title: Evidence of functional myocardial ischemia associated with myocardial dysfunction in brain-dead pigs.
abstract: BACKGROUND
  Cardiac dysfunction after brain death has been documented, but its mechanisms remain unclear. Myocardial ischemia has been suggested as a possible cause. The aim of the present study was to investigate the existence of an imbalance between myocardial oxygen delivery and demand as a possible cause of myocardial dysfunction in brain-dead pigs.
  
  
  RESULTS
  Interstitial myocardial lactate and adenosine concentrations were assessed with cardiac microdialysis in 2 groups of animals: brain-dead pigs (n=7) and brain-dead pigs treated with labetalol (10+/-3 mg/kg) (n=7). Heart rate (HR), left ventricular (LV) dP/dt(max), rate-pressure product (RPP), cardiac output (CO), and left anterior descending coronary artery blood flow (QLAD) were continuously monitored. Brain-dead pigs exhibited a transient significant increase in HR, LV dP/dt(max), RPP, and CO and a limited increase in QLAD. This resulted in functional myocardial ischemia attested to by the significantly increased adenosine and lactate microdialysate concentrations. In brain-dead pigs treated with labetalol, there was a moderate increase in HR, QLAD, and adenosine microdialysate concentrations; LV dP/dt(max), RPP, CO, and myocardial lactate concentrations remained stable, confirming the preservation of aerobic metabolism.
  
  
  CONCLUSIONS
  Brain death was associated with an increase in myocardial interstitial adenosine and lactate concentrations, as well as with myocardial dysfunction; all were attenuated by labetalol, suggesting an imbalance between oxygen consumption and oxygen delivery as a possible cause of myocardial dysfunction after brain death.
authors.affiliation: Laboratoire de Chirurgie Expérimentale, Faculté de Médecine de Nancy, Université Henri Poincaré, Nancy I, France.
authors.forename: C
authors.initials: C
authors.lastname: Seguin
authors.forename: Y
authors.initials: Y
authors.lastname: Devaux
authors.forename: S
authors.initials: S
authors.lastname: Grosjean
authors.forename: E M
authors.initials: EM
authors.lastname: Siaghy
authors.forename: P
authors.initials: P
authors.lastname: Mairose
authors.forename: F
authors.initials: F
authors.lastname: Zannad
authors.forename: N
authors.initials: N
authors.lastname: de Talancé
authors.forename: D
authors.initials: D
authors.lastname: Ungureanu-Longrois
authors.forename: P M
authors.initials: PM
authors.lastname: Mertes
mesh_terms: D000241:Adenosine / Q000378:metabolism; D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects; D001784:Blood Gas Analysis; D001794:Blood Pressure; D001926:Brain Death / Q000503:physiopathology*; D002302:Cardiac Output / Q000187:drug effects; D009202:Cardiomyopathies / Q000150:complications / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D007741:Labetalol / Q000494:pharmacology; D019344:Lactic Acid / Q000378:metabolism; D017551:Microdialysis; D017202:Myocardial Ischemia / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption; D013552:Swine; D013565:Sympatholytics / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D013565:Sympatholytics; D019344:Lactic Acid; D000241:Adenosine; D007741:Labetalol; D010100:Oxygen