首页> 外文期刊>Angiology: the Journal of Vascular Diseases >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.
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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.

机译:在兔急性心肌梗塞模型中,碱性成纤维细胞生长因子可增加局部心肌血流量并挽救梗塞边界区的心肌。

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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.
机译:一些人已显示碱性成纤维细胞生长因子(bFGF)在实验性急性心肌梗死中可促进血管生成和心肌抢救。尽管这些发现激发了许多临床兴趣,但并未普遍观察到它们,bFGF的真正功效仍不清楚。作者使用兔急性心肌梗死模型进一步阐明了bFGF对急性侧支含很少侧支的心肌的作用。结扎左冠状动脉引起心肌梗塞。结扎前,将100微克bFGF(bFGF组; n = 15)或生理盐水(对照组; n = 22)注射到结扎动脉供血的心肌中。使用非放射性彩色微球,在冠状动脉结扎之前,之后和4周测量局部血流量(Qm)。在切除的心脏的横截面切片中测量梗塞和边界区的大小,并在组织学上确定每个区域的存活心肌量(心肌评分)和纤维化程度。结扎后四周,bFGF组和对照组之间梗死区的Qm值无显着差异(0.54 +/- 0.36 vs 0.48 +/- 0.30 mL / min / g);在边界区域,bFGF组的Qm倾向于更高(3.39 +/- 2.68 vs 1.47 +/- 0.80 mL / min / g),但差异不显着。最后,在非梗塞区域,bFGF组的Qm显着升高(p <0.05)(6.06 +/- 3.85 vs 2.09 +/- 0.82 mL / min / g)。两组的梗死区域中存活心肌的数量或纤维化程度无显着差异。然而,在边界区域,bFGF组的存活心肌数量明显更大(p <0.005)(视野的61.8 +/- 8.5%与35.8 +/- 20.3%)。同样,按照从0到5的等级进行评分,bFGF组的纤维化程度明显减少(p <0.005)(2.1 +/- 0.5 vs 3.3 +/- 0.8)。总之,向急性梗死心肌注射bFGF可以增加流向非梗死区域的血流量,并挽救边界区域的心肌。

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