The Effect of Adenosine A1 Receptor Antagonism on Return of Spontaneous Circulation andShort-Term Survival in Prolonged Ventricular Fibrillation

Background. Endogenous adenosine (ADO) is cardioprotective during ischemia andits myocardial concentration increases during untreated ventricular fibrillation (VF). We have previously shown that ADO A1 receptor (ADOA1R) antagonism hastens the time-dependent decay in VF waveform morphology during the circulatory phase of cardiac arrest. Objective. To determine the effect of ADOA1R antagonism on ROSC andshort-term survival in prolonged VF. Methods. Thirty-six swine were assigned by block randomization to one of three groups: a group that received only vehicle (control), an ADOA1R antagonist pretreatment group (pre), anda group that was given ADOA1R antagonist during resuscitation (during). The animals were instrumented under anesthesia, andADOA1R antagonist or vehicle, per group assignment, was infused 5 minutes prior to VF induction. At minute 8 of untreated VF, chest compression with ventilation was initiated anda standard drug cocktail, with ADOA1R antagonist or vehicle, was given. The first rescue shock (150 J biphasic) was delivered after 11 minutes of VF. Proportions with 95% confidence intervals (CIs) were calculated for the two outcome measures. Results. The baseline characteristics andchemistry values for the three groups were mathematically the same. The during group had a greater proportion of female animals (seven of 12) in comparison with the control group (two of 12) (p = 0.03). ADOA1R antagonism hastened the decay of VF as previously demonstrated, but the rate of ROSC was the same for all groups: control = seven of 12, pre = six of 12, andduring = seven of 12. There were also no differences in short-term survival: control = four of 12, pre = five of 12, andduring = seven of 12. Conclusions. In this study, ADOA1R antagonism had no effect on outcome whether given before induction of VF or upon resuscitation after 8 minutes of untreated VF. The role of endogenous ADO in prolonged VF remains unclear.

[1]  C. Callaway,et al.  Adenosine A1 receptor antagonism hastens the decay in ventricular fibrillation waveform morphology during porcine cardiac arrest. , 2006, Resuscitation.

[2]  A. Voors,et al.  Neovascularisation after erythropoietin treatment in heart failure is associated with increased myocardial homing and vascular incorporation of endothelial progenitor cells , 2006 .

[3]  C. Callaway,et al.  Abstract 1780: Sex Differences Exist in Porcine Ventricular Fibrillation Morphology , 2006 .

[4]  D. Beiser,et al.  Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation* , 2006, Critical care medicine.

[5]  T. Aufderheide,et al.  Effect of an inspiratory impedance threshold device on hemodynamics during conventional manual cardiopulmonary resuscitation. , 2005, Resuscitation.

[6]  T. Aufderheide,et al.  Clinical evaluation of an inspiratory impedance threshold device during standard cardiopulmonary resuscitation in patients with out-of-hospital cardiac arrest* , 2005, Critical care medicine.

[7]  Henry E. Wang,et al.  Ventricular Fibrillation Scaling Exponent Can Guide Timing of Defibrillation and Other Therapies , 2004, Circulation.

[8]  Henry E. Wang,et al.  Immediate defibrillation versus interventions first in a swine model of prolonged ventricular fibrillation. , 2003, Resuscitation.

[9]  Nremt-P,et al.  Dynamic nature of electrocardiographic waveform predicts rescue shock outcome in porcine ventricular fibrillation. , 2003, Annals of emergency medicine.

[10]  W. Voelckel,et al.  Vasopressor Response in a Porcine Model of Hypothermic Cardiac Arrest Is Improved with Active Compression-Decompression Cardiopulmonary Resuscitation Using the Inspiratory Impedance Threshold Valve , 2002, Anesthesia and analgesia.

[11]  W. Voelckel,et al.  Improving Standard Cardiopulmonary Resuscitation with an Inspiratory Impedance Threshold Valve in a Porcine Model of Cardiac Arrest , 2001, Anesthesia and analgesia.

[12]  C. Callaway,et al.  Effects of biphasic vs monophasic defibrillation on the scaling exponent in a swine model of prolonged ventricular fibrillation. , 2001, Academic emergency medicine : official journal of the Society for Academic Emergency Medicine.

[13]  Vincent N. Mosesso,et al.  Scaling Exponent Predicts Defibrillation Success for Out-of-Hospital Ventricular Fibrillation Cardiac Arrest , 2001, Circulation.

[14]  C. Callaway,et al.  Ventricular fibrillation exhibits dynamical properties and self-similarity. , 2000, Resuscitation.

[15]  K. Lurie,et al.  Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest. , 2000, Circulation.

[16]  C. Callaway,et al.  Scaling Structure of Electrocardiographic Waveform During Prolonged Ventricular Fibrillation in Swine , 2000, Pacing and clinical electrophysiology : PACE.

[17]  K. Lurie,et al.  Improving Active Compression-Decompression Cardiopulmonary Resuscitation With an Inspiratory Impedance Valve , 1995 .

[18]  B. Lerman,et al.  Metabolic determinants of defibrillation. Role of adenosine. , 1995, Circulation.

[19]  L. Belardinelli,et al.  Role of endogenous adenosine in postdefibrillation bradyarrhythmia and hemodynamic depression. , 1989, Circulation.

[20]  R. Berne,et al.  The cardiac effects of adenosine. , 1989, Progress in cardiovascular diseases.

[21]  W. Giles,et al.  Ionic mechanisms of adenosine actions in pacemaker cells from rabbit heart. , 1988, The Journal of physiology.

[22]  T. Higuchi Approach to an irregular time series on the basis of the fractal theory , 1988 .

[23]  J. Dobson Adenosine reduces catecholamine contractile responses in oxygenated and hypoxic atria. , 1983, The American journal of physiology.

[24]  G. Isenberg,et al.  Isolated atrial myocytes: adenosine and acetylcholine increase potassium conductance. , 1983, The American journal of physiology.

[25]  G. Baumann,et al.  Adenosine as inhibitor of myocardial effects of catecholamines , 1977, Pflügers Archiv.

[26]  R. Berne,et al.  Effect of Ischemia on Adenine Nucleotides in Cardiac and Skeletal Muscle , 1964, Circulation research.

[27]  R. Berne Cardiac nucleotides in hypoxia: possible role in regulation of coronary blood flow. , 1963, The American journal of physiology.

[28]  Margaret Hsieh,et al.  Angular velocity: a new method to improve prediction of ventricular fibrillation duration. , 2004, Resuscitation.

[29]  T. Aufderheide,et al.  Use of an Inspiratory Impedance Valve Improves Neurologically Intact Survival in a Porcine Model of Ventricular Fibrillation , 2002, Circulation.