摘要
目的 :建立冷挛缩模型 ,探讨冷挛缩对未成熟心肌功能、能量代谢与超微结构的影响。方法 :在离体工作心模型基础上 ,30只新西兰幼兔 ( 3～ 4周 )随机分成三组 : 组 (对照组 ,n =10 ) , 组 (冷挛缩组 ,n =10 ) , 组 (冷挛缩 +低钙心肌保护液组 ,n =10 )。离体缺血再灌注复苏 ,测试缺血前、后心功能 ,心输出量 ,左室收缩压 ,左室舒张末压 ,最大压力变化速率 ,缺血后冠状静脉窦流出液乳酸脱氢酶 ( L DH) ,肌酸激酶 ( CK) ,心肌组织水含量 ,三磷酸腺苷 ( ATP)、二磷酸腺苷、一磷酸腺苷含量 ,电镜观察缺血后心肌超微结构。结果 :离体心缺血再灌注复苏后 ,心功能恢复、电镜观察缺血后超微结构 、 组优于 组 , 、 组 ATP含量始终高于 组 ( P <0 .0 5 ) ,而 组 L DH、CK和心肌组织水含量高于 、 组 ( P <0 .0 5 )。结论 :冷挛缩对缺血后心功能恢复和能量代谢不利 。
Objective:To establish cooling contracture model and study effects of cooling contracture on immature myocardial function,energic metabolism and structure.Method:On an isolated working heart model,thirty New Zealand rabbits(aged 3 to 4 weeks) were randomly divided into three groups:Group Ⅰ(normothermia,n=10);Group Ⅱ(cooling,n=10)and Group Ⅲ (cooling+low Ca 2+ cardioplegia,n=10).The preischemic and postischemic heart function (CO,LVSP,LVEDP,±dp/dt),postischemic LDH,CK of coronary sinus fluid,myocardial water content and ATP,ADP,AMP were measured and ultrastructure was observed.Result:The recovery of heart postischemia function;Group Ⅰ,Ⅲ better than Group Ⅱ(P< 0.05 ),myocardial ultrastructure was more excellent in GroupⅠ,Ⅲ than GroupⅡ,ATP in Group Ⅰ,Ⅲ were higher than GroupⅡ(P< 0.05 ),but LDH,CK and postischemic myocardial water content in Group Ⅱ were higher than GroupⅠ,Ⅲ (P< 0.05 )。Conclusion:Cooling contracture impairs the immature myocardial function and metabolism.Low Ca 2+ cardioplegia can decrease the trauma of cooling contracture.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
1999年第2期77-80,共4页
Journal of Clinical Cardiology
关键词
冷挛缩
未成熟心肌
心功能
能量代谢
超微结构
Immature myocardium Cooling contracture Heart function Energic metablism
