Decrease in cardiac stroke volume in humans during inhalations of 8% hypoxic gas mixture

2006 ◽  
Vol 141 (3) ◽  
pp. 281-283
Author(s):  
S. V. Nesterov
2006 ◽  
Vol 27 (5) ◽  
pp. S139-S146 ◽  
Author(s):  
S Zlochiver ◽  
D Freimark ◽  
M Arad ◽  
A Adunsky ◽  
S Abboud

1996 ◽  
Vol 199 (3) ◽  
pp. 569-578
Author(s):  
C Airriess ◽  
B Mcmahon

Changes in cardiac function and arterial haemolymph flow associated with 6 h of emersion were investigated in the crab Cancer magister using an ultrasonic flowmeter. This species is usually found sublittorally but, owing to the large-scale horizontal water movements associated with extreme tides, C. magister may occasionally become stranded on the beach. Laboratory experiments were designed such that the emersion period was typical of those that might be experienced by this crab in its natural environment. The frequency of the heart beat began to decline sharply almost immediately after the start of the experimental emersion period. Cardiac stroke volume fell more gradually. The combined reduction in these two variables led to a maximum decrease in cardiac output of more than 70 % from the control rate. Haemolymph flow through all the arteries originating at the heart, with the exception of the anterior aorta, also declined markedly during emersion. As the water level in the experimental chamber fell below the inhalant branchial openings, a stereotypical, dramatic increase in haemolymph flow through the anterior aorta began and this continued for the duration of the emersion period. The rapid time course of the decline in heart-beat frequency and the increase in haemolymph flow through the anterior aorta suggest a neural mechanism responding to the absence of ventilatory water in the branchial chambers. These responses may be adaptations, respectively, to conserve energy by reducing the minute volume of haemolymph pumped by the heart and to protect the supply of haemolymph to cephalic elements of the central nervous system. The decline in cardiac stroke volume, which occurs more slowly over the emersion period, may be a passive result of the failure to supply sufficient O2 to meet the aerobic demands of the cardiac ganglion.


2020 ◽  
Vol 195 ◽  
pp. 105553
Author(s):  
Rachel Smith ◽  
Joel Balmer ◽  
Christopher G. Pretty ◽  
Tashana Mehta-Wilson ◽  
Thomas Desaive ◽  
...  

1991 ◽  
Vol 70 (2) ◽  
pp. 740-747 ◽  
Author(s):  
J. D'Brot ◽  
T. Ahmed

We tested the hypothesis that prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity, possibly via a cyclooxygenase-dependent mechanism. In 15 sheep, specific lung resistance (sRL) was measured before and after 30 min of exposure to either air or a hypoxic gas mixture (13% O2). The sheep then inhaled 50 breaths of aerosolized 5% histamine solution (n = 9) or 10 breaths of 2.5% carbachol solution (n = 9), and measurements of sRL were repeated. On subsequent days the above protocols were repeated after a 30-min exposure to hyperoxia (O2 greater than or equal to 95%), without or after pretreatment with indomethacin (2 mg/kg). After air-sham exposure, carbachol and histamine increased mean sRL to 370 +/- 40 (SE) and 309 +/- 65% of baseline, respectively. Exposure to the hypoxic gas mixture had no effect on baseline sRL but enhanced the airway responsiveness to carbachol and histamine; mean sRL increased to 740 +/- 104 and 544 +/- 76% of baseline, respectively (P less than 0.05). Prior 30-min exposure to hyperoxia prevented the hypoxia-induced enhancement of bronchial reactivity to carbachol (sRL = 416 +/- 66% of baseline) and histamine (sRL = 292 +/- 41% of baseline) without affecting the airway responsiveness to these agents after air. Pretreatment with indomethacin did not reverse the protective effects of hyperoxia or the hypoxia-induced enhancement of bronchial reactivity. We conclude that 1) prior exposure to alveolar hyperoxia prevents the hypoxia-induced enhancement of bronchial reactivity and 2) neither the protective effects of hyperoxia nor the hypoxia-induced enhancement of bronchial reactivity is mediated via a cyclooxygenase-dependent mechanism.


1995 ◽  
Vol 20 (2) ◽  
pp. 198-210 ◽  
Author(s):  
Richard L. Hughson ◽  
John M. Kowalchuk

This study evaluated the dynamic response of [Formula: see text] in 6 healthy men at the onset and end of submaximal step changes in work rate during a pseudorandom binary sequence (PRBS) exercise test and during ramp incremental exercise to exhaustion while breathing three different gas mixtures. The fractional concentrations of inspired O2 were 0.14, 0.21, and 0.70 for the hypoxic, normoxic, and hyperoxic tests, respectively. Both maximal [Formula: see text] and work rate was significantly reduced in hypoxic tests compared to normoxic and hyperoxic tests. Maximal work rate was greater in hyperoxia than in normoxia. Work rate at ventilatory threshold was lower in hypoxia than in normoxia and hyperoxia but above the upper limit of exercise for the submaximal tests. Hypoxia significantly slowed the response of [Formula: see text] both at the onset and end of exercise compared to normoxia and hyperoxia. Hypoxia also modified the response to PRBS exercise, and again there was no difference between normoxia and hyperoxia. These data support the concept that [Formula: see text] kinetics can be slowed from the normoxic response by a hypoxic gas mixture. Key words: [Formula: see text]max, ventilatory threshold, oxygen deficit, pseudorandom binary sequence


1987 ◽  
Vol 59 (9) ◽  
pp. 975-978 ◽  
Author(s):  
Halfdan Ihlen ◽  
Knut Endresen ◽  
Yngvar Myreng ◽  
Erik Myhre

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