Metabolic and respiratory effects of infused sodium acetate in healthy human subjects

1992 ◽  
Vol 263 (6) ◽  
pp. R1271-R1276 ◽  
Author(s):  
P. Burnier ◽  
L. Tappy ◽  
E. Jequier ◽  
D. Schneeberger ◽  
R. Chiolero
Keyword(s):  
Sodium Acetate ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Open Circuit ◽  
Alveolar Ventilation ◽  
Co2 Production ◽  
Healthy Human ◽  
Respiratory Effects ◽  
Normal Human ◽  
Arterial Po2

The metabolic and respiratory effects of intravenous 0.5 M sodium acetate (at a rate of 2.5 mmol/min during 120 min) were studied in nine normal human subjects. O2 consumption (VO2) and CO2 production (VCO2) were measured continuously by open-circuit indirect calorimetry. VO2 increased from 251 +/- 9 to 281 +/- 9 ml/min (P < 0.001), energy expenditure increased from 4.95 +/- 0.17 kJ/min baseline to 5.58 +/- 0.16 kJ/min (P < 0.001), and VCO2 decreased nonsignificantly (211 +/- 7 ml/min vs. 202 +/- 7 ml/min, NS). The extrapulmonary CO2 loss (i.e., bicarbonate generation and excretion) was estimated at 48 +/- 5 ml/min. This observation is consistent with 1 mol of bicarbonate generated from 1 mol of acetate metabolized. Alveolar ventilation decreased from 3.5 +/- 0.2 l/min basal to 3.1 +/- 0.2 l/min (P < 0.001). The minute ventilation (VE) to VO2 ratio decreased from 22.9 +/- 1.3 to 17.6 +/- 0.9 l/l (P < 0.005), arterial PO2 decreased from 93.2 +/- 1.9 to 78.7 +/- 1.6 mmHg (P < 0.0001), arterial PCO2 increased from 39.2 +/- 0.7 to 42.1 +/- 1.1 mmHg (P < 0.0001), pH from 7.40 +/- 0.005 to 7.50 +/- 0.007 (P < 0.005), and arterial bicarbonate concentration from 24.2 +/- 0.7 to 32.9 +/- 1.1 (P < 0.0001). These observations indicate that sodium acetate infusion results in substantial extrapulmonary CO2 loss, which leads to a relative decrease of total and alveolar ventilation.

Time course of ozone-induced changes in breathing pattern in healthy exercising humans

2007 ◽  
Vol 102 (2) ◽  
pp. 688-697 ◽  
Author(s):  
Edward S. Schelegle ◽  
William F. Walby ◽  
William C. Adams
Keyword(s):  
Time Course ◽  
Breathing Pattern ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Cumulative Exposure ◽  
Healthy Human ◽  
Percent Change ◽  
Atropine Treatment ◽  
Induced Changes ◽  
Time To Onset

We examined the time course of O3-induced changes in breathing pattern in 97 healthy human subjects (70 men and 27 women). One- to five-minute averages of breathing frequency (fB) and minute ventilation (V̇e) were used to generate plots of cumulative breaths and cumulative exposure volume vs. time and cumulative exposure volume vs. cumulative breaths. Analysis revealed a three-phase response; delay, no response detected; onset, fB began to increase; response, fB stabilized. Regression analysis was used to identify four parameters: time to onset, number of breaths at onset, cumulative inhaled dose of ozone at onset of O3-induced tachypnea, and the percent change in fB. The effect of altering O3 concentration, V̇e, atropine treatment, and indomethacin treatment were examined. We found that the lower the O3 concentration, the greater the number of breaths at onset of tachypnea at a fixed ventilation, whereas number of breaths at onset of tachypnea remains unchanged when V̇e is altered and O3 concentration is fixed. The cumulative inhaled dose of O3 at onset of tachypnea remained constant and showed no relationship with the magnitude of percent change in fB. Atropine did not affect any of the derived parameters, whereas indomethacin did not affect time to onset, number of breaths at onset, or cumulative inhaled dose of O3 at onset of tachypnea but did attenuate percent change in fB. The results are discussed in the context of dose response and intrinsic mechanisms of action.

Finite difference analysis of respiratory heat transfer

1986 ◽  
Vol 61 (6) ◽  
pp. 2252-2259 ◽  
Author(s):  
E. P. Ingenito ◽  
J. Solway ◽  
E. R. McFadden ◽  
B. M. Pichurko ◽  
E. G. Cravalho ◽  
...  
Keyword(s):  
Heat Transfer ◽  
Heat Loss ◽  
Air Temperature ◽  
Breathing Pattern ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Tracheobronchial Tree ◽  
Temperature Profiles ◽  
Opposite Pattern ◽  
Normal Human

A numerical computer model of heat and water transfer within the tracheobronchial tree of humans was developed based on an integral formulation of the first law of thermodynamics. Simulation results were compared with directly measured intraluminal airway temperature profiles previously obtained in normal human subjects, and a good correlation was demonstrated. The model was used to study aspects of regional pulmonary heat transfer and to predict the outcomes of experiments not yet performed. The results of these simulations show that a decrease in inspired air temperature and water content at fixed minute ventilation produces a proportionately larger increase in heat loss from extrathoracic airways relative to intrathoracic, whereas an increase in minute ventilation at fixed inspired air conditions produces the opposite pattern, with cold dry air penetrating further into the lung, and that changes in breathing pattern (tidal volume and frequency) at fixed minute ventilation and fixed inspiratory-to-expiratory (I/E) ratio do not affect local air temperature profiles and heat loss, whereas changes in I/E ratio at fixed minute ventilation do cause a significant change.

Continuous measurement of minute ventilation and gaseous metabolism of newborn infants

1981 ◽  
Vol 50 (5) ◽  
pp. 1098-1103 ◽  
Author(s):  
K. Schulze ◽  
R. Kairam ◽  
M. Stefanski ◽  
R. Sciacca ◽  
L. S. James
Keyword(s):  
Continuous Measurement ◽  
Minute Ventilation ◽  
Newborn Infants ◽  
Minute Volume ◽  
Open Circuit ◽  
Co2 Production ◽  
Low Birth Weight Infants ◽  
Human Newborn ◽  
Bias Flow ◽  
Circuit Techniques

A system of instrumentation for continuous measurement of gaseous metabolism and minute volume (VI) in the human newborn is described. O2 uptake and CO2 production are measured by open-circuit techniques utilizing a Servomex OA184 differential paramagnetic O2 analyzer and a BEckman LB-2 infrared CO2 analyzer. VI is measured with bias-flow pneumotachometry. Bench performance is described, methodological errors are defined, and clinical data are presented. The instrumentation is capable of safe, accurate, and continuous measurement of respiratory and metabolic variables in low-birth-weight infants.

Somatostatin inhibits the ventilatory response to hypoxia in humans

1986 ◽  
Vol 60 (3) ◽  
pp. 997-1002 ◽  
Author(s):  
D. L. Maxwell ◽  
P. Chahal ◽  
K. B. Nolop ◽  
J. M. Hughes
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Open Circuit ◽  
Co2 Production ◽  
Adult Males ◽  
Hypoxic Response ◽  
Ventilatory Responses ◽  
End Tidal ◽  
Hypercapnic Response ◽  
Ventilatory Response To Hypoxia

The effects of a 90-min infusion of somatostatin (1 mg/h) on ventilation and the ventilatory responses to hypoxia and hypercapnia were studied in six normal adult males. Minute ventilation (VE) was measured with inductance plethysmography, arterial 02 saturation (SaO2) was measured with ear oximetry, and arterial PCO2 (Paco2) was estimated with a transcutaneous CO2 electrode. The steady-state ventilatory response to hypoxia (delta VE/delta SaO2) was measured in subjects breathing 10.5% O2 in an open circuit while isocapnia was maintained by the addition of CO2. The hypercapnic response (delta VE/delta PaCO2) was measured in subjects breathing first 5% and then 7.5% CO2 (in 52–55% O2). Somatostatin greatly attenuated the hypoxic response (control mean -790 ml x min-1.%SaO2 -1, somatostatin mean -120 ml x min-1.%SaO2 -1; P less than 0.01), caused a small fall in resting ventilation (mean % fall - 11%), but did not affect the hypercapnic response. In three of the subjects progressive ventilatory responses (using rebreathing techniques, dry gas meter, and end-tidal Pco2 analysis) and overall metabolism were measured. Somatostatin caused similar changes (mean fall in hypoxic response -73%; no change in hypercapnic response) and did not alter overall O2 consumption nor CO2 production. These results show an hitherto-unsuspected inhibitory potential of this neuropeptide on the control of breathing; the sparing of the hypercapnic response is suggestive of an action on the carotid body but does not exclude a central effect.

Precision and accuracy of a noninvasive inert gas washin method for determination of cardiac output in men

1994 ◽  
Vol 76 (4) ◽  
pp. 1560-1565 ◽  
Author(s):  
O. W. Nielsen ◽  
S. Hansen ◽  
J. Gronlund
Keyword(s):  
Measurement Errors ◽  
Human Subjects ◽  
Open Circuit ◽  
Lung Model ◽  
Inert Gas ◽  
Healthy Human ◽  
Pulmonary Capillary Blood Flow ◽  
Pulmonary Capillary Blood ◽  
Anesthetized Dogs ◽  
Experimental Errors

Stout et al. (J. Appl. Physiol. 38:913–918, 1975) suggested an open-circuit multibreath (MB) inert gas method for determining pulmonary capillary blood flow (Qc) in anesthetized dogs receiving artificial ventilation. In the present work we investigated the accuracy and reproducibility of the MB method in nine healthy human subjects at spontaneous ventilation, and we compared the MB method with the inert gas rebreathing (RB) method. Qc was calculated at rest and during exercise at 50 or 100 W, and experimental errors were evaluated in computer simulations of a two-alveoli lung model. The calculated mean Qc values of the MB method were 5.56 +/- 1.23 (SD), 10.02 +/- 0.78, and 13.2 +/- 0.84 l/min, and the mean difference (MB Qc - RB Qc) was not significantly different (P > 0.05). The variation in Qc of the MB method was found to be significantly larger than that in Qc of the RB method (P < 0.01). Random measurement errors and uneven distribution of ventilation contributed to the experimental errors. We conclude that the MB method is inferior to the RB method but that the MB method may be useful under exercise conditions.

Long-term facilitation of ventilation is not present during wakefulness in healthy men or women

2002 ◽  
Vol 93 (6) ◽  
pp. 2129-2136 ◽  
Author(s):  
A. S. Jordan ◽  
P. G. Catcheside ◽  
F. J. O'Donoghue ◽  
R. D. McEvoy
Keyword(s):  
Repeated Measures ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Menstrual Phase ◽  
Healthy Human ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Long Term Facilitation

Obstructive sleep apnea (OSA) is more common in men than in women for reasons that are unclear. The stability of the respiratory controller has been proposed to be important in OSA pathogenesis and may be involved in the gender difference in prevalence. Repetitive hypoxia elicits a progressive rise in ventilation in animals [long-term facilitation (LTF)]. There is uncertainty whether LTF occurs in humans, but if present it may stabilize respiration and possibly also the upper airway. This study was conducted to determine 1) whether LTF exists during wakefulness in healthy human subjects and, if so, whether it is more pronounced in women than men and 2) whether inspiratory pump and upper airway dilator muscle activities are affected differently by repetitive hypoxia. Twelve healthy young men and ten women in the luteal menstrual phase were fitted with a nasal mask and intramuscular genioglossal EMG (EMGgg) recording electrodes. After 5 min of rest, subjects were exposed to ten 2-min isocapnic hypoxic periods (∼9% O2 in N2, arterial O2 saturation ∼80%) separated by 2 min of room air. Inspired minute ventilation (V˙i) and peak inspiratory EMGgg activity were averaged over 30-s intervals, and respiratory data were compared between genders during and after repetitive hypoxia by using ANOVA for repeated measures. V˙i during recovery from repetitive hypoxia was not different from the resting level and not different between genders. There was no facilitation of EMGgg activity during or after repetitive hypoxia. EMGgg activity was reduced below baseline during recovery from repetitive hypoxia in women. In conclusion, we have found no evidence of LTF of ventilation or upper airway dilator muscle activity in healthy subjects during wakefulness.

scholarly journals Corin Is Present in the Normal Human Heart, Kidney, and Blood, with Pro–B-Type Natriuretic Peptide Processing in the Circulation

2011 ◽  
Vol 57 (1) ◽  
pp. 40-47 ◽  
Author(s):  
Tomoko Ichiki ◽  
Brenda K Huntley ◽  
Denise M Heublein ◽  
Sharon M Sandberg ◽  
Paul M McKie ◽  
...  
Keyword(s):  
Protein Expression ◽  
Western Blot ◽  
Natriuretic Peptide ◽  
Human Heart ◽  
Human Subjects ◽  
Active Form ◽  
Healthy Human ◽  
His Tag ◽  
Normal Human ◽  
Processed Form

BACKGROUND B-type natriuretic peptide (BNP), which is activated in heart failure (HF), is processed to an active form by corin. The corin gene is expressed in the human heart and kidney, but corin protein expression in the heart, kidney, and circulation, along with whether proBNP is processed by circulating corin, remains unknown. METHODS We examined corin protein expression by immunostaining and Western blot in human heart and kidney, and we assessed the circulating corin concentration by ELISA. We examined histidine-tagged (His-tag) proBNP1–108 processing in serum and plasma by immunoprecipitation and Western blot and sequenced the processed form. RESULTS Normal human heart and kidney displayed the presence of corin, especially in cells around the vasculature. Both corin and proBNP1–108 were present in the plasma of healthy human subjects, with circulating corin significantly higher in men than women (P &lt; 0.0001) and a positive correlation of corin to age (P = 0.0497, r = 0.27). In fresh normal plasma and serum, His-tag proBNP1–108 was processed to a lower molecular weight form confirmed to be BNP. Processed BNP was higher in men than women (P = 0.041) and was positively correlated to plasma corin concentrations (P = 0.041, r = 0.65). CONCLUSIONS Our results support the concept that proBNP1–108 may be processed outside of the heart in the circulation where the proprotein convertase is present. Moreover, sex may impact this process, since corin concentrations are higher in men. These findings may have important physiologic and pathophysiologic implications for the proBNP/corin system in the human.

Effect of metabolic rate on ventilatory roll-off during hypoxia

1994 ◽  
Vol 76 (6) ◽  
pp. 2310-2314 ◽  
Author(s):  
W. M. Gershan ◽  
H. V. Forster ◽  
T. F. Lowry ◽  
M. J. Korducki ◽  
A. L. Forster ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Minute Ventilation ◽  
Face Mask ◽  
Co2 Production ◽  
O2 Consumption ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Series Of Experiments ◽  
Carotid Arterial ◽  
Arterial Po2

This study was done to determine 1) whether goats demonstrate the roll-off phenomenon, i.e., a secondary decrease in minute ventilation (VE), after an initial hyperventilation during various levels of hypoxia and, if so, 2) whether roll-off could be due to changes in metabolic rate. We hypothesized that roll-off occurs in the goat during hypoxia but is not due to hypometabolism. To answer question 1, eight unanesthetized adult goats were exposed to 15–20 min of hypoxia at 0.15, 0.12, and 0.09 inspired O2 fraction (FIO2), resulting in 60, 40, and 30 Torr arterial PO2, respectively. Goats were fitted with a face mask connected to a spirometer to measure VE, and arterial blood gas samples were obtained via carotid arterial catheters. Roll-off was seen with 0.15 and 0.12 FIO2, whereas VE steadily increased with 0.09 FIO2. During hypoxia, arterial PCO2 fell 2, 3, and 7 Torr at 0.15, 0.12, and 0.09 FIO2, respectively. In the second series of experiments, nine different goats were exposed to 30 min of 0.12 FIO2. O2 consumption and CO2 production were measured five times during baseline and hypoxia. VE increased to 32% above baseline values after 2 min of hypoxia and then gradually decreased by 18%. Changes in breathing frequency and tidal volume contributed to the roll-off. O2 consumption decreased (P = 0.0029, analysis of variance) and CO2 production increased (P = 0.0027) during hypoxia, although both changes were small (< 7%) compared with the eventual 18% decrease in VE. We conclude that the adult goat demonstrates the roll-off phenomenon during moderate levels of hypoxia. (ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory responses to dead space and CO2 breathing under inspiratory resistive load

1995 ◽  
Vol 78 (2) ◽  
pp. 555-561 ◽  
Author(s):  
D. A. Sidney ◽  
C. S. Poon
Keyword(s):  
Breathing Pattern ◽  
Human Subjects ◽  
Minute Ventilation ◽  
Resistive Load ◽  
Healthy Human ◽  
Ventilatory Responses ◽  
Ventilatory Pattern ◽  
Volume Relationship ◽  
The Mean ◽  
End Tidal

To investigate how breathing is controlled during CO2 stimulation, steady-state ventilatory responses to rebreathing through a tube (DS) and inspiring a fixed PCO2 (INH) were compared in healthy human subjects. Tests were performed in hyperoxia with (IRL) and without (NL) an inspiratory resistive load (15 cmH2O.l–1.s at 1 l/s). The mean slope of the minute ventilation (VE)-end-tidal PCO2 relationship was significantly higher in DS-IRL than in INH-IRL [1.86 +/- 0.67 (SD) vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.01], and it was significantly different between INH-NL and INH-IRL (1.64 +/- 0.41 vs. 1.40 +/- 0.32 l.min-1.Torr-1, P < 0.05) but not between DS-NL and DS-IRL (1.85 +/- 0.72 vs. 1.86 +/- 0.67 l.min-1.Torr-1). The slope of the VE-tidal volume relationship was significantly lower in DS-NL than in INH-NL (19.6 +/- 3.8 vs. 21.2 +/- 5.1 min-1, P < 0.05), but other comparisons in breathing pattern between NL and IRL and between DS and INH failed to reach significance. We concluded that 1) alterations in alveolar PCO2 temporal profile by DS could induce changes in VE-end-tidal PCO2 sensitivity and ventilatory pattern, 2) these changes may be modified by increased mechanical impairment resulting from IRL, and 3) carotid chemoreceptor mediation is not necessary for the observed effects of DS.

Is the hyperpnea of muscular contractions critically dependent on spinal afferents?

1988 ◽  
Vol 64 (1) ◽  
pp. 226-233 ◽  
Author(s):  
A. G. Brice ◽  
H. V. Forster ◽  
L. G. Pan ◽  
A. Funahashi ◽  
M. D. Hoffman ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Human Subjects ◽  
Lactate Concentration ◽  
Muscle Contractions ◽  
Co2 Production ◽  
Central Command ◽  
Afferent Pathways ◽  
Co2 Partial Pressure ◽  
Normal Human ◽  
Spinal Afferents

We studied the role of spinal afferent pathways in the hyperpnea of electrically induced muscle contractions (ExE). The ventilatory (VE) and arterial CO2 partial pressure (PaCO2) responses were measured at rest and during two levels of ExE in awake human paraplegic subjects with clinically complete lesions of the spinal cord (range T4-T11). We hypothesized that if peripheral neural drive is critical to a normal ventilatory response, then ExE in the absence of intact pathways should cause a lower ventilatory response resulting in hypercapnia at the onset of ExE. ExE was induced by stimulation of the quadriceps and hamstring muscles that approximately doubled the resting level of CO2 production (VCO2). PaCO2 during work transitions and in the latter stages of ExE did not differ significantly from that at rest. Arterial pH progressively declined over time during ExE (P less than 0.01) as a result of increased lactate concentration (P less than 0.01). The linear relationship between VE and VCO2 was similar to that found for normal human subjects during ExE (P = 0.73). These data suggest that VE and presumably alveolar ventilation (VA) can be appropriately matched to VCO2 during low-intensity muscle contractions of the lower extremities in the absence of intact spinal afferent pathways. Moreover, since it is unlikely that postulated "central command" mechanisms were initiated during ExE in these paraplegic subjects, the data provide support for our previous conclusion that central command is not obligatory for matching VA to VCO2 (J. Appl. Physiol. 64: 218-225, 1988).

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