不同浓度2,3-丁二酮单肟初始复灌对停搏心脏的保护作用

The effects of initial reperfusion with different concentration of 2,3-butanedione monoxime on hearts following cardioplegic arrest

目的研究不同浓度的2,3-丁二酮单肟(BDM)初始复灌对停搏心脏机械功能和氧代谢恢复的影响,确定理想作用浓度并初步探讨其机制。方法48只Langendorff灌流豚鼠心脏用4℃St.Thomas Hospital液保存12h,随机分为4组,分别以37℃改良Krebs-Ringer液(CON组),含20mmol/L BDM的Krebs液(BDM20组)、含30mmol/L BDM的Krebs液(BDM30组)、含40mmol/L BDM的Krebs液(BDM40组)进行初始复灌30min,随后所有心脏以37℃改良Krebs-Ringer液进行复灌60min。结果与CON组比较,BDM初始灌流后左室作用压、左室压力增加速率峰值(dP/dtmax)和左室压力减少速率峰值(-dP/dtmax)、氧消耗速度和用氧效率恢复更为迅速,BDM30组最为显著。电镜检查发现,CON组心肌呈明显的肌节过度收缩和线粒体破坏,BDM30组则明显减轻。结论BDM初始灌流可显著改善停搏心肌的机械功能和氧代谢,且理想作用浓度为30mmol/L,其机制可能与BDM减轻缺血-再灌注引起的心肌过度收缩和细胞破坏有关。

Objective To evaluate the effects of initial reperfusion with different concentration of 2,3 butanedione monoxime （BDM） on the mechanical function and oxygen metabolism in hearts following cold cardioplegic arrest. Methods 48 Langendorff perfused guinea pig hearts were subjected to 12 h of cardioplegie arrest in 4℃ St. Thomas Hospital solution. Control group（CON group, n=12） were reperfused with a modified Krebs-Ringer solution for 30 rain immediately. Hearts in BDM20 group, BDM30 group and BDM 40 group （n=12,each） were initial reperfused with Krebs solution at 37℃ which contained 20 mmol/L,30 mmol/L and 40 mmol/L BDM, respectively, for 30 min. Then the perfusate in all groups were switched to the modified Krebs-Ringer solution for 60 min. Results Compared to CON group, initial reperfusion with BDM enhanced the recovery of left ventricular developed pressure, dPn=dtmax and - dPn=dtmax and alleviate oxygen consumption and cardiac efficacy in utilizing consumed oxygen. The most markedly effect was observed in BDM30 group. Myocardial ultrastructure was best preserved in hearts of BDM30 group too. Condusion Initial BDM reperfusion were superior to immediate Krebs-Ringer＇reperfusion in preserving myocardial mechanical function. 30 mmol/L of BDM was the optimal concentration, comparing with either 20 mmol/L or 40 mmol/L. The underlying mechanism of protecting effect of BDM may be its alleviation of myocardial hypercontracture and ultrastructure damage induced by reperfusion injury.