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Ann Thorac Surg 1998;66:1658-1661
© 1998 The Society of Thoracic Surgeons

Protective action of 17ß-estradiol in cardiac cells: implications for hyperkalemic cardioplegia

^a Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic and Foundation, Rochester, Minnesota, USA

Accepted for publication May 22, 1998.

Address reprint requests to Dr Terzic, Division of Cardiovascular Diseases, Department of Medicine, Guggenheim-7F, Mayo Clinic and Foundation, Rochester, MN 55905

Background. Hyperkalemic cardioplegic solutions effectively arrest the heart, but may also induce intracellular Ca²⁺ loading and cellular hypercontracture, which could contribute to ventricular dysfunction associated with global surgical ischemia. Recently, it has been proposed that 17ß-estradiol may possess protective properties in the ischemic myocardium. The purpose of the present study was to examine the action of 17ß-estradiol on cardiac cells exposed to hyperkalemic stress.

Methods. Single ventricular cardiomyocytes, a preparation devoid of vascular and neuronal elements, were isolated from guinea pig hearts, loaded with a Ca²⁺-sensitive fluorescent probe, and imaged by digital epifluorescent microscopy. The emitted fluorescence of the probe, a measure of intracellular Ca²⁺ concentration, and cell length were simultaneously recorded during hyperkalemic challenge, in the absence or presence of 17ß-estradiol.

Results. In control cardiomyocytes, the cytosolic concentration of Ca²⁺ was 138 ± 11 nmol/L and cell length 93 ± 11 µm. Exposure to high K⁺ (+16 mmol/L KCl) significantly increased cytosolic Ca²⁺ to 2,191 ± 187 nmol/L (p < 0.001), and produced cell shortening (length at 39 ± 5 µm; p < 0.001). 17ß-Estradiol (10 µmol/L) acutely prevented high K⁺ to induce either intracellular Ca²⁺ loading (144 ± 13 nmol/L, p < 0.001) or hypercontracture (91 ± 10 µm, p < 0.001). Tamoxifen (10 µmol/L), an antiestrogen, abolished the protective effect of 17ß-estradiol.

Conclusions. We conclude that 17ß-estradiol prevents hyperkalemia-induced Ca²⁺ loading and hypercontracture through a direct and tamoxifen-sensitive action in cardiomyocytes. This study raises the possibility that 17ß-estradiol should be considered as a cardioprotective adjunct toward a safer hyperkalemic cardioplegia.

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