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Rate of oxygen disappearance from arterioles in rat mesentery measured with scanning phosphorescence quenching microscopy (PQM)
Author(s) -
Golub Aleksander Sergeevich,
Song Bjorn Kyungsuck,
Pittman Roland Natan
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.973.4
Subject(s) - oxygen–haemoglobin dissociation curve , chemistry , arteriole , kinetics , oxygen , microcirculation , anatomy , blood flow , hamster , biophysics , medicine , biology , physics , organic chemistry , quantum mechanics
The oxygen disappearance curve (ODC) recorded in an arteriole after rapid arrest of blood flow reflects the complex interaction between the HbO 2 dissociation curve and the kinetics of tissue respiration. We have collected 75 ODCs in mesenteric arterioles using the scanning PQM technique in order to exclude the artifact of oxygen photo‐consumption in stationary blood. The ODC signatures were practically linear in contrast to reported exponential decays of intra‐arteriolar PO 2 . The initial rate of O 2 disappearance was 0.38 – 0.46 mmHg/s in large and small (mean i.d. = 26 and 15 μm) arterioles. The duration of the ODC was 3–4 min, many times longer than 12.8 s, reported by other workers. A group of arterioles associated with lymphatic vessels had a wider range of the ODC rate of 0.24–0.92 mmHg/s (27 and 18 μm arterioles, respectively). The linear shape of the experimental ODC was in a good agreement with results of computer simulations of ODCs accounting for HbO 2 dissociation and Michaelis‐Menten kinetics of oxygen consumption by the tissue. The maximal oxygen flux from arterioles calculated from the highest ODC rate (0.92 mmHg/s) was 0.95 nl O 2 /(cm 2 s) which was 37 times lower than that found in arterioles of the hamster dorsal skinfold window chamber. Our results do not support the hypothesis of a high oxygen consumption by the arteriolar wall. Support: AHA‐0655449U and NIH‐HL18292.