Arterial oxygen content regulates plasma erythropoietin independent of arterial oxygen tension: a blinded crossover study

2019 ◽  
Vol 95 (1) ◽  
pp. 173-177 ◽  
Author(s):  
David Montero ◽  
Carsten Lundby
1997 ◽  
Vol 272 (1) ◽  
pp. H67-H75 ◽  
Author(s):  
S. Mouren ◽  
R. Souktani ◽  
M. Beaussier ◽  
L. Abdenour ◽  
M. Arthaud ◽  
...  

In isolated rabbit hearts perfused with suspension of red blood cells, we investigated the role of the endothelium and of several substances in the coronary vasoconstriction induced by a high arterial blood oxygen tension (PaO2). Red blood cells in Krebs-Henseleit buffer were oxygenated to obtain control and high-PaO2 perfusates. Arterial oxygen content was kept constant in both perfusates by reducing hemoglobin concentration in the high-PaO2 perfusate. Coronary blood flow was kept constant so that oxygen supply would not vary with the rise in PaO2. Increases in perfusion pressure therefore reflected increased coronary resistance. The high PaO2-induced coronary vasoconstriction was not affected by administration of indomethacin, nordihydroguaiaretic acid, NG-nitro-L-arginine, or superoxide dismutase and catalase but was abolished after endothelium damage or by cromakalim. These results demonstrate that 1) the endothelium contributes to the high PaO2-induced coronary vasoconstriction; 2) this effect is independent of cyclooxygenase or lipoxygenase products, nitric oxide, or free radicals; and 3) the closure of ATP-sensitive K+ channels mediates this vasoconstriction.


1987 ◽  
Vol 25 (3) ◽  
pp. 199-208 ◽  
Author(s):  
STEVEN J. BARKER ◽  
KEVIN K. TREMPER

1996 ◽  
Vol 23 (2) ◽  
pp. 75-77
Author(s):  
P. Dobromylskyj ◽  
P.M. Taylor ◽  
J.C. Brearley ◽  
C.B. Johnson ◽  
S.P.L. Luna

1979 ◽  
Vol 135 (5) ◽  
pp. 637-646 ◽  
Author(s):  
Louis L.H. Peeters ◽  
Roger E. Sheldon ◽  
M. Douglas Jones ◽  
Edgar L. Makowski ◽  
Giacomo Meschia

1973 ◽  
Vol 59 (2) ◽  
pp. 323-338 ◽  
Author(s):  
ALAN G. HEATH ◽  
G. M. HUGHES

1. Trout were subjected to a steady increase in water temperature (1.5 °C/h) from 15 °C until death occurred, while several respiratory and cardiovascular parameters were monitored. 2. Oxygen consumption increased during the warming (Q10 = 2.35 between 16 and 20 °C). At the higher temperatures the increase was more marked (Q10 =4.96 between 20 and 26 °C). 3. Ventilatory frequency increased during the rising temperature with a general levelling off observed above 23 °C. The amplitude of the pressure changes in the buccal and opercular cavities increased more than did the ventilatory frequency. Further analysis of the differential pressure across the gills suggests that the adjustment of respiratory pumping to the increased oxygen demand is predominantly in the volume pumped per stroke (cycle). 4. Heart rate rose steadily with the increasing temperature until about 24-25 °C, when a bradycardia usually became evident. Synchrony between the heart beat and the respiratory pumps was observed in some preparations at the higher temperatures. 5. Blood pressure increases during the warming were more marked in the ventral aorta than in the dorsal aorta. At the highest temperatures, abnormal cardiac cycles were frequently observed. 6. Arterial oxygen content declined slightly during warming and venous oxygen content dropped to zero above 23 °C. 7. It is suggested that cardiovascular adjustments may be a limiting factor in this type of stress.


PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 219-228
Author(s):  
Henrique Rigatto ◽  
June P. Brady

We studied nine healthy preterm infants during the first 35 days of life to define the relationship between periodic breathing, apnea, and hypoxia. For this purpose we compared ventilation/apnea (V/A), minute ventilation, and alveolar and capillary blood gases during periodic breathing induced by hypoxia and during spontancous periodic breathing in room air. We induced periodic breathing by giving the baby in sequence 21, 19, 17, and 15% O2 to breathe for 5 minutes each, and also by giving 21, 15, and 21% O2. We measured ventilation with a nosepiece and a screen flowmeter. With a decrease in arterial oxygen tension, preterm infants (1) hypoventilated, (2) breathed periodically more frequently, and (3) showed a decrease in V/A due to an increase in the apneic interval. In one baby this led to apnea lasting 30 seconds. These findings support our hypothesis that preterm infants breathing periodically hypoventilate and suggest that hypoxia may be a primary event leading to periodic breathing and apnea.


1974 ◽  
Vol 85 (2) ◽  
pp. 254-261 ◽  
Author(s):  
Arnold W. Strauss ◽  
Marilyn Escobedo ◽  
David Goldring

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