摘要
ObjectivePrevious 研究证明组织缺氧 preconditioning 能保护心脏的功能免于随后的心肌的梗塞损害。然而,在在心肌的梗塞以后室的左的组织缺氧的效果仍然是不清楚的。这研究因此试图调查在在兔子柱子的左室的改变上训练的组织缺氧的效果心肌的 infarction.MethodsAdult 男性兔子随机被划分成三个组:那么组织(假冒操作) ,组 MI (心肌的梗塞仅仅) 并且组 MI-HT (加组织缺氧训练的心肌的梗塞) 。心肌的梗塞被左室的分支结扎导致。训练的组织缺氧在一个比重低於脑脊髓液的房间被执行(在 4000 m 的高度有相等的状况, F <sub > i </sub > 为 1 h/day 的 O <sub>2</sub>14.9%) ,为四个星期的 5 天 / 星期。在端点,在血浆的脉管的 endothelial 生长因素(VEGF ) 被测量。梗塞尺寸和毛状的密度被组织学检测。左室的改变和功能被 echocardiography.ResultsAfter 估计 4 星期的实验,与这个组相比那么,在组 MI 的血浆 VEGF 层次(130.27 ±;18.58 pg/mL, P <;0.01 ) 并且 MI-HT (181.93 ±;20.29 pg/mL, P <;0.01 ) 显著地被增加。在组 MI-HT 的梗塞尺寸(29.67%±;7.73%) 显著地被死亡,当时它的毛状的密度(816.0 ±;122.2/mm <sup>2</sup>) 显著地被增加。为组 MI 和 MI-HT,而左室的喷射部分被减少,左室的结束心脏舒张、结束收缩的尺寸被增加。与组 MI 相比,然而,组 MI-HT 减少了留给室结束心脏舒张(15.86 ±;1.09 公里, P <;0.05 ) 并且结束收缩的尺寸(12.10 ±;1.20 公里, P <;0.01 ) 显著地并且改进左室的喷射部分(54.39 ±;12.74 公里, P <;0.05 ) 训练可以改进的 .ConclusionHypoxia 让室的功能和还原剂与 MI 在兔子经由 angiogenesis 改变。
Objective Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myo-cardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infarction is still unclear. This study therefore aims to investigate the effects of hypoxia training on left ventricular remodeling in rabbits post myocardial infarction. Methods Adult male rabbits were randomly divided into three groups: group SO (sham operated), group MI (myocardial infarc-tion only) and group MI-HT (myocardial infarction plus hypoxia training). Myocardial infarction was induced by left ventricular branch ligation. Hypoxia training was performed in a hypobaric chamber (having equivalent condition at an altitude of 4000 m, FiO214.9%) for 1 h/day, 5 days/week for four weeks. At the endpoints, vascular endothelial growth factor (VEGF) in the plasma was measured. Infarct size and capillary density were detected by histology. Left ventricular remodeling and function were as-sessed by echocardiography.Results After the 4-week experiment, compared with the group SO, plasma VEGF levels in groups MI (130.27 ± 18.58 pg/mL,P〈 0.01) and MI-HT (181.93 ± 20.29 pg/mL,P〈 0.01) were significantly increased. Infarct size in Group MI-HT (29.67% ± 7.73%) was deceased remarkably, while its capillary density (816.0 ± 122.2/mm2) was significantly increased. For both groups MI and MI-HT, left ventricular end-diastolic and end-systolic dimensions were increased whereas left ventricular ejection fraction was decreased. However, compared with group MI, group MI-HT diminished left ventricular end-diastolic (15.86 ± 1.09 mm,P〈 0.05) and end-systolic dimensions (12.10 ± 1.20 mm,P〈 0.01) significantly and im-proved left ventricular ejection fraction (54.39 ± 12.74 mm,P〈 0.05).ConclusionHypoxia training may improve left ven-tricular function and reduce remodeling via angiogenesis in rabbits with MI.
基金
We are grateful to the support of Dr. Lei Yuan and Shao-Shao Zhao for their technical assistance. This work was supported in part by China Postdoctoral Science Foundation Province, China
关键词
心肌梗死
心室重构
训练
低氧
雄兔
血管内皮生长因子
VEGF
血管密度
Hypobaric hypoxia Myocardial infarction Left ventricular remodelling Infarct size Vascular endothelial growth factor