Effects of nitric oxide donor and inhibitor on prostaglandin E-2-like activity, malondialdehyde and reduced glutathione levels after skeletal muscle ischemia-reperfusion

Sayan H., Babul A., Ugurlu B.

PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS, vol.65, no.4, pp.179-183, 2001 (SCI-Expanded) identifier identifier identifier


Oxygen free radicals are implicated in the pathophysiology of ischemia-reperfusion (I/R) injury in skeletal muscle. Nitric oxide (NO) and prostaglandin E-2 (PGE(2)) are important regulators of the microcirculation in skeletal muscle. The effects of L-arginine, substrate for NO, and NG-nitro L-arginine methyl ester (L-NAME) on PGE2 synthesis, lipid peroxidation and reduced glutathione (GSH) levels was investigated in the rat gastrocnemius muscle after 3 h of reperfusion following 2 h of ischemia. Lipid peroxidation and GSH levels showed a non-significant changes in the I/R groups compared to the control group. According to these results, it can be assumed that skeletal muscle can resist 2 h of ischemia followed by 3 h of reperfusion-induced oxidative stress.