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Ann Thorac Surg 1994;58:351-358
© 1994 The Society of Thoracic Surgeons
Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama USA
* Address reprint request to Dr Holman, Department of Surgery. University of Alabama at Birmingham, University Stalion, Birmingham, AL 35294.
This study compared myocardial blood flow during postcardioplegia reperfusion asystole and ventricular fibrillation. Pigs (n = 20) were placed on cardiopulmonaiy bypass and blood cardioplegic solution at 38°C was then infused, A preischemia microsphere injection was given in asystolic hearts. All animals then had 1 hour of hypothermie cardioplegic arrest and underwent reperfusion with high-dose (n = 10) or low-dose (n = 10) 38°C blood cardioplegia. At 30 seconds after reperfusion, all hearts were asystolic. The second microsphere injection was then given. At 3 and 6 minutes after leperfusion, the animals' hearts were either in asystole (n = 10) or ventricular fibrillation (n = 10), and the third and fourth microsphere injections were then given. At 10 minutes after reperfusion, all hearts were beating and the final (fifth) microsphere injection was given. There was an initial increase in the global myocardiat blood flow during reperfusion versus the prcischemic control value. However, later, during reperfusion (ie, at the third and fourth injections), there was a significant (p < 0,05) decrease in the global myocardial blood flow. There was no discernible response in either the global myocardial blood flow or regional myocardial blood flow distribution to electromechanical activity (ie, ventricular fibrillation) for the third and fourth injections, suggesting that coronary autoregulation was abnormal. Postcardioplegia reperfusion ventricular fibrillation imposes metabolic demands that may cause reperfusion injury, especially in hearts affected by hypertrophy, ventricular distention, or coronary obstruction.
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