A thyroid hormone analog stimulates angiogenesis in the post-infarcted rat heart.
A thyroid hormone analog stimulates angiogenesis in the post-infarcted rat heart.
复制标题
甲状腺激素类似物刺激梗塞后大鼠心脏的血管生成。
DOI：
10.1006/jmcc.1998.0671
复制
发表时间：
1998
影响因子：
5
通讯作者：
Goldman,S
中科院分区：
文献类型：
--
作者：
Tomanek,RJ;Zimmerman,MB;Suvarna,PR;Morkin,E;Pennock,GD;Goldman,S
鉴于甲状腺激素给药对肥大心肌具有血管生成作用的证据，我们测试了这样的假设：给予甲状腺激素类似物二碘甲腺丙酸（DITPA）可以改善梗死后肥大心肌的毛细血管供应。我们皮下给予DITPA（MI-DITPA）或盐水（MI-盐水），在实验性左心室（LV）梗塞后对大鼠进行10天。采用形态测量方法评估左心室三个区域的毛细血管和肌细胞横截面积：（1）边缘（靠近梗死瘢痕）;（2）邻近（靠近边缘）;（3）远端（室间隔）。心肌梗死范围为左室游离壁的20-85%，两组的平均梗死面积相似。毛细血管长度密度（Lv）显着高于在MI-盐水大鼠的治疗组的偏远地区。在心脏细胞横截面积增加最显著的边缘区域，Lvin并不显著低于其他区域，表明血管生成反应更显著。在大面积梗死（≥40%）的心脏中，DITPA组边缘区域的Lvin高于未治疗大鼠。在MI-DITPA组中，边缘区域的心肌细胞大小与其他区域的心肌细胞大小呈正相关，这与MI-盐水大鼠的负相关性形成对比。这些数据表明，DITPA治疗（1）可以改善心肌梗死后存活的肥厚心肌的最大灌注电位，（2）在大面积梗死心脏的边缘区域选择性有效。
In view of the evidence that thyroid hormone administration has angiogenic effects on the hypertrophic myocardium, we tested the hypothesis that the capillary supply in the hypertrophic myocardium surviving infarction would be improved by administration of the thyroid hormone analog, diiodothyroproprionic acid (DITPA). We administered DITPA (MI-DITPA) or saline (MI-saline), s.c., to rats for 10 days following experimental infarction of the left ventricle (LV). Morphometric methods were used to assess capillarity and myocyte cross-sectional area in three regions of the left ventricle: (1) border (next to the scar of infarction); (2) adjacent (next to the border); and (3) remote (interventricular septum). Infarct size ranged from 20–85% of the LV free-wall, and both groups had similar mean infarct size. Capillary length density (Lv) was significantly higher in the remote region of the treated group than in the MI-saline rats. Lvin the border region, which experienced the most marked increase in cardiocyte cross-sectional area, was not significantly lower than in the other regions, indicating a more marked angiogenic response. In hearts with large infarcts (≥40%) Lvin the border region was higher in the DITPA group than in the non-treated rats. In the MI-DITPA group, cardiocyte size in the border region was positively correlated with that of the other regions, which contrasts with the negative correlations noted for the MI-saline rats. These data suggest that DITPA therapy (1) may improve maximal perfusion potential of the hypertrophied myocardium surviving a myocardial infarction, and (2) is selectively effective in the border region of hearts with large infarcts.