摘要
目的：建立冷挛缩模型，探讨冷挛缩中未成熟心肌钙离子与心功能的关系。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：Ⅰ组：对照组（ｎ＝１０）；Ⅱ组：冷挛缩组（ｎ＝１０）；Ⅲ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（ＣＯ，ＬＶＳＰ，ＬＶＥＤＰ，±ｄｐ／ｄｔ），冠状静脉窦流出液丙二醛（ＭＤＡ）和氧自由基清除剂超氧化物歧化酶（ＳＯＤ），缺血后心肌组织钙离子含量，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Ⅰ、Ⅲ组优于Ⅱ组，Ⅰ、Ⅲ组ＳＯＤ含量始终高于Ⅱ组（Ｐ＜０．０５），而Ⅱ组ＭＤＡ和缺血后心肌组织钙离子含量高于Ⅰ、Ⅲ组（Ｐ＜０．０５）。结论：冷灌注使未成熟心肌产生冷挛缩，对缺血后心功能恢复不利，心肌钙离子超负荷与氧自由基是造成心肌冷挛缩损伤的重要因素。
Objective: To establish the model of cooling contracture and to evaluate the relation between immature myocardial ionized calcium and cardiac function during cooling process. Methods: In 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, Ca 2+ 0.6mmol/L, n=10). The preischemic and postischemic heart function (CO, LVSP, LVEDP,±dp/dt),MDA、SOD of coronary sinus fluid, postischemic myocardium ionized calcium were measured and postischemic ultrastructure was observed. Results: The recovery of postischemic heart function in group Ⅰ、Ⅲ was better than that of group Ⅱ (P<0.05), myocardial ultra structure was more also better in group Ⅰ、Ⅲ.SOD in group Ⅰ、Ⅲ were higher than that in Group Ⅱ (P<0.05),but MDA and postischemic myocardium ionized calcium in group Ⅱ were higher than that in group Ⅰ、Ⅲ (P<0.05). Conclusion: The heart functional recovery was impaired postischemically if prolonged cold perfusion was used in working neonate heart; the myocardial ionized calcium overloading and oxygen free radical were detrimental elements during cooling contracture; low Ca 2+ cardioplegia could decrease the trauma of cooling contracture.
出处
《上海医学》
CAS
CSCD
北大核心
1998年第11期642-644,共3页
Shanghai Medical Journal
基金
国家自然科学基金
