The mechanism of myocardial damage following potassium citrate (Melrose) cardioplegia.

摘要: To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable 2-1/2 hours. After 1/2 hour work, 42 experimental subjected to 1 ischemis by aortic cross-clamping with unmodified ischemia eight and simultaneous intracoronary injection 5 ml. 4 degrees C. (1)Krebs-Henseleit buffer seven (2)potassium chloride six hearts, (3)potassium citrate (both 26 mEq. per liter K, approximately 300 mOsm. liter), (4)Melrose solution (greater than 200 greater 400 (5)hypertonic (26 liter). The pH all solutions 7.8 plus or minus 0.1. recovery isotonic citrate- chloride-arrested time-matched showed no significant differences cardiac output, coronary flow, systolic pressure, heart rate. Hypertonic decreased function after not significantly different from ischemia. Intracoronary cold Krebs-Henseleit better but inferior er arrest. Arrest augments perfusion hypothermia prevents functional histologic myocardial damage during ischemis. Previous authors assumed that hypertonicity responsible poor results high concentration is major deleterious factor playing a contributory role.