scholarly journals Increases in coronary vascular resistance related to high arterial oxygen tension in dogs.

1980 ◽  
Vol 44 (9) ◽  
pp. 749-754 ◽  
Author(s):  
KINJI ISHIKAWA ◽  
KEN KANAMASA ◽  
TETSU YAMAKADO ◽  
YASUYUKI KOHASHI ◽  
ARATA KATO ◽  
...  
2006 ◽  
Vol 12 (6) ◽  
pp. S11
Author(s):  
Thomas P. Olson ◽  
Robert P. Frantz ◽  
Kathy A. O'Malley ◽  
Bruce D. Johnson

1999 ◽  
Vol 91 (4) ◽  
pp. 945-945 ◽  
Author(s):  
Albert Benzing ◽  
Torsten Loop ◽  
Georg Mols ◽  
Klaus Geiger

Background Compressed air from a hospital's central gas supply may contain nitric oxide as a result of air pollution. Inhaled nitric oxide may increase arterial oxygen tension and decrease pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. Therefore, the authors wanted to determine whether unintentional nitric oxide inhalation by contamination of compressed air influences arterial oxygen tension and pulmonary vascular resistance and interferes with the therapeutic use of nitric oxide. Methods Nitric oxide concentrations in the compressed air of a university hospital were measured continuously by chemiluminescence during two periods (4 and 2 weeks). The effects of unintended nitric oxide inhalation on arterial oxygen tension (n = 15) and on pulmonary vascular resistance (n = 9) were measured in patients with acute lung injury and acute respiratory distress syndrome by changing the source of compressed air of the ventilator from the hospital's central gas supply to a nitric oxide-free gas tank containing compressed air. In five of these patients, the effects of an additional inhalation of 5 ppm nitric oxide were evaluated. Results During working days, compressed air of the hospital's central gas supply contained clinically effective nitric oxide concentrations (> 80 parts per billion) during 40% of the time. Change to gas tank-supplied nitric oxide-free compressed air decreased the arterial oxygen tension by 10% and increased pulmonary vascular resistance by 13%. The addition of 5 ppm nitric oxide had a minimal effect on arterial oxygen tension and pulmonary vascular resistance when added to hospital-supplied compressed air but improved both when added to tank-supplied compressed air. Conclusions Unintended inhalation of nitric oxide increases arterial oxygen tension and decreases pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. The unintended nitric oxide inhalation interferes with the therapeutic use of nitric oxide.


1969 ◽  
Vol 47 (1) ◽  
pp. 93-98 ◽  
Author(s):  
R. F. P. Cronin ◽  
A. Kovacs

In 11 anesthetized open-chest dogs, controlled perfusion of the left circumflex coronary artery was accomplished by shunting blood from the femoral artery and vein via a peristaltic pump. The pO2 of the perfusing blood was altered by changing the proportion of arterial and venous blood reaching the inflow side of the pump. Coronary perfusion pressure (CPP) was measured during stepwise reduction in the left circumflex coronary flow (LCF) over the range 120–10 cc/min. Resistance to coronary blood flowin the perfused myocardial segment was calculated as the ratio CPP/LCF and plotted against flow. Resistance-flow curves for the perfused coronary segments were obtained at pO2 values ranging between 95 and 25 mm Hg. Lowering the pO2 of the perfusing blood caused a reduction in coronary vascular resistance (CVR) in the perfused segment. When nitroglycerine was infused in a dosage of 3–6 μg/kg per minute, arterial blood pressure and heart rate were unaltered but CVR was reduced. The reduction in CVR was inversely proportional to the pO2 of the perfusing blood, the maximal vasodilator effect being observed at pO2 > 60 mm Hg. Nitroglycerine caused no significant change in coronary vascular resistance at pO2 < 39 mm Hg and did not prevent or delay the appearance of excess lactate in the coronary venous blood.


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

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.


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