Role and mechanism of PKC in ischemic preconditioning of pig skeletal muscle against infarction

1  Research Institute, The Hospital for Sick Children, Toronto; and Departments of 2  Surgery and 3  Physiology, University of Toronto, Toronto, Ontario M5G 1X8, Canada Protein kinase C (PKC) inhibitors, chelerythrine (Chel, 0.6 mg) and polymyxin B (Poly B, 1.0 mg), and PKC activators, phorbol 12-my...

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Veröffentlicht in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2000-08, Vol.279 (2), p.666-R676
Hauptverfasser: Hopper, Richard A, Forrest, Christopher R, Xu, Huai, Zhong, Anguo, He, Wei, Rutka, James, Neligan, Peter, Pang, Cho Y
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Sprache:eng
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Zusammenfassung:1  Research Institute, The Hospital for Sick Children, Toronto; and Departments of 2  Surgery and 3  Physiology, University of Toronto, Toronto, Ontario M5G 1X8, Canada Protein kinase C (PKC) inhibitors, chelerythrine (Chel, 0.6 mg) and polymyxin B (Poly B, 1.0 mg), and PKC activators, phorbol 12-myristate 13-acetate (PMA, 0.05 mg) and 1-oleoyl-2-acetyl glycerol (OAG, 0.1 mg), were used as probes to investigate the role of PKC in mediation of ischemic preconditioning (IPC) of noncontracting pig latissimus dorsi (LD) muscles against infarction in vivo. These drugs were delivered to each LD muscle flap (8 × 12 cm) by 10 min of local intra-arterial infusion. It was observed that LD muscle flaps sustained 43 ± 5% infarction when subjected to 4 h of global ischemia and 24 h of reperfusion. IPC with three cycles of 10 min ischemia-reperfusion reduced muscle infarction to 25 ± 3% ( P  
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.2000.279.2.R666