Effects of high energy phosphates and l-arginine on the electrical parameters of ischemic-reperfused rat skeletal muscle fibers

In skeletal muscle, 4 h of ischemia followed by 30 min of reperfusion depolarizes the fibers, markedly increases the Cl- and glibenclamide-sensitive K+ conductances and reduces the excitability of the fibers. The ischemia-reperfusion also significantly decreases the ATP content of the muscles. In the present work, the electrical parameters of reperfused extensor digitorum longus muscle of rats were measured in vitro at 30°C, by a computerized two-intracellular microelectrode technique, before and after in vivo pretreatment with equimolar doses of phosphocreatine disodium salt tetrahydrate, phosphocreatine di-l-arginine salt and l-arginine hydrochloride. In the same experimental situations the ATP content of the muscles was also measured. Both phosphocreatine salts prevented the increase of membrane ion conductance due to muscle reperfusion by preloading the muscle fibers with extra ATP. Phosphocreatine disodium salt also prevented the depolarization and restored the normal excitability of the reperfused fibers. In contrast, phosphocreatine di-l-arginine salt did not restore the resting potential nor the excitability of the fibers, but it decreased the amplitude of the action potential by reducing the overshoot. The pretreatment with l-arginine also failed to protect the electrical parameters of the fibers from the ischemic-reperfusion insult. Furthermore, the l-amino acid produced a more pronounced reduction of the excitability of the fibers by increasing the threshold current needed to elicit an action potential and reducing its overshoot. The in vitro application of l-arginine to the muscle also reduced the overshoot of the action potential, suggesting a direct interaction of the l-amino acid with Na+ channels. © 1995.