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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，低钙心肌保护液有利于减轻冷挛缩损伤
OBJECTIVE: To establish a cold contracture model to investigate the relationship between heart function and immature myocardial calcium in cold contracture. Methods: Thirty New Zealand rabbits (3-4 weeks) were randomly divided into three groups: group Ⅰ: control group (n = 10); group Ⅱ: cold contracture group (n = 10); Group Ⅲ: cold contracture + low calcium cardioplegia group (n = 10). The ischemia / reperfusion resuscitation was performed in vitro. The changes of cardiac function (CO, LVSP, LVEDP, ± dp / dt), malondialdehyde (MDA) and oxygen radical scavenger superoxide dismutase Enzyme (SOD), calcium content in myocardial tissue after ischemia, myocardial ultrastructure after ischemia. Results: After revascularization of isolated heart, cardiac function recovered and ultrastructure of ischemic postischemic ultrastructure was better than that of group Ⅱ in group Ⅰ, Ⅲ. The SOD level of group Ⅰ and Ⅲ was always higher than that of group Ⅱ (P <0.05 ), While the content of calcium in myocardial tissue of group Ⅱ and ischemia group was higher than that of group Ⅰ and Ⅲ (P <0.05). CONCLUSION: Cold perfusion can cause cold contracture in immature myocardium, and adversely affect cardiac function recovery after ischemia. Cardiac calcium overload and oxygen free radical are important factors that cause cold contracture injury in myocardium. Low calcium cardioplegic solution is beneficial to relieve cold contracture damage