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J Thorac Cardiovasc Surg 2002;124:361-370
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Protective effect of magnesium on the endothelial function mediated by endothelium-derived hyperpolarizing factor in coronary arteries during cardioplegic arrest in a porcine model

From the Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Hong Kong SAR, China,^a and Providence Heart Institute, Albert Starr Academic Center, the Department of Surgery, Oregon Health & Science University, Portland, Ore.^b

Supported in full by grants from the Research Grant Council of the Hong Kong Special Administrative Region (Projects CUHK7246/99M and CUHK4127/01M), China, and the Providence St Vincent Medical Foundation, Portland, Ore.

Received for publication July 23, 2001. Revisions requested Sept 12, 2001; revisions received Dec 20, 2001. Accepted for publication Dec 27, 2001. Address for reprints: Guo-Wei He, MD, PhD, Department of Surgery, Block B, 5A, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China (E-mail: gwhe{at}cuhk.edu.hk).

Objectives: Hyperkalemia in cardioplegia impairs the function mediated by endothelium-derived hyperpolarizing factor. This study examined the effect and mechanism of magnesium ion on the relaxation mediated by endothelium-derived hyperpolarizing factor.
Methods: In the isometric force study, porcine coronary microarteries in a myograph (diameter 200-450 µm) were incubated in Krebs solution (subgroups Ia, IIa, and IIIa), potassium ion (20 mmol/L, subgroups Ib, IIb, and IIIb), magnesium ion (16 mmol/L, subgroups Ic, IIc, and IIIc), or potassium ion plus magnesium ion (subgroups Id, IId, and IIId) for 1 hour at 37°C in group I or II, followed by washout for 45 minutes in group III (n = 8). Relaxation to bradykinin (groups I and III) or sodium nitroprusside (group II) in U₄₆₆₁₉-stimulated contraction was established. In the electrophysiologic study, the membrane potentials of single smooth muscle cells of arteries were measured by microelectrode after superfusion with the previously described solutions (subgroups IVa-IVc).
Results: In group I, 20-mmol/L potassium ion greatly reduced the bradykinin-induced relaxation (35.0% ± 4.9% vs 86.0% ± 5.3%, P < .001), which was significantly restored by magnesium ion (51.9% ± 4.0%, P = .017). In groups II and III, the bradykinin- or nitroprusside-induced relaxation had no significant differences. In group IV, potassium ion depolarized the smooth muscle and decreased the bradykinin-induced hyperpolarization (-72.0 ± 1.5 vs -61.7 ± 0.7 mV, n = 7, P < .001), which was significantly restored by magnesium ion (-68.0 ± 2.5 mV vs -72.5 ± 1.5 mV, n = 6, P = .029).
Conclusions: Magnesium ion, either alone or added to hyperkalemic solutions, preserves or helps to restore the endothelial function mediated by endothelium-derived hyperpolarizing factor. The mechanism is related to preservation of the membrane hyperpolarization and reversal of the potassium-induced membrane depolarization of the smooth muscle cell.

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