Effect of SNAP‐generated NO on PO2 and VO2 in contracting skeletal muscle

Abstract

The effect of supplemental NO flux produced by the NO donor SNAP on interstitial PO2 and oxygen consumption (VO2) 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 PO2 was sampled at 2 Hz in 0.8 mm diam regions of muscle. In order to evoke reactive hyperemia and to evaluate VO2, the muscle was pneumatically compressed for 60 s to instantly remove blood and to record the rate of oxygen disappearance. The PO2 data were corrected for photo‐consumption. Interstitial PO2 at normal perfusion (Po), and VO2 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 VO2 (276 vs 281 nlO2/s•cm3). In SNAP‐treated muscles contraction caused VO2 to increase to 622 nlO2/s•cm3 (vs 650 in control), with a moderate decrease of Po from 95 to 61 mmHg. In SNAP‐treated muscles the post‐occlusion PO2 “overshoot” transient was absent and PO2 returned to Po, while the PO2 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 PO2. Support: NHLBI HL18292