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Right arrow Cardiac - pharmacology

Ann Thorac Surg 2001;72:1970-1976
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

Epoxyeicosatrienoic acids (EET11,12) may partially restore endothelium-derived hyperpolarizing factor–mediated function in coronary microarteries

Wei Zou, MDa, Qin Yang, MDa, Anthony P.C. Yim, MDa, Guo-Wei He, MD, PhD*a,b

a Cardiovascular Research Laboratory, Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Hong Kong SAR, China
b Cardiovascular Research, Providence Heart Institute & Starr Academic Center, Providence St. Vincent Hospital, Portland, Oregon, USA

Accepted for publication July 16, 2001.

* Address reprint requests to Dr He, Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Block B, 5A, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China
e-mail: gwhe{at}cuhk.edu.hk

Background. Endothelial cells derive nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF). The cytochrome P-450–monooxygenase metabolites of arachidonic acid (epoxyeicosatrienoic acids [EETs]) have been suggested to be EDHF. This study was designed to examine the effect of EET11,12 with regard to the possibility of restoring EDHF function when added into hyperkalemic cardioplegic solution.

Methods. Porcine coronary microartery rings were studied in a myograph. In groups 1 and 2, paired arteries were incubated in either hyperkalemic solution (K+ 20 mmol/L) or Krebs’ solution (control). In group 3, the paired arteries were incubated in hyperkalemia plus EET11,12 (1 x 10-6.5 mol/L) or hyperkalemia alone (control) at 37°C for 1 hour, followed by Krebs’ washout and then precontracted with 1 x 10-8.5 mol/L U46619. The EDHF-mediated relaxation to EET11,12 (group 1) or bradykinin (groups 2 and 3) was studied in the presence of NG-nitro-L-arginine, indomethacin, and oxyhemoglobin.

Results. After exposure to hyperkalemia, the EDHF-mediated maximal relaxation by bradykinin (72.5% ± 7.8% versus 41.6% ± 10.6%; p < 0.05), but not by EET11,12 (18.4% ± 3.3% versus 25.1% ± 4.9%; p > 0.05) was significantly reduced. Incubation with EET11,12 partially restored EDHF function (33.3% ± 9.5% versus 62.0% ± 8.5%; p < 0.05).

Conclusions. In coronary microarteries, hyperkalemia impairs EDHF-mediated relaxation, and EET11,12 may partially mimic the EDHF function. Addition of EET11,12 into cardioplegic solution may partially restore EDHF-mediated function reduced by exposure to hyperkalemia.




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