Interstitial nitric oxide concentrations are elevated in rat gastrocnemius muscle following recovery from femoral occlusion

Abstract

The present study examined the effects of ischemia‐reperfusion on the interstitial levels of nitric oxide (NO) and adenosine (Ado). Eight anesthetized rats had two microdialysis fibers inserted into the gastrocnemius muscle of each leg and perfused with Ringers (control) or 500 μM AOPCP (5'ectonucleotidase inhibitor). Following baseline collections both femoral arteries were clamped for 60 min (samples at 20, 40 and 60 min) and then released (samples at 20 min). With Ringers perfusion there were no increases in interstitial NO (baseline = 4.2±0.4 μM) during ischemia but NO was elevated (P<0.05) following reperfusion (5.4±0.5 μM). Prior to occlusion AOPCP treatment resulted in an increase (P<0.05) in NO from 4.3±0.6 to 5.5±0.5 μM as compared to Ringers. No further increases in NO were observed with AOPCP during ischemia, but NO was further elevated (P<0.05) following reperfusion (6.5±0.6 μM). Interstitial NO concentrations were higher (P<0.05) during AOPCP treatment compared to Ringers at all time points. There were no changes in interstitial Ado during the study. These data show that NO and Ado are not altered during femoral occlusion, but NO is elevated during reperfusion and that NO is even higher during ischemia‐reperfusion when Ado production is inhibited. These findings suggest that NO plays an important role in interstitially mediating vasodialtion during skeletal muscle reperfusion.Supported by NSERC