Preservation of Myocardial High-Energy Phosphates with Vagal Stimulation and Hypothermic Cardioplegia

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We examined three methods of inducing hypothermic cardioplegic arrest and related each to preservation of high-energy phosphates. Levels of adenosine triphosphate (ATP) and creatine phosphate (CP) in baseline rat hearts were compared with levels found after (1) vagal stimulation combined with cardioplegia containing 15 mEq of potassium chloride (KCl) per liter, (2) cardioplegia with 15 mEq of KCl per liter alone, and (3) cardioplegia with 30 mEq of KCl per liter alone. Vagal stimulation produced complete electromechanical arrest in a shorter time than either 15 or 30 mEq of KCl alone ( p < 0.001 for both cardioplegic solutions compared with vagal stimulation), with fewer ventricular beats after ischemia than cardioplegic solution containing 15 or 30 mEq of KCl ( p < 0.001 and < 0.01, respectively). Levels of ATP and CP, although less than baseline levels ( p < 0.01 and < 0.001, respectively), were greater with vagal stimulation than with either 15 or 30 mEq of KCl ( p < 0.001 and < 0.05, respectively, for ATP and p < 0.001 for both CP levels). Furthermore, when all groups were combined, ATP and CP levels were found to correlate negatively with arrest time ( r = -0.851 and -0.788, respectively; both r values significant at p < 0.01) and with the number of ventricular beats after ischemia ( r = -0.927 and -0.851, respectively; both r values significant at p < 0.01). We conclude that electromechanical work quantified as time to arrest after aortic cross-clamping and as number of ventricular beats after ischemia correlates negatively with ATP and CP levels. Vagal stimulation combined with hypothermic crystalloid cardioplegia reduces the amount of ischemic electromechanical work the heart undergoes prior to arrest, thereby resulting in preservation of myocardial high-energy phosphates.