Vascular endothelial growth factor regulation of endothelial nitric oxide synthase phosphorylation is involved in isoflurane cardiac preconditioning

• Published in: Cardiovascular research 2019-01, Vol.115 (1), p.168-178
• Main Authors: Liu, Yanan, Paterson, Mark, Baumgardt, Shelley L, Irwin, Michael G, Xia, Zhengyuan, Bosnjak, Zeljko J, Ge, Zhi-Dong
• Format: Article
• Language: English
• Subjects: Animals; Cell Communication; Cells, Cultured; Coculture Techniques; Disease Models, Animal; Endothelial Cells - enzymology; Endothelial Cells - pathology; Female; Humans; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism; Ischemic Preconditioning, Myocardial - methods; Isoflurane - pharmacology; Male; Myocardial Reperfusion Injury - enzymology; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - physiopathology; Myocardial Reperfusion Injury - prevention & control; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Nitric Oxide Synthase Type III - metabolism; Original; Phosphorylation; Rats, Wistar; Signal Transduction; Vascular Endothelial Growth Factor A - metabolism
• ISSN: 0008-6363; 1755-3245
• DOI: 10.1093/cvr/cvy157

Abstract Aims Previous studies indicate that nitric oxide derived from endothelial nitric oxide synthase (eNOS) serves as both trigger and mediator in anaesthetic cardiac preconditioning. The mechanisms underlying regulation of eNOS by volatile anaesthetics have not been fully understood. Therefore, this study examined the role of vascular endothelial growth factor (VEGF) in isoflurane cardiac preconditioning. Methods and results Wistar rats underwent 30 min of coronary artery occlusion followed by 2 h of reperfusion. Isoflurane given prior to ischaemia/reperfusion significantly decreased myocardial infarct size from 60 ± 1% in control to 40 ± 3% (n = 8 rats/group, P