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Ann Thorac Surg 2002;74:143-148
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Hypoxic preconditioning in coronary microarteries: role of EDHF and K+ channel openers

Zhen Ren, MDa, Qin Yang, MDb, H. Storm Floten, MDa, Guo-Wei He, MD, PhD*a,b

a Providence Heart Institute, Albert Starr Academic Center, Department of Surgery, Oregon Health and Science University, Portland, Oregon, USA
b Department of Surgery, The Chinese University of Hong Kong, Hong Kong, People’s Republic Of China

Accepted for publication April 2, 2002.

* Address reprint requests to Prof. He, Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Block B, 5A, Prince of Wales Hospital, Shatin, NT, Hong Kong, People’s Republic Of China
e-mail: gwhe{at}cuhk.edu.hk

Background. Hypoxic preconditioning may provide a useful method of myocardial protection in cardiac operations. The present study was designed to investigate the possible mechanisms of preconditioning regarding endothelium-derived hyperpolarizing factor (EDHF) and the effect of a potassium channel opener KRN4884 on the porcine coronary microartery in mimicking hypoxic preconditioning.

Methods. Porcine coronary microartery rings (diameter 200 to 500 µm) studied in a myograph were divided into seven groups: (1) control group; (2) hypoxia-reoxygenation group (hypoxia for 60 minutes followed by reoxygenation for 30 minutes); (3) preconditioning group (hypoxia for 5 minutes followed by reoxygenation for 10 minutes before hypoxia reoxygenation); (4) KRN4884 pretreatment group (KRN4884 was added into the myograph chamber 20 minutes before hypoxia reoxygenation); (5) 5-hydroxydecanoate + KRN group (5-hydroxydecanoate was given 20 minutes before KRN4884 pretreatetment); (6) glibenclamide (GBC) + KRN group (GBC was added 20 minutes before KRN4884 pretreatment); and (7) endothelium denuded group (the endothelium was removed). The endothelium-derived hyperpolarizing factor-mediated relaxation to bradykinin was studied in the rings precontracted with U46619 in the presence of N{omega}-nitro-L-arginine and indomethacin.

Results. The maximal relaxation induced by bradykinin was reduced in hypoxia reoxygenation (40.7% ± 2.8% vs 66.9% ± 2.5% in control, p = 0.000). This reduced relaxation was recovered in either preconditioning (64.6% ± 4.6%, p = 0.002), or KRN4884 pretreatment (67.1% ± 3.6%, p = 0.000). The 5-hydroxydecanoate, but not GBC pretreatment abolished the effect of KRN44884 pretreatment (67.1% ± 3.6% vs 42.9% ± 3%, p = 0.001).

Conclusions. Hypoxia reoxygenation reduces the relaxation mediated by endothelium-derived hyperpolarizing factor in the coronary microartery. This function can be restored by either hypoxic preconditioning or the KATP channel opener KRN4884, and therefore KATP channel openers may provide similar effect as preconditioning. The mechanism is mainly related to the mitochondrial ATP-sensitive K+ channels.




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