title: The role of magnesium in the endothelial dysfunction caused by global ischemia followed by reperfusion: in vitro study of canine coronary arteries.
abstract: OBJECTIVE
  To study the role of magnesium in the endothelial dysfunction of canine coronary arteries caused by cardiopulmonary bypass (CPB) global ischemia followed by reperfusion.
  
  
  METHODS
  Segments of canine coronary arteries were suspended in organ chambers to measure isometric contraction by prostaglandin F (2alpha), and relaxed by acetylcholine (ACh), sodium fluoride (NaF), calcium ionophore (A23187) and sodium nitroprusside (SNP) in crescent concentrations. The investigation protocol had groups with six dogs: CONTROL group (without CPB), CPB group (105 min of CPB without aortic cross-clamping), ISCH group (45 min of CPB with aortic cross-clamping), ISCH/REP group (45 min of aortic cross-clamping followed by 60 min of reperfusion). The coronary relaxations were evaluated with (phase I), without (phase II) and restored magnesium (phase III) to the organ bath.
  
  
  RESULTS
  The presence of magnesium in the organ bath was associated with the greater relaxation in response to agonists of the nitric oxide production. The removal of magnesium from the organ bath was associated with the reduction in the intensity of vessel relaxation. The magnesium restoration to the organ bath was associated with the additional reduction in the intensity of relaxation with the exception of NaF that allowed re-acquisition of the relaxation observed in the presence of magnesium.
  
  
  CONCLUSIONS
  This in vitro study demonstrates that magnesium ion favorably influences the nitric oxide production by the coronary endothelium, attenuating the endothelial dysfunction caused by global ischemia followed by reperfusion.
authors.affiliation: Endothelium Laboratory, Division of Experimental Surgery, Department of Surgery and Anatomy, Faculdade de Medicina de Ribeirão Preto, USP, Brazil.
authors.forename: Marco A
authors.initials: MA
authors.lastname: Volpe
authors.forename: João J
authors.initials: JJ
authors.lastname: Carneiro
authors.forename: Luís Alberto
authors.initials: LA
authors.lastname: Magna
authors.forename: Fernanda
authors.initials: F
authors.lastname: Viaro
authors.forename: Eliana Aparecida L
authors.initials: EA
authors.lastname: Origuela
authors.forename: Paulo R B
authors.initials: PR
authors.lastname: Evora
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002315:Cardiopulmonary Bypass; D003331:Coronary Vessels / Q000378:metabolism*; D015237:Dinoprost / Q000494:pharmacology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D019204:GTP-Binding Proteins; D066298:In Vitro Techniques; D008274:Magnesium / Q000502:physiology* / Q000627:therapeutic use; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D015425:Myocardial Reperfusion; D009569:Nitric Oxide / Q000096:biosynthesis; D009599:Nitroprusside / Q000494:pharmacology; D015398:Signal Transduction / Q000502:physiology; D012969:Sodium Fluoride / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D009599:Nitroprusside; D009569:Nitric Oxide; D000001:Calcimycin; D012969:Sodium Fluoride; D015237:Dinoprost; D019204:GTP-Binding Proteins; D008274:Magnesium; D000109:Acetylcholine