Hashimoto K, Hahimoto K [corrected to Hashimoto K ], Mashburn J P, Cartier R, Schaff H V
Division of Thoracic and Cardiovascular Surgery, Mayo Clinic, Rochester, Minnesota.
Jpn Circ J. 1993 Mar;57(3):237-44. doi: 10.1253/jcj.57.237.
Maximum deactivation of the contractile elements using Ca2+ minimizes oxygen requirements during global ischemia, Ca2+ antagonists and Ca(2+)-free cardioplegia solutions are methods by which the Ca2+ flux can be manipulated. This study was performed with 5 experimental groups: 1) Standard cardioplegia (with Ca2+), 2) Ca(2+)-free cardioplegia, 3) Ca(2+)-free cardioplegia plus verapamil (0.5 mg/L), 4) Verapamil cardioplegia (with Ca2+), and 5) Ca(2+)-free cardioplegia, in which verapamil was administered at the onset of reperfusion (0.5 mg/L). Cardiac functions, heart rate, edema formation, and creatine kinase concentration were measured before and after 70 min of ischemia at a myocardial temperature of 20 degrees C. Ca(2+)-free cardioplegia may be beneficial under hypothermic conditions, but the "Ca2+ paradox" was still a matter of concern. Reperfusion with verapamil did not protect from reperfusion-related injuries. However, the use of verapamil provided more protection than did standard or Ca(2+)-free cardioplegic solutions. Since verapamil did not maintain membrane integrity during ischemia when combined with Ca(2+)-free cardioplegic solutions (prominent edema formation was observed), its combination with Ca(2+)-containing cardioplegic solutions is recommended.
