Gas Exchange and Ventilatory Responses to Hypoxia and Hypercapnia in Amphisbaena Alba (Reptilia: Amphisbaenia)

1987 ◽  
Vol 127 (1) ◽  
pp. 159-172 ◽  
Author(s):  
AUGUSTO S. ABE ◽  
KJELL JOHANSEN
Keyword(s):  
Gas Exchange ◽  
Oxygen Uptake ◽  
Large Fraction ◽  
Breath Hold ◽  
Low Oxygen ◽  
Hold Period ◽  
Ventilatory Responses ◽  
Variable Duration ◽  
End Tidal ◽  
A Minor

1. Total and cutaneous gas exchange and ventilatory responses to breathing hypoxic and hypercapnic gases were studied in Amphisbaena alba (Linnaeus), a burrowing squamate reptile. 2. This species shows a very low oxygen uptake rate (VO2) compared with other squamates of the same size (VO2 = 15.4, 36.2 and 49.0 mlkg−1 h−1 at 20, 25 and 30°C, respectively). Cutaneous gas exchange represents a large fraction of the total uptake. Oxygen uptake was strongly affected by temperature [Q10 = 5.5 (20–25°C); 1.8 (25–30°C); 3.2 (20–30°C)]. 3. A. alba shows a biphasic ventilatory pattern under hypoxic and hypercapnic conditions. A single breathing cycle, consisting of expiration-inspiration, includes a ventilatory period (VP) followed by a non-ventilatory (breath hold) period (NVP) of variable duration. When breathing air at 25°C the NVP typically occupied about 2 min. The ventilatory period occupied only 0.075 parts of a complete breath-tobreath cycle. Breathing hypoxic gases caused a pronounced rise in ventilation volume (Ve) from an increase in tidal volume (Vt) and frequency (f) at inspired O2 concentrations below 7%. Breathing hypercapnic gas mixtures induced a minor change in Vt at CO2 concentrations below 3%, and Ve increased mostly because of increases in f. End tidal O2 (PetOO2) and CO2 (PetOO2) tensions changed with increasing VE while breathing hypoxic and hypercapnic gas. 4. The results are discussed in relation to the fossorial habits of A. alba, and are compared with data from other squamates.

Alteration by hyperoxia of ventilatory dynamics during sinusoidal work

1980 ◽  
Vol 48 (6) ◽  
pp. 1083-1091 ◽  
Author(s):  
R. Casaburi ◽  
R. W. Stremel ◽  
B. J. Whipp ◽  
W. L. Beaver ◽  
K. Wasserman
Keyword(s):  
Gas Exchange ◽  
Work Load ◽  
Cycle Ergometer ◽  
Work Rate ◽  
Phase Lag ◽  
Ventilatory Responses ◽  
Load Tests ◽  
The Mean ◽  
End Tidal ◽  
End Tidal Co2

The effects of hyperoxia on ventilatory and gas exchange dynamics were studied utilizing sinusoidal work rate forcings. Five subjects exercised on 14 occasions on a cycle ergometer for 30 min with a sinusoidally varying work load. Tests were performed at seven frequencies of work load during air or 100% O2 inspiration. From the breath-by-breath responses to these tests, dynamic characteristics were analyzed by extracting the mean level, amplitude of oscillation, and phase lag for each six variables with digital computer techniques. Calculation of the time constant (tau) of the ventilatory responses demonstrated that ventilatory kinetics were slower during hyperoxia than during normoxia (P less than 0.025; avg 1.56 and 1.13 min, respectively). Further, for identical work rate fluctuations, end-tidal CO2 tension fluctuations were increased by hyperpoxia. Ventilation during hyperoxia is slower to respond to variations in the level of metabolically produced CO2, presumably because hyperoxia attenuates carotid body output; the arterial CO2 tension is consequently less tightly regulated.

Mass Spectrometry Analysis of Oxygen Gas Exchange in High- and LOW-CO2 Cells of Chlorella vulgaris

1988 ◽  
Vol 43 (9-10) ◽  
pp. 709-716 ◽  
Author(s):  
Y. Shiraiwa ◽  
K. P. Bader ◽  
G. H. Schmid
Keyword(s):  
Gas Exchange ◽  
Oxygen Uptake ◽  
Chlorella Vulgaris ◽  
Mitochondrial Respiration ◽  
Mass Spectrometry Analysis ◽  
Strong Light ◽  
Inlet System ◽  
Light Intensities ◽  
Oxygen Gas ◽  
A Minor

Abstract Oxygen gas exchange was monitored in the unicellular green alga Chlorella vulgaris 211 - 11 h by means of a mass spectrometer equipped with a special membrane gas-inlet-system and a photosynthetic reaction vessel. CO2-dependent 18O2-uptake as well as 16O2-evolution were analyzed in both High- and Low-CO2 cells. In High-CO2 cells, the 18O2-ruptake in the light (UL) decreased by 65% upon addition of 3 mᴍ NaHCO3 , while 16O2-evolution (E) was increased approx. 1.8 times by the same treatment. 18O2-uptake in the dark (UD) was not affected by the addition of external inorganic carbon (Ci). The addition of 3.3 mᴍ NaHCO3 also affected UL and E in Low CO2-cells, however, to a minor extent. UL under CO2-saturating conditions was light intensity-independent up to 2 klux and 1.2 klux in High- and Low-CO2 cells, respectively. Above these light intensities UL increased approx. 4-fold in High- and approx. 6-fold in Low-CO2 cells. Under CO2-limiting conditions, however, UL increased in High-CO2 cells even under very low light intensities, showing that photorespiratory oxygen uptake occurred even in the near vicinity of the light compensation point. Under C02-saturating and strong light conditions UL represented almost half of E in Low-CO2 cells and about 30 % of E in High-CO2 cells. In Low-CO2 cells addition of ethoxyzolamide (EZA), an inhibitor of carbonic anhydrase, enhanced UL and suppressed E and NET under CO2-limiting conditions, whereas the compound had only a minor effect on High-CO2 cells. DCMU (3 μᴍ) strongly inhibited E and UL under CO2-saturating conditions, with the remaining UL being smaller than UD . KCN (1 mᴍ) and SHAM (1.5 mᴍ) added to DCMU-treated Low-CO2 cells suppressed UL by approx. 50 % . The resulting value corresponded to half of UD . KCN also inhibited E under CO2-saturating conditions, with UL being strongly enhanced showing a maximal uptake at 0.4 mᴍ KCN . Under these conditions NET was nearly zero. The effect seems to be due to an inhibition of RubisCO and an enhancement of Mehler reactions. At 0.7 mᴍ KCN , DCMU entirely inhibited UL , but oxygen uptake appeared increased after turning the light off. This uptake corresponded to approx. 60 % of UD . Whereas KCN and SHAM inhibited approx. 70 % of UD , only 16% of UL was suppressed. These results suggest that the contribution of mitochondrial respiration to UL was negligeable, since UL seemed to be suppressed in the light under CO2-saturated conditions. Iodoacetamide, which is an inhibitor of the Calvin cycle and thereby diverts carbon into the respiratory pathway, inhibited E and NET under CO2-saturating conditions, but did not affect UL . This result also shows that UL is not due to mitochondrial respiration. A hydroxylamine derivative [20, 21] which changes the ratio of the RuBP carboxylation to oxygenation activity in tobacco leaves did not affect this ratio in Chlorella.

The Ventilatory Effects of Doxapram in Normal Man

1983 ◽  
Vol 65 (1) ◽  
pp. 65-69 ◽  
Author(s):  
P. M. A. Calverley ◽  
R. H. Robson ◽  
P. K. Wraith ◽  
L. F. Prescott ◽  
D. C. Flenley
Keyword(s):  
Oxygen Uptake ◽  
Ventilatory Response ◽  
Co2 Production ◽  
Central Action ◽  
Ventilatory Responses ◽  
Ventilatory Effects ◽  
Normal Man ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Ventilatory Response To Co2

1. To determine the mode of action of doxapram in man we have measured ventilation, oxygen uptake, CO2 production, hypoxic and hypercapnic ventilatory responses in six healthy men before and during intravenous infusion to maintain a constant plasma level. 2. Doxapram changed neither resting oxygen uptake nor CO2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO2 studied. 3. Doxapram increased the ventilatory response to isocapnic hypoxia from − 0.8 ± 0.4 litre min−1 (%Sao2)−1 to −1.63 ± 0.9 litres min−1 (%Sao2)−1. This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO2 by 0.5 kPa without adding doxapram. 4. The slope of the ventilatory response to rebreathing CO2 rose from 11.6 ± 5.3 litres min−1 kPa−1 to 20,4 ± 9.8 litres min−1 kPa−1 during doxapram infusion. 5. The marked increase in the ventilatory response to CO2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanaesthetized subjects.

Ventilatory responses to cardiac output changes in patients with pacemakers

1981 ◽  
Vol 51 (5) ◽  
pp. 1103-1107 ◽  
Author(s):  
P. W. Jones ◽  
W. French ◽  
M. L. Weissman ◽  
K. Wasserman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Blood Gas ◽  
Cardiac Pacemakers ◽  
Ventilatory Responses ◽  
Mean Delay ◽  
Arterial Blood ◽  
End Tidal

Cardiac output changes were induced by step changes of heart rate (HR) in six patients with cardiac pacemakers during monitoring of ventilation and gas exchange, breath-by-breath. Mean low HR was 48 beats/min; mean high HR was 82 beats/min. The change of oxygen uptake immediately after the HR change was used as an index of altered cardiac output. After HR increase, oxygen uptake (V02) rose by 34 +/- 20% (SD), and after HR decrease, Vo2 fell by 24 +/- 11%. There was no change in arterial blood pressure. After HR increase, ventilation increased, after a mean delay of 19 +/- 4 s; after HR reduction, ventilation fell, after a mean delay of 29 +/- 7 s. In the period between HR increase and the resulting increase in ventilation, end-tidal PCO2 (PETCO2) rose by 2.6 +/- 2.0 Torr, and in the period between HR decreases and the fall in ventilation, PETCO2 dropped by 2.9 +/- 2.2 Torr. The response time and end-tidal gas tension changes implicate the chemoreceptors in the reflex correction of blood gas disturbances that may result from imbalances between cardiac output and ventilation.

Unsteady-state gas exchange and storage in diving marine mammals: the harbor porpoise and gray seal

2001 ◽  
Vol 281 (2) ◽  
pp. R490-R494 ◽  
Author(s):  
R. G. Boutilier ◽  
J. Z. Reed ◽  
M. A. Fedak
Keyword(s):  
Gas Exchange ◽  
Marine Mammals ◽  
Lung Ventilation ◽  
The Body ◽  
Breath Hold ◽  
Unsteady State ◽  
Harbor Porpoise ◽  
Per Se ◽  
End Tidal ◽  
And Storage

Breath-by-breath measurements of end-tidal O2 and CO2 concentrations in harbor porpoise reveal that the respiratory gas exchange ratio (RR; CO2 output/O2 uptake) of the first lung ventilation in a breathing bout after a prolonged breath-hold is always well below the animal's metabolic respiratory quotient (RQ) of 0.85. Thus the longest apneic pauses are always followed by an initial breath having a very low RR(0.6–0.7), which thereafter increases with each subsequent breath to values in excess of 1.2. Although the O2 stores of the body are fully readjusted after the first three to four breaths following a prolonged apneic pause, a further three to four ventilations are always needed, not to load more O2 but to eliminate built-up levels of CO2. The slower readjustment of CO2 stores relates to their greater magnitude and to the fact that they must be mobilized from comparatively large and chemically complex HCO[Formula: see text]/CO2 stores that are built up in the blood and tissues during the breath-hold. These data, and similar measurements on gray seals (12), indicate that it is the readjustment of metabolic RQ and not O2 stores per se that governs the amount of time an animal must spend ventilating at the surface after a dive.

scholarly journals Pulmonary ventilation–perfusion mismatch: a novel hypothesis for how diving vertebrates may avoid the bends

2018 ◽  
Vol 285 (1877) ◽  
pp. 20180482 ◽  
Author(s):  
Daniel Garcia Párraga ◽  
Michael Moore ◽  
Andreas Fahlman
Keyword(s):  
Gas Exchange ◽  
Marine Mammals ◽  
Decompression Sickness ◽  
Large Fraction ◽  
Pulmonary Ventilation ◽  
Flow Distribution ◽  
Theoretical Modelling ◽  
Breath Hold ◽  
Air Breathing ◽  
Marine Vertebrates

Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N 2 uptake and avoiding gas emboli (GE) as they ascend. However, studies of beached and bycaught cetaceans and sea turtles imply that air-breathing marine vertebrates may, under unusual circumstances, develop GE that result in decompression sickness (DCS) symptoms. Theoretical modelling of tissue and blood gas dynamics of breath-hold divers suggests that changes in perfusion and blood flow distribution may also play a significant role. The results from the modelling work suggest that our current understanding of diving physiology in many species is poor, as the models predict blood and tissue N 2 levels that would result in severe DCS symptoms (chokes, paralysis and death) in a large fraction of natural dive profiles. In this review, we combine published results from marine mammals and turtles to propose alternative mechanisms for how marine vertebrates control gas exchange in the lung, through management of the pulmonary distribution of alveolar ventilation ( ) and cardiac output/lung perfusion ( ), varying the level of in different regions of the lung. Man-made disturbances, causing stress, could alter the mismatch level in the lung, resulting in an abnormally elevated uptake of N 2 , increasing the risk for GE. Our hypothesis provides avenues for new areas of research, offers an explanation for how sonar exposure may alter physiology causing GE and provides a new mechanism for how air-breathing marine vertebrates usually avoid the diving-related problems observed in human divers.

scholarly journals Oxygen-Sensitivity and Pulmonary Selectivity of Vasodilators as Potential Drugs for Pulmonary Hypertension

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 155
Author(s):  
Daniel Morales-Cano ◽  
Bianca Barreira ◽  
Beatriz De Olaiz Navarro ◽  
María Callejo ◽  
Gema Mondejar-Parreño ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Pulmonary Circulation ◽  
Pulmonary Arteries ◽  
Blood Perfusion ◽  
Mesenteric Arteries ◽  
Oxygen Sensitivity ◽  
Low Oxygen ◽  
Oxygen Selectivity

Current approved therapies for pulmonary hypertension (PH) aim to restore the balance between endothelial mediators in the pulmonary circulation. These drugs may exert vasodilator effects on poorly oxygenated vessels. This may lead to the derivation of blood perfusion towards low ventilated alveoli, i.e., producing ventilation-perfusion mismatch, with detrimental effects on gas exchange. The aim of this study is to analyze the oxygen-sensitivity in vitro of 25 drugs currently used or potentially useful for PH. Additionally, the study analyses the effectiveness of these vasodilators in the pulmonary vs. the systemic vessels. Vasodilator responses were recorded in pulmonary arteries (PA) and mesenteric arteries (MA) from rats and in human PA in a wire myograph under different oxygen concentrations. None of the studied drugs showed oxygen selectivity, being equally or more effective as vasodilators under conditions of low oxygen as compared to high oxygen levels. The drugs studied showed low pulmonary selectivity, being equally or more effective as vasodilators in systemic than in PA. A similar behavior was observed for the members within each drug family. In conclusion, none of the drugs showed optimal vasodilator profile, which may limit their therapeutic efficacy in PH.

Pulmonary Gas Exchange and Oxygen Uptake During Exercise in Patients with Type 1 Diabetes Mellitus

1992 ◽  
Vol 9 (3) ◽  
pp. 252-257 ◽  
Author(s):  
Th. Wanke ◽  
D. Formanek ◽  
M. Auinger ◽  
H. Zwick ◽  
K. Irsigler
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Gas Exchange ◽  
Oxygen Uptake ◽  
Type 1 Diabetes Mellitus ◽  
Pulmonary Gas Exchange

Direct effect of PaCO2 on respiratory sinus arrhythmia in conscious humans

2002 ◽  
Vol 282 (3) ◽  
pp. H973-H976 ◽  
Author(s):  
Nobuko Sasano ◽  
Alex E. Vesely ◽  
Junichiro Hayano ◽  
Hiroshi Sasano ◽  
Ron Somogyi ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Direct Effect ◽  
Respiratory Sinus Arrhythmia ◽  
Random Order ◽  
Mean Amplitude ◽  
Frequency Component ◽  
Pulmonary Gas Exchange ◽  
High Frequency Component ◽  
Sinus Arrhythmia ◽  
End Tidal

Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2directly affects RSA in conscious humans even when changes in tidal volume (VT) and breathing frequency ( F B), which indirectly affect RSA, are prevented. In seven healthy subjects, we adjusted end-tidal Pco 2 (Pet CO2 ) to 30, 40, or 50 mmHg in random order at constant VT and F B. The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with Pet CO2 ( P < 0.001). Mean R-R interval did not differ at Pet CO2 of 40 and 50 mmHg but was less at 30 mmHg ( P < 0.05). Because VT and F B were constant, these results support our hypothesis that increased CO2directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.

scholarly journals Coca chewing for exercise: hormonal and metabolic responses of nonhabitual chewers

1996 ◽  
Vol 81 (5) ◽  
pp. 1901-1907 ◽  
Author(s):  
Roland Favier ◽  
Esperanza Caceres ◽  
Laurent Guillon ◽  
Brigitte Sempore ◽  
Michel Sauvain ◽  
...  
Keyword(s):  
Heart Rate ◽  
Gas Exchange ◽  
Oxygen Uptake ◽  
Metabolic Responses ◽  
Physiological Data ◽  
Respiratory Gas Exchange ◽  
Gum Chewing ◽  
Arterial Blood ◽  
Before And After ◽  
Exercise Induced

Favier, Roland, Esperanza Caceres, Laurent Guillon, Brigitte Sempore, Michel Sauvain, Harry Koubi, and Hilde Spielvogel. Coca chewing for exercise: hormonal and metabolic responses of nonhabitual chewers. J. Appl. Physiol. 81(5): 1901–1907, 1996.—To determine the effects of acute coca use on the hormonal and metabolic responses to exercise, 12 healthy nonhabitual coca users were submitted twice to steady-state exercise (∼75% maximal O2 uptake). On one occasion, they were asked to chew 15 g of coca leaves 1 h before exercise, whereas on the other occasion, exercise was performed after 1 h of chewing a sugar-free chewing gum. Plasma epinephrine, norepinephrine, insulin, glucagon, and metabolites (glucose, lactate, glycerol, and free fatty acids) were determined at rest before and after coca chewing and during the 5th, 15th, 30th, and 60th min of exercise. Simultaneously to these determinations, cardiorespiratory variables (heart rate, mean arterial blood pressure, oxygen uptake, and respiratory gas exchange ratio) were also measured. At rest, coca chewing had no effect on plasma hormonal and metabolic levels except for a significantly reduced insulin concentration. During exercise, the oxygen uptake, heart rate, and respiratory gas exchange ratio were significantly increased in the coca-chewing trial compared with the control (gum-chewing) test. The exercise-induced drop in plasma glucose and insulin was prevented by prior coca chewing. These results contrast with previous data obtained in chronic coca users who display during prolonged submaximal exercise an exaggerated plasma sympathetic response, an enhanced availability and utilization of fat (R. Favier, E. Caceres, H. Koubi, B. Sempore, M. Sauvain, and H. Spielvogel. J. Appl. Physiol. 80: 650–655, 1996). We conclude that, whereas coca chewing might affect glucose homeostasis during exercise, none of the physiological data provided by this study would suggest that acute coca chewing in nonhabitual users could enhance tolerance to exercise.

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