RESUMEN
Nitric oxide(NO) has been known to play an important role as a signal molecule in many parts of the organism as well as a cytotoxic effector molecule of the nonspecific immune response. Excessive NO has been reported to exert cytotoxic effect by direct toxicity or by reacting to superoxide radicals during ischemia-reperfusion. Therefore is strongly needed a study directly measuring NO release designed to better clarify roles of NO in ischemia-reperfusion injury and its mechanism. Male Sprague-Dawley rats were anesthetized with urethane(1g/kg) intraperitoneally, and pedicled gastrocnemius muscle flaps were elevated. The elevated flaps were subjected to 4 hours of arterial ischemia and then reperfused for 2 hours. And then NO current was measured in the gastrocnemius muscle using NO-selective microelectrode system. NO release gradually increased and then decreased in the rat gastrocnemius muscle during both ischemic and reperfusion period. The average NO releases from baseline during ischemia and reperfusion were 10405 +/- 2663 and 2513 +/- 970 picoamperes(pA), respectively. The ischemia-reperfusion caused substantial histological damage in the skeletal muscle, in which a profusion of red blood cells was observed due to extravasation of vessels, rupturing of microcirculation, and leukocyte infiltration, compared to the damage in control and ischemic rat gastrocnemius muscles. From the above results, ischemia-reperfusion injury was developed more severely during reperfusion than ischemia, and NO increased during ischemia and reperfusion as a biphasic pattern in the rat gastrocnemius muscle.
Asunto(s)
Animales , Humanos , Masculino , Ratas , Eritrocitos , Isquemia , Leucocitos , Microcirculación , Microelectrodos , Músculo Esquelético , Músculos , Óxido Nítrico , Ratas Sprague-Dawley , Reperfusión , Daño por Reperfusión , SuperóxidosRESUMEN
No abstract available.