Effects of warm blood cardioplegic solution on myocardial protection.
To evaluate the effects of warm blood cardioplegic solution on myocardial protection, normothermic induction and terminal perfusion of oxygenated blood cardioplegia in combination with intermittent administration of cold blood cardioplegia during ischemia were studied in an isolated working rat heart model. The experimental protocol consisted of a 120 min cardioplegic arrest followed by 45 min normothermic reperfusion. Myocardial content of adenosine triphosphate (ATP), recovery of the left ventricular function, release of creatine phosphokinase (CPK) and ultrastructure of myocardium were assessed before and after ischemia. The results showed that the hearts preserved with warm blood cardioplegic induction and terminal perfusion had significantly higher levels of ATP, better recovery of cardiac function and lower releases and lower releases of CPK than those receiving cold blood cardioplegia alone, with myocardial tissue being of generally normal structure. These findings suggest that warm induction and terminal perfusion of blood cardioplegic solution can accelerate myocardial metabolic and functional recovery, preserve high-energy phosphate, reduce myocardial injury and enhance myocardial protection.
Du
X L
XL
Institute of Cardiovascular Diseases, Tongji Medical University, Wuhan.
Lan
H J
HJ
Sun
Z Q
ZQ
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001769:Blood; D002314:Cardioplegic Solutions; D003402:Creatine Kinase / Q000378:metabolism; D006324:Heart Arrest, Induced / Q000379:methods; D066298:In Vitro Techniques; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013696:Temperature; D016277:Ventricular Function, Left
D002314:Cardioplegic Solutions; D000255:Adenosine Triphosphate; D003402:Creatine Kinase