Effect of coronary artery flow on left ventricular contractile dysfunction induced by brain death

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Background : Massive catecholamine release after brain death is thought to be one of the most important causes to cardiac dysfunction after heart transplantation. However, the exact mechanism for cardiac failure in brain-dead heart has not been fully elucidated. The aim of this study was to investigate the response of coronary artery to vasodilator and their contribution to hemodynamic deterioration using canine brain death model.Methods: Brain death was induced by rapid inflation of a subdurally placed balloon catheter. Hemodynamic measurements including assessment of left ventricular contractility using pressure-volume relations and biochemical analysis of blood samples was performed in 7 dogs. Coronary flow reserve was assessed by endothelium-dependent (acetylcholine ; Ach) and -independent (sodium nitroprusside ; SNP) coronary vasodilation in 8 dogs.Results: Hyperdynamic response was observed transiently after induction of brain death followed by decreases in arterial pressure, cardiac output and coronary blood flow. Left ventricular contractility was deteriorated at 60-minute after brain death. Coronary flow reserve both by Ach and SNP were significantly impaired at 30- and 60-minute after brain death (Ach 3μg 320.5 % to 189.1 % and 202.8 % ; SNP 100μg 255.6 % to 145.8 % and 153.5 %). Coronary resistance ratios were significantly increased at 30- and, 60-minute after brain death.Conclusions : Impairement of coronary flow reserve and left ventricular function was observed in brain-dead canine heart. This impaired coronary circulation could be a disadvantage of preservation and recovery of cardiac dysfunction.