Augmentation of CO2 drives by chlormadinone acetate, a synthetic progesterone

1984 ◽  
Vol 56 (6) ◽  
pp. 1627-1632 ◽  
Author(s):  
H. Kimura ◽  
F. Hayashi ◽  
A. Yoshida ◽  
S. Watanabe ◽  
I. Hashizume ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Pressure Response ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Physiological Basis ◽  
Load Compensation ◽  
Chlormadinone Acetate ◽  
Arterial Blood ◽  
Resistive Loading

We studied 10 male subjects who were administered chlormadinone acetate (CMA), a potent synthetic progesterone, to clarify the physiological basis of its respiratory effects. Arterial blood gas tension, resting ventilation, and respiratory drive assessed by ventilatory and occlusion pressure response to CO2 with and without inspiratory flow-resistive loading were measured before and 4 wk after CMA administration. In all subjects, arterial PCO2 decreased significantly by 5.7 +/- 0.6 (SE) Torr with an increase in minute ventilation by 1.8 +/- 0.6 l X min-1, whereas no significant changes were seen in O2 uptake. During unloaded conditions, both slopes of occlusion pressure and ventilatory response to CO2 increased, being statistically significant in the former but showing nonsignificant trends in the latter. Furthermore, inspiratory flow-resistive loading (16 cmH2O X l(-1) X s) increased both slopes more markedly after CMA. The magnitudes of load compensation, assessed by the ratio of loaded to unloaded slope of the occlusion pressure response curve, were increased significantly. We concluded CMA is a potent respiratory stimulant that increases the CO2 chemosensitivity and neuromechanical drives in the load-compensation mechanism.

Respiration during exercise in conscious laryngectomized humans

1989 ◽  
Vol 66 (5) ◽  
pp. 2071-2078 ◽  
Author(s):  
W. N. Gardner ◽  
M. S. Meah
Keyword(s):  
Minute Ventilation ◽  
Work Rate ◽  
Inspiratory Flow ◽  
Control Group ◽  
Respiratory Drive ◽  
Upper Airways ◽  
Expiratory Time ◽  
Expiratory Flow ◽  
End Tidal ◽  
Normal Controls

We compared respiratory patterning at rest and during steady cycle exercise at work rates of 30, 60, and 90 W in 7 male chronically laryngectomized subjects and 13 normal controls. Breathing was measured with a pneumotachograph and end-tidal PCO2 by mass spectrometer. Inspired air was humidified and enriched to 35% O2. Peak flow, volume, and times for the inspiratory and expiratory half cycles, time for expiratory flow, minute ventilation, and mean inspiratory flow were computer averaged over at least 40 breaths at rest and during the last 2 min of 5-min periods at each work rate. During the transition from rest to exercise and with increasing work rate in both groups, there was an increase in respiratory rate and depth with selective and progressive shortening of expiratory time; these responses were not significantly different between the two groups, but there was a suggestion that respiratory “drive” as quantitated by mean inspiratory flow may limit in the laryngectomized subjects at high work rates. Time for expiratory flow increased on transition from rest to exercise and then decreased in both groups as the work rate increased; it was shorter in the laryngectomy than control group at all levels. In the laryngectomized subjects there was significantly more breath-by-breath scatter in some variables at rest, but there was no difference during exercise. It is concluded that chronic removal of the larynx and upper airways in mildly hyperoxic conscious humans has only subtle and, therefore, functionally insignificant effects on breathing during moderate exercise. Evidence is provided that the upper airways can modulate expiratory flow but not expiratory time during exercise.

Effect of hypoxia on the pressure developed by inspiratory muscles during airway occlusion

1976 ◽  
Vol 40 (3) ◽  
pp. 372-378 ◽  
Author(s):  
S. G. Kelsen ◽  
M. D. Altose ◽  
N. N. Stanley ◽  
R. S. Levinson ◽  
N. S. Cherniack ◽  
...  
Keyword(s):  
Pressure Response ◽  
Occlusion Pressure ◽  
Airway Occlusion ◽  
Single Breath ◽  
Inspiratory Muscles ◽  
Resistive Loading ◽  
Expired Gas ◽  
Motoneuron Activity ◽  
Maximal Pressure ◽  
Ventilatory Response To Hypoxia

The effect of progressive isocapnic hypoxia on the pressure generated by the inspiratory muscle during airway occlusion was studied in 10 awake subjects during normal and obstructed breathing. Isocapnic hypoxia was produced by rebreathing a gas mixture of 6% CO2 in air while the expired gas was passed through a CO2 scrubber so as to maintain PACO2 constant (42.6 mmHg +/- 2.2 SE). Occlusion of the airway was performed randomly for a single breath at FRC. In all 10 subjects maximal pressure (Ppeak) and the pressures measured 100, 200, 300, and 400 ms after the onset of inspiration increased during hypoxia. Furthermore, good correlation was noted between the occlusion pressure response to hypoxia (delta P/DELTA[1/PO2-32]) and simultaneous changes in ventilatory response to hypoxia (delta VI/DELTA[1/PO2-32]). The occlusion pressure response to hypoxia therefore seems to be a reliable measure of respiratory center output. When rebreathing was repeated during inspiratory resistive loading, the occlusion pressure at any given PO2 and delta P/DELTA(1PO2-32) measured in the first 400 ms of inspiration increased in 9 of 10 subjects. Since PACO2 and PAO2 during both control and loaded experiments were the same, the increase in occlusion pressure in the presence of flow-resistive loading appeared to represent a neurally mediated increase in inspiratory motoneuron activity.

Relationship between inspiratory drive and perceived inspiratory effort in normal man

1990 ◽  
Vol 78 (5) ◽  
pp. 493-496 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley
Keyword(s):  
Ventilatory Response ◽  
Free Breathing ◽  
Normal Subjects ◽  
Inspiratory Effort ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Resistive Loading ◽  
Mouth Occlusion Pressure ◽  
The Individual ◽  
Induced Changes

1. To examine the relationship between the inspiratory effort sensation (IES) and respiratory drive as reflected by mouth occlusion pressure (P0.1) we have studied loaded and unloaded ventilatory responses to CO2 in 12 normal subjects. 2. The individual coefficient of variation of the effort sensation response to CO2 (IES/Pco2) between replicate studies was 21% and was similar to the variability of the ventilatory response (VE/Pco2) (18%) and the occlusion pressure response (P0.1/Pco2) (22%). 3. IES was well correlated with P0.1 (r >0.9) for both free-breathing and loaded runs. 4. Resistive loading reduced the ventilatory response to hypercapnia from 19.3 1 min−1 kPa−1 (sd 7.5) to 12.6 1 min−1 kPa−1 (sd 3.9) (P <0.01). IES and P0.1 responses increased with resistive loading from 2.28 (sd 0.9) to 3.15 (sd 1.1) units/kPa and 2.8 (sd 1.2) to 3.73 (sd 1.5) cmH2O/kPa, respectively (P <0.01). 5. Experimentally induced changes in Pco2 and respiratory impedance were accompanied by increases in IES and P0.1. We found no evidence that CO2 increased IES independently of its effect on respiratory drive.

scholarly journals The Relationship Between Airway Occlusion Pressure and Severity of liver Cirrhosis in Candidates for Liver Transplantation

2020 ◽  
Vol 12 (2) ◽  
pp. 111-115
Author(s):  
Delara Gholamipoor ◽  
Mohssen Nassiri-Toosi ◽  
Masumeh Azadi ◽  
Mehrnaz Asadi Gharabaghi
Keyword(s):  
Liver Transplantation ◽  
Liver Cirrhosis ◽  
Liver Disease ◽  
Pulmonary Function Tests ◽  
Meld Score ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Arterial Blood ◽  
End Stage ◽  
The Relationship

BACKGROUND End-stage cirrhosis is an irreversible condition, and liver transplantation is the only treatment option in for the affected patients. Respiratory problems and abnormal breathing are common findings among these patients. In this study, for the first time, we examined the relationship between the severity of liver cirrhosis and respiratory drive measured by mouth occlusion pressure (P0.1). METHODS This was a cross-sectional study conducted on 50 candidates for liver transplantation who were referred to the pulmonary clinic of Imam Khomeini Hospital for pre-operative pulmonary evaluations. Arterial blood gas analysis (ABG), pulmonary function tests, and measurement of P0.1 were performed for all patients. The severity of liver disease was assessed using the Model for End-Stage Liver Disease (MELD) score. RESULTS The median P0.1 was 5 cm H2 O. P0.1 was negatively associated with PaCO2 (r = -0.466, p = 0.001) and HCO3 - (r = -0.384, p = 0.007), and was positively correlated with forced expiratory volume at 1s (FEV1 )/ forced vital capacity (FVC) (r = 0.282, p = 0.047). There was a strong correlation between P0.1 and MELD score (r = 0.750, p < 0.001). Backward multivariate linear regression revealed that a higher MELD score and lower PaCO2 were associated with increased P0.1. CONCLUSION High levels of P0.1 and strong direct correlation between P0.1 and MELD score observed in the present study are suggestive of the presence of abnormal increased respiratory drive in candidates for liver transplantation, which is closely related to their disease severity.

The effects of hypoxia on load compensation during sustained incremental resistive loading in patients with obstructive sleep apnea

2007 ◽  
Vol 103 (1) ◽  
pp. 234-239 ◽  
Author(s):  
Michael C. Hlavac ◽  
Peter G. Catcheside ◽  
Amanda Adams ◽  
Danny J. Eckert ◽  
R. Doug McEvoy
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Minute Ventilation ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Load Compensation ◽  
Significant Fall ◽  
Obstructive Sleep ◽  
Resistive Loading ◽  
Increasing Load

Inspiratory load compensation is impaired in patients with obstructive sleep apnea (OSA), a condition characterized by hypoxia during sleep. We sought to compare the effects of sustained hypoxia on ventilation during inspiratory resistive loading in OSA patients and matched controls. Ten OSA patients and 10 controls received 30 min of isocapnic hypoxia (arterial oxygen saturation 80%) and normoxia in random order. Following the gas period, subjects were administered six incremental 2-min inspiratory resistive loads while breathing room air. Ventilation was measured throughout the loading period. In both patients and controls, there was a significant increase in inspiratory time with increasing load ( P = 0.006 and 0.003, respectively), accompanied by a significant fall in peak inspiratory flow ( P = 0.006 and P < 0.001, respectively). The result was a significant fall in minute ventilation in both groups with increasing load ( P = 0.003 and P < 0.001, respectively). There was no difference between the two groups for these parameters. The only difference between the two groups was a transient increase in tidal volume in controls ( P = 0.02) but not in OSA patients ( P = 0.57) during loading. Following hypoxia, there was a significant increase in minute ventilation during loading in both groups ( P < 0.001). These results suggest that ventilation during incremental resistive loading is preserved in OSA patients and that it appears relatively impervious to the effects of hypoxia.

Volume acceleration as an index of respiratory drive during exercise

1999 ◽  
Vol 98 (1) ◽  
pp. 91-101
Author(s):  
Takahiro URUMA ◽  
Hiroshi KIMURA ◽  
Akira KOJIMA ◽  
Kiyoshi HASAKO ◽  
Shigeru MASUYAMA ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Minute Ventilation ◽  
Forced Expiratory Volume ◽  
Inspiratory Flow ◽  
Chronic Obstructive ◽  
Respiratory Drive ◽  
Obstructive Pulmonary Disease ◽  
Co2 Partial Pressure ◽  
Co2 Rebreathing ◽  
End Tidal

In order to evaluate the applicability of volume acceleration (AI) at the onset of inspiration as an index of neuromuscular output, CO2 rebreathing in six healthy subjects and incremental-load exercise in eight healthy subjects was performed while measuring AI and mouth occlusion pressure (P0.1). During CO2 rebreathing, AI increased linearly with end-tidal CO2 partial pressure and P0.1. During incremental-load exercise, P0.1 and AI increased exponentially with minute ventilation and mean inspiratory flow, and AI increased linearly with P0.1. Dyspnoea sensation at rest and exercise with or without the circuit system in eight healthy subjects was examined. Dyspnoea sensation increased markedly with the circuit system in some subjects. Incremental-load exercise was carried out by 13 healthy subjects and 21 patients with chronic obstructive pulmonary disease (COPD) to evaluate the difference in AI as respiratory drive between the two groups in the absence of a respiratory circuit. In patients with COPD, AI responses to minute ventilation, mean inspiratory flow and carbon dioxide output (co2) were greater than those in healthy subjects. In patients with COPD, the AI response to co2 was greater in those with a lower FEV1.0 (forced expiratory volume in 1.0 s), but the ventilatory response to co2 was lower in those with a lower FEV1.0. These data suggest that AI reflects neuromuscular output during CO2 rebreathing and incremental-load exercise under conditions where mechanical properties of the respiratory system are expected to be involved. During exercise, flow increased markedly, and the influence of the resistance of the respiratory circuit also increased. Therefore the use of AI has the advantage of less resistance (no respiratory circuit) and less additional respiratory effort, in comparison with the use of P0.1, especially in patients with COPD.

Effects of acute exposure to high altitude on ventilatory drive and respiratory pattern

1984 ◽  
Vol 56 (4) ◽  
pp. 1027-1031 ◽  
Author(s):  
N. K. Burki
Keyword(s):  
High Altitude ◽  
Minute Ventilation ◽  
Progressive Increase ◽  
Acute Exposure ◽  
Respiratory Pattern ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Ventilatory Pattern ◽  
Ventilatory Drive ◽  
Mouth Occlusion Pressure

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.

scholarly journals Methylphenidate Actively Induces Emergence from General Anesthesia

2011 ◽  
Vol 115 (4) ◽  
pp. 791-803 ◽  
Author(s):  
Ken Solt ◽  
Joseph F. Cotten ◽  
Aylin Cimenser ◽  
Kin F. K. Wong ◽  
Jessica J. Chemali ◽  
...  
Keyword(s):  
General Anesthesia ◽  
Minute Ventilation ◽  
Gas Analysis ◽  
Respiratory Drive ◽  
Dependent Manner ◽  
General Anesthetic ◽  
Adult Rats ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Induced Changes

Background Although accumulating evidence suggests that arousal pathways in the brain play important roles in emergence from general anesthesia, the roles of monoaminergic arousal circuits are unclear. In this study, the authors tested the hypothesis that methylphenidate (an inhibitor of dopamine and norepinephrine transporters) induces emergence from isoflurane general anesthesia. Methods Using adult rats, the authors tested the effect of intravenous methylphenidate on time to emergence from isoflurane general anesthesia. They then performed experiments to test separately for methylphenidate-induced changes in arousal and changes in minute ventilation. A dose-response study was performed to test for methylphenidate-induced restoration of righting during continuous isoflurane general anesthesia. Surface electroencephalogram recordings were performed to observe neurophysiological changes. Plethysmography recordings and arterial blood gas analysis were performed to assess methylphenidate-induced changes in respiratory function. Intravenous droperidol was administered to test for inhibition of methylphenidate's actions. Results Methylphenidate decreased median time to emergence from 280 to 91 s. The median difference in time to emergence without methylphenidate compared with administration of methylphenidate was 200 [155-331] s (median, [95% CI]). During continuous inhalation of isoflurane, methylphenidate induced return of righting in a dose-dependent manner, induced a shift in electroencephalogram power from delta (less than 4 Hz) to theta (4-8 Hz), and induced an increase in minute ventilation. Administration of intravenous droperidol (0.5 mg/kg) before intravenous methylphenidate (5 mg/kg) largely inhibited methylphenidate-induced emergence behavior, electroencephalogram changes, and changes in minute ventilation. Conclusions Methylphenidate actively induces emergence from isoflurane general anesthesia by increasing arousal and respiratory drive, possibly through activation of dopaminergic and adrenergic arousal circuits. The authors' findings suggest that methylphenidate may be useful clinically as an agent to reverse general anesthetic-induced unconsciousness and respiratory depression at the end of surgery.

Metabolic, hemodynamic, and ventilatory responses to respiratory load in sedated neonatal piglets

1993 ◽  
Vol 75 (1) ◽  
pp. 181-184 ◽  
Author(s):  
S. Duara ◽  
C. Suguihara ◽  
T. Gerhardt ◽  
E. Bancalari
Keyword(s):  
Metabolic Rate ◽  
Minute Ventilation ◽  
Mechanical Loads ◽  
Neonatal Piglets ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Resistive Loading ◽  
Loaded Breathing ◽  
Baseline Values ◽  
Spontaneously Breathing

Some neonatal species fail to develop the expected degree of hypercapnia during hypoventilation with mechanical loads. We studied 13 spontaneously breathing, sedated piglets (1–9 days old), grouped by age as young (< or = 3 day old) or old (> 3 day old). Baseline measurements of minute ventilation, arterial blood pressure (BP), cardiac output, and O2 consumption were repeated after continuous (inspiratory and expiratory) flow-resistive loading of 330 cmH2O.l-1 x s for 10 min. Older animals [n = 6, age 6.6 +/- 1.9 (SD) days, wt 1.99 +/- 0.5 kg] increased metabolic rate (9.8 +/- 1.4 to 10.5 +/- 1.3 ml.min-1 x kg-1, P < 0.01), whereas younger animals (n = 7, 2.6 +/- 0.6 days, 1.37 +2- 0.3 kg) invariably decreased metabolic rate with loading (9.7 +/- 1.6 to 7.9 +/- 2.6 ml.min-1 x kg-1); changes were different between groups (P < 0.02). Although ventilation decreased with loading in both groups (P < 0.01), younger animals showed a relatively greater fall from baseline values (38 vs. 27%). Despite differences in the degree of hypoventilation, arterial CO2 tension increased similarly in both groups (21%). BP increased (P < 0.01) with loading in older but not younger animals. We conclude that the decreased metabolic rate and limited hemodynamic response in younger piglets reflect an accomodative response to hypoventilation in contrast to that of older animals, which display an adult pattern of increased metabolic rate and BP with loaded breathing.

Background ventilatory stimulus as a determinant of load compensation

1989 ◽  
Vol 66 (3) ◽  
pp. 1352-1358 ◽  
Author(s):  
H. E. Greenberg ◽  
D. M. Rapoport ◽  
P. J. Gloeggler ◽  
R. M. Goldring
Keyword(s):  
Interindividual Variability ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Co2 Production ◽  
Control Mechanisms ◽  
Co2 Response ◽  
Co2 Partial Pressure ◽  
Load Compensation ◽  
Resistive Loading

Compensation for inspiratory flow-resistive loading was compared during progressive hypercapnia and incremental exercise to determine the effect of changing the background ventilatory stimulus and to assess the influence of the interindividual variability of the unloaded CO2 response on evaluation of load compensation in normal subjects. During progressive hypercapnia, ventilatory response was incompletely defended with loading (mean unloaded delta VE/delta PCO2 = 3.02 +/- 2.29, loaded = 1.60 +/- 0.67 1.min-1.Torr-1 CO2, where VE is minute ventilation and PCO2 is CO2 partial pressure; P less than 0.01). Furthermore the degree of defense of ventilation with loading was inversely correlated with the magnitude of the unloaded CO2 response. During exercise, loading produced no depression in ventilatory response (mean delta VE/delta VCO2 unloaded = 20.5 +/- 1.9, loaded = 19.2 +/- 2.5 l.min-1.l-1.min-1 CO2 where VCO is CO2 production; P = NS), and no relationship was demonstrated between degree of defense of the exercise ventilatory response and the unloaded CO2 response. Differences in load compensation during CO2 rebreathing and exercise suggest the presence of independent ventilatory control mechanisms in these states. The type of background ventilatory stimulus should therefore be considered in load compensation assessment.

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