◽  
Jeffrey B. Gross
Keyword(s):  
Carbon Dioxide ◽  
Respiratory Depression ◽  
Response Curve ◽  
Time Course ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Effect Site ◽  
Ventilatory Drive ◽  
Ventilatory Depression ◽  
Carbon Dioxide Response

Background In doses typically administered during conscious sedation, remifentanil may be associated with ventilatory depression. However, the time course of ventilatory depression after an initial dose of remifentanil has not been determined previously. Methods In eight healthy volunteers, the authors determined the time course of the ventilatory response to carbon dioxide using the dual isohypercapnic technique. Subjects breathed via mask from a to-and-fro circuit with variable carbon dioxide absorption, allowing the authors to maintain end-tidal pressure of carbon dioxide (PET(CO2)) at approximately 46 or 56 mm Hg (alternate subjects). After 6 min of equilibration, subjects received 0.5 microg/kg remifentanil over 5 s, and minute ventilation (V(E)) was recorded during the next 20 min. Two hours later, the study was repeated using the other carbon dioxide tension (56 or 46 mm Hg). The V(E) data were used to construct two-point carbon dioxide response curves at 30-s intervals after remifentanil administration. Using published pharmacokinetic values for remifentanil and the method of collapsing hysteresis loops, the authors estimated the effect-site equilibration rate constant (k(eo)), the effect-site concentration producing 50% respiratory depression (EC50), and the shape parameter of the concentration-response curve (gamma). Results The slope of the carbon dioxide response decreased from 0.99 [95% confidence limits 0.72 to 1.26] to a nadir of 0.27 l x min(-1) x mm Hg(-1) [-0.12 to 0.66] 2 min after remifentanil (P&lt;0.001); within 5 min, it recovered to approximately 0.6 l x min(-1) x mm Hg(-1), and within 15 min of injection, slope returned to baseline. The computed ventilation at PET = 50 mm Hg (VE50) decreased from 12.9 [9.8 to 15.9] to 6.1 l/min [4.8 to 7.4] 2.5 min after remifentanil injection (P&lt;0.001). This was caused primarily by a decrease in tidal volume rather than in respiratory rate. Estimated pharmacodynamic parameters based on computed mean values of VE50 included k(eo) = 0.24 min(-1) (T1/2 = 2.9 min), EC50 = 1.12 ng/ml, and gamma = 1.74. Conclusions After administration of 0.5 microg/kg remifentanil, there was a decrease in slope and downward shift of the carbon dioxide ventilatory response curve. This reached its nadir approximately 2.5 min after injection, consistent with the computed onset half-time of 2.9 min. The onset of respiratory depression appears to be somewhat slower than previously reported for the onset of remifentanil-induced electroencephalographic slowing. Recovery of ventilatory drive after a small dose essentially was complete within 15 min.

Developmental changes in chemoreceptive control of gill ventilation in larval bullfrogs (Rana catesbeiana). II. Sites of O2-sensitive chemoreceptors

1997 ◽  
Vol 200 (16) ◽  
pp. 2237-2248
Author(s):  
X Jia ◽  
W Burggren
Keyword(s):  
Blood Circulation ◽  
Time Course ◽  
Developmental Stages ◽  
Rana Catesbeiana ◽  
Ventilatory Response ◽  
Venous Blood ◽  
Gill Arch ◽  
Gill Ventilation ◽  
Hypoxic Water ◽  
Two Populations

The time course of reflex changes in gill ventilation variables caused by a step-wise change in PO2 of inspired water and by the introduction of NaCN into inspired water was measured in two populations of unanesthetized larval bullfrogs (Rana catesbeiana) &shy; one with intact gill arches and a second with bilateral ablation of the first gill arch. Developmental stages TK V&shy;VII, IX&shy;XI and XVII&shy;XIX were examined. Inspiring hypoxic water or a pulse of NaCN significantly increased gill ventilation within 7 s in control larvae. Ablation of the first gill arches in larval R. catesbeiana eliminated the initial, quick response of gill ventilation to changes in the PO2 of inspired water and to the presence of NaCN in all three developmental groups. These data suggest that O2-sensitive chemoreceptors are located on the first gill arch and are responsible for the initial rapid ventilatory response. However, a slow response (&gt;15 s) to changes in PO2 of inspired water persisted even after removal of the first gill arch. This response is far slower than the minimum blood circulation time (approximately 5&shy;8 s as measured in all three groups), indicating that a second population of receptors is not directly monitoring arterial or venous blood. Instead, this second population of receptors is likely to be located 'behind' a significant diffusion barrier, possibly monitoring cerebrospinal fluid.

Time course of the ventilatory response to adjuvant arthritis in the rat

Life Sciences ◽  
1983 ◽  
Vol 33 (11) ◽  
pp. 1065-1073 ◽  
Author(s):  
F.C. Colpaert ◽  
R.H.W.M. van den Hoogen
Keyword(s):  
Adjuvant Arthritis ◽  
Time Course ◽  
Ventilatory Response
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