Adipose stromal vascular fraction cell construct sustains coronary microvascular function after acute myocardial infarction
Adipose stromal vascular fraction cell construct sustains coronary microvascular function after acute myocardial infarction
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DOI：
10.1152/ajpheart.00735.2011
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发表时间：
2012-02-01
影响因子：
4.8
通讯作者：
Williams, Stuart K.
中科院分区：
文献类型：
--
作者：
LeBlanc, Amanda J.;Touroo, Jeremy S.;Williams, Stuart K.
王晓明，王晓明，王晓明，等。心肌梗死后脂肪间质血管碎片细胞的构建及其对冠状动脉微血管功能的影响。[J]中国生物医学工程杂志，2012。首次发表于2011年12月2日；doi: 10.1152 / ajpheart.00735.2011。-使用脂肪来源的基质血管部分（SVF）细胞构建三维组织结构，并评估其在心肌梗死（MI）模型中的微血管保护治疗作用。本研究评估冠脉血流量（BF）和整体左心室功能在心肌梗死后与不SVF结构。将fisher -344大鼠分为假手术组（sham）、心肌梗死组（MI）、心肌梗死贴片组（无细胞）和心肌梗死SVF构建组（MI SVF）。用绿色荧光蛋白（GFP）标记SVF细胞。梗死后立即将构建体植入缺血部位的心外膜。术后4周，与假手术组相比，心肌梗死组冠状动脉BF储备明显减少67%，心肌梗死Vicryl组明显减少75%。假手术组和心肌梗死组在危险区域的冠状动脉BF储备无显著差异（假手术组：83 +/- 22%，心肌梗死组：57 +/- 22%）。单纯格里菲尼亚1和gfp阳性的SVF免疫染色显示移植后4周梗死区微血管周围的SVF细胞。心肌梗死SVF心脏的整体心功能，特别是射血分数明显高于心肌梗死和心肌梗死Vicryl心脏（心肌梗死SVF: 66 +/- 4%，心肌梗死：37 +/- 8%，心肌梗死Vicryl: 29 +/- 6%）。综上所述，脂肪来源的SVF细胞可以通过植入心脏外膜表面来构建一种治疗微血管不稳定和缺血的新治疗模式。心肌梗死后立即植入的SVF结构不仅能维持心功能，还能通过维持冠状动脉BF储备来维持梗死区微血管灌注和功能。
LeBlanc AJ, Touroo JS, Hoying JB, Williams SK. Adipose stromal vascular fraction cell construct sustains coronary microvascular function after acute myocardial infarction. Am J Physiol Heart Circ Physiol 302: H973-H982, 2012. First published December 2, 2011; doi:10.1152/ajpheart.00735.2011.-A three-dimensional tissue construct was created using adipose-derived stromal vascular fraction (SVF) cells and evaluated as a microvascular protection treatment in a myocardial infarction (MI) model. This study evaluated coronary blood flow (BF) and global left ventricular function after MI with and without the SVF construct. Fischer-344 rats were separated into four groups: sham operation (sham), MI, MI Vicryl patch (no cells), and MI SVF construct (MI SVF). SVF cells were labeled with green fluorescent protein (GFP). Immediately postinfarct, constructs were implanted onto the epicardium at the site of ischemia. Four weeks postsurgery, the coronary BF reserve was significantly decreased by 67% in the MI group and 75% in the MI Vicryl group compared with the sham group. The coronary BF reserve of the sham and MI SVF groups in the area at risk was not significantly different (sham group: 83 +/- 22% and MI SVF group: 57 +/- 22%). Griffonia simplicifolia I and GFP-positive SVF immunostaining revealed engrafted SVF cells around microvessels in the infarct region 4 wk postimplant. Overall heart function, specifically ejection fraction, was significantly greater in MI SVF hearts compared with MI and MI Vicryl hearts (MI SVF: 66 +/- 4%, MI: 37 +/- 8%, and MI Vicryl: 29 +/- 6%). In conclusion, adipose-derived SVF cells can be used to construct a novel therapeutic modality for treating microvascular instability and ischemia through implantation on the epicardial surface of the heart. The SVF construct implanted immediately after MI not only maintains heart function but also sustains microvascular perfusion and function in the infarct area by sustaining the coronary BF reserve.