摘要
Direct effects of a high-dose aprotinin on the normally perfused hearts and the myocardial protection after ischemia and reperfusion were investigated in an isolated working rat heart model. In trial I, hearts had no ischemia and were perfused with either K-H solution or the K-H solution containing aprotinin (200KIU/ml) for 55 min. No statistically significant difference was observed in hemodynamics betweem the two groups. In trial Ⅱ, hearts were exposed to 150 minperiod of global ischemia at 15℃ with 4℃ multidose St. Thomas'Ⅱ solution (STS). The control group I received norma1 K-H solution; the group Ⅱ was treated with the solution with aprotinin added. The group, was similar to the group Ⅰ and received the STS enriched with aprotinin. On reperfusion, the recovery of hearts in group, was significantly better than those of the group Ⅰand Ⅱ, as reflected by better hemodynamics and myocardial oxygen consumption,lower level myocardial enzymes, higher myocardial ATP levels and milder myocardial ultrastructural injury. There was no difference between the group Ⅰand Ⅱ. These results suggest that the aprotinin at a dose of 200 KIU/ml has no harmful effects on normally perfused hearts and has a marked myocardial protective effect on the prolonged myocardial ischemia when used in cold crystalloid cardioplegia.
Direct effects of a high-dose aprotinin on the normally perfused hearts and the myocardial protection after ischemia and reperfusion were investigated in an isolated working rat heart model. In trial I, hearts had no ischemia and were perfused with either K-H solution or the K-H solution containing aprotinin (200KIU/ml) for 55 min. No statistically significant difference was observed in hemodynamics betweem the two groups. In trial Ⅱ, hearts were exposed to 150 minperiod of global ischemia at 15℃ with 4℃ multidose St. Thomas'Ⅱ solution (STS). The control group I received norma1 K-H solution; the group Ⅱ was treated with the solution with aprotinin added. The group, was similar to the group Ⅰ and received the STS enriched with aprotinin. On reperfusion, the recovery of hearts in group, was significantly better than those of the group Ⅰand Ⅱ, as reflected by better hemodynamics and myocardial oxygen consumption,lower level myocardial enzymes, higher myocardial ATP levels and milder myocardial ultrastructural injury. There was no difference between the group Ⅰand Ⅱ. These results suggest that the aprotinin at a dose of 200 KIU/ml has no harmful effects on normally perfused hearts and has a marked myocardial protective effect on the prolonged myocardial ischemia when used in cold crystalloid cardioplegia.
