Effects of altered nitric oxide availability on rat muscle microvascular oxygenation during contractions

Aim: To explore the role of nitric oxide (NO) in controlling microvascular O-2 pressure (PO(2)mv) at rest and during contractions (1 Hz). We hypothesized that at the onset of contractions sodium nitroprusside (SNP) would raise PO(2)mv and slow the kinetics of PO(2)mv change whereas L-nitro arginine methyl ester L-NAME) would decrease PO(2)mv and speed its kinetics. Methods: We superfused the spinotrapezius muscle of female Sprague-Dawley rats (n = 7, body mass = 298 +/- 10 g) with SNP (300 mu M) and L-NAME (1.5 MM and measured PO(2)mv (phosphorescence quenching) during contractions. Results: SNP decreased mean arterial pressure (92 +/- 5 mmHg) below that of control (CON, 124 +/- 4 mmHg) and L-NAME (120 +/- 4 mmHg) conditions. SNP did not raise PO(2)mv at rest but it did elevate the PO(2)mv-to-MAP ratio (50% increase, P < 0.05) and slow the kinetics by lengthening the time-delay (TD, 14.0 +/- 5.0 s) and time constant (tau, 24.0 +/- 10.0 s) of the response compared with CON (TD, 8.4 +/- 3.3 s; tau, 16.0 +/- 4.5 s, P < 0.05 vs. SNP). L-NAME decreased PO(2)mv at rest and tended to speed tau (10.1 +/- 3.8 s, P =0.1), while TD (8.1 +/- 1.0 s) was not significantly different. L-NAME also caused PO(2)mv to fall transiently below steady-state contracting values. Conclusions: These results indicate that NO availability can significantly affect PO(2)mv at rest and during contractions and suggests that PO(2)mv derangements in ageing and chronic disease conditions may potentially result from impairments in NO availability.