title: Brain damage and myocardial dysfunction: protective effects of magnesium in the newborn pig.
abstract: BACKGROUND
  Brain damage is associated with myocardial dysfunction resulting from excessive release of endogenous catecholamines and Ca2+ overload. Magnesium ion, a natural Ca2+ blocker, has recently been recognized as a myoprotective agent.
  
  
  METHODS
  Myocardial function was assessed in 3- to 7-day-old piglets from pressure-volume data (obtained by the conductance catheter/micromanometer technique) before and for 4 hours after ligation of the aortic arch vessels and was correlated with ultrastructural changes. Group a (n = 6) received MgSO4 immediately after induction of brain damage for 4 hours, whereas group b (n = 6) did not receive MgSO4 and served as control.
  
  
  RESULTS
  In both groups after induction of brain damage, there was a significant (p < 0.05) increase in end-systolic elastance and preload-recruitable stroke work that persisted for 1 hour. However, after 2 and 4 hours, there was a significant (p < 0.05) reduction in both variables in group b (end-systolic elastance, 74% +/- 5% and 59% +/- 6%, respectively, and preload-recruitable stroke work, 77% +/- 4% and 64% +/- 3%, respectively, compared with baseline), and in group a, the values returned to baseline. The chamber stiffness index rose significantly (p < 0.05) in group b 15 minutes after induction of brain damage and remained significantly (p < 0.05) higher for 4 hours versus no significant change in group a. Plasma levels of epinephrine and norepinephrine were similar in the groups before and after brain damage. Electron microscopic study showed severe ultrastructural changes in group b and significantly milder changes in group a.
  
  
  CONCLUSIONS
  We conclude that MgSO4 may protect the neonatal myocardium when administered immediately after brain damage.
authors.affiliation: Department of Pathology, The Hospital for Sick Children, Toronto, Ontario, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Caspi
authors.forename: J G
authors.initials: JG
authors.lastname: Coles
authors.forename: L N
authors.initials: LN
authors.lastname: Benson
authors.forename: G J
authors.initials: GJ
authors.lastname: Wilson
mesh_terms: D000322:Adrenergic Agonists / Q000097:blood; D000316:Adrenergic alpha-Agonists / Q000097:blood; D000818:Animals; D000831:Animals, Newborn; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D006328:Cardiac Catheterization / Q000295:instrumentation; D002306:Cardiac Volume / Q000187:drug effects / Q000502:physiology; D004837:Epinephrine / Q000097:blood; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D008278:Magnesium Sulfate / Q000627:therapeutic use*; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000648:ultrastructure; D009638:Norepinephrine / Q000097:blood; D013318:Stroke Volume / Q000187:drug effects; D013552:Swine; D013599:Systole; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology; D017725:Ventricular Pressure / Q000187:drug effects / Q000502:physiology
chemical_list: D000322:Adrenergic Agonists; D000316:Adrenergic alpha-Agonists; D002121:Calcium Channel Blockers; D008278:Magnesium Sulfate; D002118:Calcium; D009638:Norepinephrine; D004837:Epinephrine