ENERGY-METABOLISM AND ADENINE-NUCLEOTIDE DEGRADATION IN TWITCH-STIMULATED RAT HINDLIMB DURING ISCHEMIA-REPERFUSION

The purpose of this study was to characterize twitch tension and energ y metabolism in ischemic, stimulated rat hindlimb to determine its sui tability as a rapid time course model of ischemia-reperfusion injury. After 15 min equilibration, rat hindlimbs were stimulated (1-Hz twitch es, 0.2 ms pulse duration, 15 V) for 5 min (control, n = 8). This twit ch protocol was maintained throughout the ischemic and reperfusion per iods. The control period was followed by 5, 20, or 40 min of ischemia (ligation of femoral artery and vein) or 40 min of ischemia with 0, 5, or 20 min of reperfusion (removal of ligature). The soleus [89% slow oxidative (SO)] and the white gastrocnemius [WG; 91 % fast glycolytic (FG)] were analyzed for phosphocreatine (PCr), adenine nucleotides, gl ycogen, and glycolytic intermediates. Ischemia was characterized by pr ogressive decreases in twitch tension, high-energy phosphagens, total adenine nucleotides (TAN), and glycogen. Also, energy metabolism was a ltered at a greater rate in WG than in soleus. Reperfusion resulted in a recovery in PCr and lactate, with little change in ATP, TAN, or gly cogen. The inability to resynthesize adenine nucleotides and glycogen during reperfusion is characteristic of damaged skeletal muscle. The e xtent of the metabolic alterations in SO and FG muscles during twitch stimulation was comparable with previously reported noncontracting isc hemia protocols of 2-4 and 4-7 h in length, respectively. The present study demonstrates that twitch stimulation of ischemic skeletal muscle is a useful model for inducing rapid metabolic changes and an ischemi c insult comparable to prolonged noncontracting ischemia-reperfusion m odels.