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-s ensitive K+ conductances and reduces the excitability of the fibers. T he ischemia-reperfusion also significantly decreases the ATP content o f the muscles. In the present work, the electrical parameters of reper fused extensor digitorum longus muscle of rats were measured in vitro at 30 degrees C, by a computerized two-intracellular microelectrode te chnique, before and after in vivo pretreatment with equimolar doses of phosphocreatine disodium salt tetrahydrate, phosphocreatine di-L-argi nine salt and L-arginine hydrochloride. In the same experimental situa tions the ATP content of the muscles was also measured. Both phosphocr eatine salts prevented the increase of membrane ion conductance due to muscle reperfusion by preloading the muscle fibers with extra ATP. Ph osphocreatine disodium salt also prevented the depolarization and rest ored the normal excitability of the reperfused fibers. In contrast, ph osphocreatine 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 fi bers from the ischemic-reperfusion insult. Furthermore, the L-amino ac id produced a more pronounced reduction of the excitability of the fib ers by increasing the threshold current needed to elicit an action pot ential and reducing its overshoot. The in vitro application of L-argin ine to the muscle also reduced the overshoot of the action potential, suggesting a direct interaction of the L-amino acid with Na+ channels.