Amelioration of the effects of ischemic cardiac arrest by the intracoronary administration of cardioplegic solutions.
Interruption of coronary flow during cardiac surgical procedures provides a bloodless flaccid heart and allows precise and rapid correction of complex cardiac defects. However, myocardial damage occurs in direct proportion to the duration of the ischemia. As the induction of cardioplegia simulataneous with the initiation of cardiac ischemia helps to preserve cardiac energy reserves and thus myocardial integrity, the identification of a consistently reliable cardioplegic technique is desirable. Isolated perfused working rat hearts were made ischemic for one hour by aortic cross-clamping and were compared with hearts rendered cardioplegic at the onset of ischemia by the intracoronary administration of 5 ml of a hypothermic solution: 1) Krebs-Henseleit buffer, 2) Ringer's lactate, 3) tetrodotoxin, 4) potassium chloride, or 5) potassium citrate. Cardiac output, heart rate, aortic pressure and coronary flow were determined pre and post-ischemia. When compared to time-matched controls and hearts arrested with potassium or tetrodotoxin, the ischemia and ischemia-Ringer's lactate groups showed significant post cross-clamp depression of all measured parameters. Intracoronary Ringer's lactate, although often used as an adjunct to ischemic arrest, was not of significant value. In contrast, hearts arrested with tetrodotoxin, potassium chloride or potassium citrate showed no significant post-ischemic functional or histologic deficit. Perfusion with hypothermic Krebs-Henseleit buffer protected the myocardium better than did Ringer's lactate but less well than the tetrodotoxin or isotonic high potassium solutions. The induction of hypothermic metabolic arrest of the heart by briefly perfusing the coronary arteries via the aortic root with isotonic buffered solutions results in markedly improved myocardial tolerance to one hour of ischemia and avoids the problems of low cardiac output and ventricular irritability previously reported with hypertonic potassium citrate arrest.
D000818:Animals; D002302:Cardiac Output; D002315:Cardiopulmonary Bypass; D002951:Citrates / Q000008:administration & dosage*; D003326:Coronary Circulation; D003327:Coronary Disease / Q000517:prevention & control*; D003331:Coronary Vessels; D006323:Heart Arrest / Q000139:chemically induced*; D006339:Heart Rate; D006982:Hypertonic Solutions; D007552:Isotonic Solutions; D009200:Myocardial Contraction / Q000187:drug effects; D010477:Perfusion; D011188:Potassium / Q000008:administration & dosage*; D011189:Potassium Chloride / Q000008:administration & dosage*; D051381:Rats; D013779:Tetrodotoxin / Q000008:administration & dosage*
D002951:Citrates; D006982:Hypertonic Solutions; D007552:Isotonic Solutions; D013779:Tetrodotoxin; D011189:Potassium Chloride; D011188:Potassium