Left ventricular myocardial adenosine triphosphate changes during reperfusion of ventricular fibrillation: the influence of flow and epinephrine.
OBJECTIVE
To determine whether epinephrine in combination with high flow worsens left ventricular (LV) myocardial high-energy phosphate stores during reperfusion of ischemic ventricular fibrillation (VF).


METHODS
Blinded, prospective block randomized, placebo controlled study.


METHODS
University medical center research laboratory.


METHODS
A total of 22 mixed breed swine weighing 22.0+/-3.3 kg (SD).


METHODS
Open-chest swine, anesthetized with alpha-chloralose, underwent 10 mins of nonperfused VF followed by reperfusion with cardiopulmonary bypass for 90 mins and then defibrillation. Animals were block randomized to four groups for reperfusion: Group 1 (n = 5), high flow (100 mL/kg/min) and epinephrine (2.5 microg/kg/min); Group 2 (n = 5), high flow and placebo; Group 3 (n = 6), low flow (30 mL/kg/min) and epinephrine; and Group 4 (n = 6), low flow and placebo.


RESULTS
In vivo LV creatine phosphate (CP) and adenosine triphosphate (ATP) were determined using whole wall and spatially localized 31P NMR spectroscopy at 4.7 Tesla. During perfusion of the fibrillating myocardium, epinephrine significantly increased aortic pressure (p < .05) and improved defibrillation rates (p < .01). ATP levels during reperfusion were significantly decreased within all groups compared with baseline. There were no differences in ATP levels between groups. High flow, independent of epinephrine, was associated with increased preservation of ATP (p < .05), increased CP/ATP ratios (p < .02) in all layers of the LV wall, and decreased aortic and cardiac vein lactates (p < .001).


CONCLUSIONS
Epinephrine, in combination with flow higher than standard cardiopulmonary resuscitation flows, increased perfusion pressure and defibrillation rates, but did not significantly alter myocardial ATP during VF reperfusion in the in vivo heart Reperfusion flow, independent of epinephrine, is a critical determinant of myocardial ATP preservation.
Angelos
M G
MG
Department of Emergency Medicine, Ohio State University, Columbus 43210, USA. angelos.1@osu.edu
Torres
C A
CA
Waite
M D
MD
Rath
D P
DP
Zhu
H
H
Beckley
P D
PD
Palmer
B S
BS
Robitaille
P M
PM
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology; D004837:Epinephrine / Q000494:pharmacology*; D009682:Magnetic Resonance Spectroscopy; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D011446:Prospective Studies; D013552:Swine; D014693:Ventricular Fibrillation / Q000503:physiopathology*; D016277:Ventricular Function, Left / Q000502:physiology
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D004837:Epinephrine