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碱性成纤维细胞生长因子可增加急性心肌梗死兔模型梗死边缘区的局部心肌血流量并挽救心肌。

Basic fibroblast growth factor increases regional myocardial blood flow and salvages myocardium in the infarct border zone in a rabbit model of acute myocardial infarction.

作者信息

Hasegawa T, Kimura A, Miyataka M, Inagaki M, Ishikawa K

机构信息

First Department of Medicine, Kinki University School of Medicine, Osakasayama, Osaka, Japan.

出版信息

Angiology. 1999 Jun;50(6):487-95. doi: 10.1177/000331979905000607.

Abstract

Basic fibroblast growth factor (bFGF) has been shown by some to promote angiogenesis and myocardial salvage in experimentally induced acute myocardial infarction. Although these findings have spurred much clinical interest, they are not universally observed, and the true efficacy of bFGF remains unclear. The authors used a rabbit model of acute myocardial infarction to further elucidate the effects of bFGF on acutely infarcted myocardium containing few collaterals. Myocardial infarction was evoked by ligation of the left coronary artery. Prior to ligation, either 100 microg of bFGF (bFGF group; n = 15) or physiological saline (control group; n = 22) was injected into the myocardium supplied by the ligated artery. With use of nonradioactive colored microspheres, regional blood flow (Qm) was measured before, immediately after, and 4 weeks after coronary artery ligation. Infarct and border zone sizes were measured in cross-sectional slices of the resected hearts, and the amount of viable myocardium (myocardium score) and the extent of fibrosis were histologically determined in each area. Four weeks after ligation, Qm values in the infarcted area did not significantly differ between the bFGF and control groups (0.54 +/- 0.36 vs 0.48 +/- 0.30 mL/min/g); in the border zone, Qm tended to be higher in the bFGF group (3.39 +/- 2.68 vs 1.47 +/- 0.80 mL/min/g), but the difference was not significant; finally in the noninfarcted area, Qm was significantly (p < 0.05) higher in the bFGF group (6.06 +/- 3.85 vs 2.09 +/- 0.82 mL/min/g). There was no significant difference in the amount of viable myocardium or the extent of fibrosis in the infarcted areas of the two groups. In the border zone, however, the amount of viable myocardium was significantly (p < 0.005) larger in the bFGF group (61.8 +/- 8.5% vs 35.8 +/- 20.3% of the visual field). Likewise, as graded on a scale from 0 to 5, the extent of fibrosis was significantly (p < 0.005) less in the bFGF group (2.1 +/- 0.5 vs 3.3 +/- 0.8). In conclusion, injection of bFGF into acutely infarcted myocardium increased blood flow to the noninfarcted area and salvaged the myocardium in the border zone.

摘要

一些研究表明,碱性成纤维细胞生长因子(bFGF)可促进实验性诱导的急性心肌梗死中的血管生成和心肌挽救。尽管这些发现引起了广泛的临床关注,但并非普遍观察到,bFGF的真正疗效仍不清楚。作者使用急性心肌梗死兔模型进一步阐明bFGF对几乎没有侧支循环的急性梗死心肌的影响。通过结扎左冠状动脉诱发心肌梗死。在结扎前,将100微克bFGF(bFGF组;n = 15)或生理盐水(对照组;n = 22)注入结扎动脉供血的心肌。使用非放射性彩色微球,在冠状动脉结扎前、结扎后立即和结扎后4周测量局部血流量(Qm)。在切除心脏的横截面切片中测量梗死区和边缘区大小,并在每个区域组织学测定存活心肌量(心肌评分)和纤维化程度。结扎后4周,bFGF组和对照组梗死区的Qm值无显著差异(0.54±0.36 vs 0.48±0.30 mL/min/g);在边缘区,bFGF组的Qm倾向于更高(3.39±2.68 vs 1.47±0.80 mL/min/g),但差异不显著;最后在非梗死区,bFGF组的Qm显著更高(p < 0.05)(6.06±3.85 vs 2.09±0.82 mL/min/g)。两组梗死区存活心肌量或纤维化程度无显著差异。然而,在边缘区,bFGF组的存活心肌量显著更大(p < 0.005)(视野的61.8±8.5% vs 35.8±20.3%)。同样,按0至5级评分,bFGF组的纤维化程度显著更低(p < 0.005)(2.1±0.5 vs 3.3±0.8)。总之,向急性梗死心肌中注射bFGF可增加非梗死区的血流量,并挽救边缘区的心肌。

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