免疫缺陷裸鼠无创性心肌缺血缺氧损伤模型的构建

目的：通过对免疫缺陷裸小鼠腹腔注射异丙肾上腺素，构建一种无创性裸小鼠的心肌缺血缺氧损伤模型。方法：16只免疫缺陷裸小鼠随机分为3组：对照组5只，实验A组7只，实验B组4只，其中实验A、B组连续3d重复腹腔注射5mg／kg异丙肾上腺素，对照组则注射等量生理盐水。对照组和实验A组于第3次注射后24h处死，实验B组则于第3次注射后2周处死。各组裸小鼠处死前取血清进行心肌酶检测，心脏标本称重，常规HE染色。结果：实验A组、B组、对照组的心脏质量分别为（94．97±6．12）mg、（79．35±7．63）mg、（81．38±10．11）mg，A组相对于B组、对照组，差异均具有统计学意义（P〈0．01）。HE染色显示A组局部心肌组织损伤与变性坏死，而B组病变程度明显较轻，未见斑痕形成。实验A组、B组、对照组的乳酸脱氢酶（LDH）分别为（6662．70±884．78）U／L、（4096．75±448．75）U／L、（4419．40±880．50）U／L，A组相对于B组、对照组，差异均具有统计学意义（P〈0．01）。结论：腹腔反复大剂量注射异丙肾上腺素可构建免疫力缺陷裸小鼠的心肌缺血缺氧损伤模型。

Construction of Noninvasive Myocardial Ischemia and Hypoxia Model in Immunodeficient Athymic Mice

Objective： To construct models of noninvasive myocardial ischemia and hypoxia in immunodeficient athymic mice through intra-abdominal injection of isoprenaline. Methods： Sixteen athymie mice were randomly divided into 3 groups： experimental group A （EGA, n=7）. experimental group B （EGB, n=4） and control group （CG, n=5）. The experimental group A and B received repeated intra-abdominal injections of isoprenaline （5 mg/kg） for 3 consecutive days, whereas the control group was given normal saline. Athymie mice in EGA and CC were sacrificed 24 hours after the last injecting and EGB were killed 2 weeks later. Serum samples were obtained from each mouse before sacrifice to be assessed for lactate dehydrogenase （LDH）, and the hearts were weighed and subjected to pathological study with routine HE staining. Results： The heart weights in EGA, EGB and CG were （94.97±6.12） mg, （79.35±7.63） mg and （81.38± 10.11） mg, respectively, The heart weight in EGA differed significantly from that in EGB or CG （P〈0.01）. HE stained histology showed local degeneration, necrosyeis and damage of cardiac muscles in EGA, which was present but obviously milder in EGB. No scarring was seen in EGA or EGB. The levels of LDH in EGA, EGB and CG were （6 662.70±884.78） U/L, （4 096.75±448.75） U/L and （4 419.40±880.50） U/L, respectively （P〈0.01）. Conclusion： Repeated injection of large dose intra-abdominal isoprenaline can be used to construct noninvasive myocardial ischemia and hypoxia model in immunodeficiency athymic mice.