Determination of alveolar–capillary O2 partial pressure gradient by using 15NO

Nitric Oxide ◽  
2005 ◽  
Vol 12 (3) ◽  
pp. 127-128 ◽  
Author(s):  
H. Heller ◽  
S. Brandt ◽  
K.-D. Schuster
2021 ◽  
Vol 5 (2) ◽  
pp. 15
Author(s):  
Paz Nativ ◽  
Yonatan Gräber ◽  
Yaron Aviezer ◽  
Ori Lahav

A new analytic approach is presented for determining the total volatile fatty acids (VFAT) concentration in anaerobic digesters. The approach relies on external determination of the inorganic carbon concentration (CT) in the analyzed solution, along with two strong-acid titration points. The CT concentration can be determined by either a direct analysis (e.g., by using a TOC device) or by estimating it from the recorded partial pressure of CO2(g) in the biogas (often a routine analysis in anaerobic digesters). The titration is carried out to pH 5.25 and then to pH 4.25. The two titration results are plugged into an alkalinity-mass-based equation and then the two terms are subtracted from each other to yield an equation in which VFAT is the sole unknown (since CT is known and the effect of the total orthophosphate and ammonia concentrations is shown to be small at this pH range). The development of the algorithm and its verification on four anaerobic reactor liquors is presented, on both the raw water and on acetic acid-spiked samples. The results show the method to be both accurate (up to 2.5% of the expected value for VFAT/Alkalinity >0.2) and repetitive when the total orthophosphate and ammonia concentrations are known, and fairly accurate (±5% for VFAT >5 mM) when these are completely neglected. PHREEQC-assisted computation of CT from the knowledge of the partial pressure of CO2(g) in the biogas (and pH, EC and temperature in the liquor) resulted in a very good estimation of the CT value (±3%), indicating that this technique is adequate for the purpose of determining VFAT for alarming operators in case of process deterioration and imminent failure.


1982 ◽  
Vol 242 (3) ◽  
pp. C200-C206 ◽  
Author(s):  
E. Mulligan ◽  
S. Lahiri

The cat carotid chemoreceptor O2 and CO2 responses can be separated by oligomycin and by antimycin A. Both of these agents greatly diminish or abolish the chemoreceptor O2 response but not the nicotine or CO2 responses. After either oligomycin or antimycin, the responses to increases and decreases in arterial CO2 partial pressure (PaCO2) consisted of increases and decreases in activity characterized respectively by exaggerated overshoots and undershoots. These were eliminated by the carbonic anhydrase inhibitor, acetazolamide, suggesting that they resulted from changes in carotid body tissue pH. The steady-state PaCO2 response remaining after oligomycin was no longer dependent on arterial O2 partial pressure (PaO2). All effects of antimycin were readily reversible in about 20 min. The separation of the responses to O2 and CO2 indicates that there may be at least partially separate pathways of chemoreception for these two stimuli. The similarity of the oligomycin and antimycin results supports the metabolic hypothesis of chemoreception.


1988 ◽  
Vol 11 (4) ◽  
pp. 752-756 ◽  
Author(s):  
Zion Sasson ◽  
Paul G Yock ◽  
Liv K Hatle ◽  
Edwin L Alderman ◽  
Richard L Popp

1987 ◽  
Vol 253 (4) ◽  
pp. H890-H897 ◽  
Author(s):  
R. W. McPherson ◽  
D. Eimerl ◽  
R. J. Traystman

The interaction of hypoxic hypoxia, hypercapnia, and mean arterial blood pressure (MABP) was studied in 15 pentobarbital-anesthetized ventilated dogs. In one group of animals (n = 5) hypercapnia [arterial CO2 partial pressure (PaCO2) approximately 50 Torr] was added to both moderate hypoxia and severe hypoxia. Moderate hypoxia [arterial O2 partial pressure (PaO2) = 36 mmHg] increased MABP and cerebral blood flow (CBF) without changes in cerebral O2 uptake (CMRO2). Superimposed hypercapnia increased CBF and MABP further with no change in CMRO2. In another group of animals (n = 5), a MABP increase of approximately 40 mmHg during moderate hypoxia without hypercapnia did not further increase CBF, suggesting intact autoregulation. Thus, during moderate hypoxia, hypercapnia is capable of increasing CBF. Severe hypoxia (PaO2 = 22 mmHg) increased CBF, but MABP and CMRO2 declined. Superimposed hypercapnia further decreased MABP and decreased CBF from its elevated level and further decreased CMRO2. Raising MABP under these circumstances in another animal group (n = 5) increased CBF above the level present during severe hypoxia alone and increased CMRO2. The change in CBF and CMRO2 during severe hypoxia plus hypercapnia with MABP elevation were not different from that severe hypoxia alone. We conclude that, during hypoxia sufficiently severe to impair CMRO2, superimposed hypercapnia has a detrimental influence due to decreased MABP, which causes a decrease in CBF and cerebral O2 delivery.


Sign in / Sign up

Export Citation Format

Share Document