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Effect of SNAP‐generated NO on PO 2 and VO 2 in contracting skeletal muscle
Author(s) -
Golub Aleksander S,
Song Bjorn K,
Pittman Roland N
Publication year - 2013
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.27.1_supplement.898.17
Subject(s) - chemistry , oxygen , reactive hyperemia , interstitial space , perfusion , snap , skeletal muscle , anatomy , vasodilation , medicine , computer graphics (images) , organic chemistry , computer science
The effect of supplemental NO flux produced by the NO donor SNAP on interstitial PO 2 and oxygen consumption (VO 2 ) was studied by phosphorescence quenching microscopy under conditions of active and reactive hyperemia in the spinotrapezius muscles of anesthetized rats. The oxygen probe and SNAP (1 mM) were loaded into the interstitial space and PO 2 was sampled at 2 Hz in 0.8 mm diam regions of muscle. In order to evoke reactive hyperemia and to evaluate VO 2 , the muscle was pneumatically compressed for 60 s to instantly remove blood and to record the rate of oxygen disappearance. The PO 2 data were corrected for photo‐consumption. Interstitial PO 2 at normal perfusion (Po), and VO 2 were recorded in resting muscle (5 s), and during stimulation (started 30 s before Po measurements, 10 V, 1 Hz, 2 ms), compression and recovery (120 s). SNAP increased Po from 33 to 95 mmHg without changing VO 2 (276 vs 281 nlO 2 /s•cm 3 ). In SNAP‐treated muscles contraction caused VO 2 to increase to 622 nlO 2 /s•cm 3 (vs 650 in control), with a moderate decrease of Po from 95 to 61 mmHg. In SNAP‐treated muscles the post‐occlusion PO 2 “overshoot” transient was absent and PO 2 returned to Po, while the PO 2 in non‐treated muscles reached 1.6–1.8 times Po. Inhibition of cell respiration by NO, found in isolated cells, apparently has no functional significance in situ because of the compensatory effect of high interstitial PO 2 . Support: NHLBI HL18292