Late anti-apoptotic effect of KATP channel opening in skeletal muscle

Summary Necrosis and apoptosis caused by ischaemia–reperfusion (IR) result in myocyte death and atrophy. ATP‐sensitive K+ (KATP) channels activation increases tissue tolerance of IR‐injury. Thus, in the present study, we evaluated the effects of KATP channel activation on skeletal muscle apoptosis after IR. Male Wistar rats were treated with 40 mg/kg, i.p., diazoxide (a KATP channel opener) or 5 mg/kg, i.p., glibenclamide (a KATP channel inhibitor) 30 min before the induction of 3 h ischaemia, followed by 6, 24 or 48 h reperfusion. At the end of the reperfusion period, the gastrocnemius muscle was removed for the analysis of tissue malondialdehyde content, superoxide dismutase (SOD) and catalase (CAT) activity, Bax and Bcl‐2 protein expression, histological damage and the number of apoptotic nuclei. Ischaemia–reperfusion increased malondialdehyde content (P