title: Protective effect of magnesium on the endothelial function mediated by endothelium-derived hyperpolarizing factor in coronary arteries during cardioplegic arrest in a porcine model.
abstract: OBJECTIVE
  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 microm) 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 degrees 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 U(46619)-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.
authors.affiliation: Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Yang
authors.forename: Yao-Chung
authors.initials: YC
authors.lastname: Liu
authors.forename: Wei
authors.initials: W
authors.lastname: Zou
authors.forename: Anthony P C
authors.initials: AP
authors.lastname: Yim
authors.forename: Guo-Wei
authors.initials: GW
authors.lastname: He
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001685:Biological Factors / Q000502:physiology*; D002314:Cardioplegic Solutions / Q000494:pharmacology*; D003331:Coronary Vessels / Q000187:drug effects*; D004594:Electrophysiology; D004730:Endothelium, Vascular / Q000502:physiology*; D006324:Heart Arrest, Induced / Q000379:methods*; D008274:Magnesium / Q000494:pharmacology*; D008564:Membrane Potentials / Q000502:physiology; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D011188:Potassium / Q000494:pharmacology; D013552:Swine
chemical_list: D001685:Biological Factors; D002314:Cardioplegic Solutions; C067410:endothelium-dependent hyperpolarization factor; D008274:Magnesium; D011188:Potassium