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左心室肥厚中心肌微循环的功能机制:心肌梗死后毛细血管重塑的一种假说模型。

Functional mechanisms of myocardial microcirculation in left ventricular hypertrophy: a hypothetical model of capillary remodeling post myocardial infarction.

作者信息

Waller Christiane, Hiller Karl-Heinz, Pfaff Daniela, Gattenlöhner Stefan, Ertl Georg, Bauer Wolfgang R

机构信息

Medizinische Klinik und Poliklinik I, Universität Würzburg, Josef-Schneider-Strasse 2, Würzburg, Germany.

出版信息

Microvasc Res. 2008 Jan;75(1):104-11. doi: 10.1016/j.mvr.2007.04.005. Epub 2007 Apr 24.

DOI:10.1016/j.mvr.2007.04.005
PMID:17540413
Abstract

OBJECTIVES

Left ventricular (LV) remodeling after myocardial infarction (MI) is characterized by myocyte hypertrophy and a disproportional capillary growth. We developed a hypothetical model of capillary remodeling mechanisms based on quantitative data of microcirculation determined by magnetic resonance (MR) imaging techniques and histology.

METHODS

Perfusion and regional capillary blood volume (RBV) were quantified 8 and 16 weeks after MI (mean 27.0+/-2.9% of the left ventricle 16 weeks post MI) or sham operation in rats using MR imaging and were correlated with morphometric data.

RESULTS

Maximum perfusion (ml/(g min)) in the remote area decreased from 5.69+/-0.63 to 3.48+/-0.48 compared to sham animals (5.33+/-0.31, p</=0.01) and showed a close inverse relation to hypertrophy. In contrast, maximum RBV in the remote area was similar to that of sham animals (16.79+/-0.42% and 16.52+/-0.33%, respectively) and did not change over time. Thus, mean transit time (MTT) was longer in remote than in sham myocardium. Morphology revealed that hypertrophy was inversely related to capillary density which was associated with an increase in capillary cross-sections.

CONCLUSIONS

Perfusion data in synopsis with histological observations demonstrate that the functional capillary length increases during hypertrophy post MI which is consistent with the increase of the mean transit time. Despite a relative decrease in capillary density, RBV may be restored by an increase in the cross-sections. In the light of almost maximum oxygen extraction under normal conditions, this hypertrophy related remodeling may be deleterious for tissue supply.

摘要

目的

心肌梗死(MI)后的左心室(LV)重构以心肌细胞肥大和不成比例的毛细血管生长为特征。我们基于磁共振(MR)成像技术和组织学确定的微循环定量数据,建立了一个毛细血管重构机制的假设模型。

方法

使用MR成像对大鼠在心肌梗死或假手术后8周和16周(心肌梗死后16周平均为左心室的27.0±2.9%)的灌注和局部毛细血管血容量(RBV)进行定量,并将其与形态学数据相关联。

结果

与假手术动物相比,梗死周边区域的最大灌注量(ml/(g·min))从5.69±0.63降至3.48±0.48(假手术动物为5.33±0.31,p≤0.01),且与肥大呈密切负相关。相比之下,梗死周边区域的最大RBV与假手术动物相似(分别为16.79±0.42%和16.52±0.33%),且随时间无变化。因此,梗死周边心肌的平均通过时间(MTT)比假手术心肌更长。形态学显示,肥大与毛细血管密度呈负相关,毛细血管密度的增加与毛细血管横截面积的增加有关。

结论

综合灌注数据和组织学观察表明,心肌梗死后肥大过程中功能性毛细血管长度增加,这与平均通过时间的增加一致。尽管毛细血管密度相对降低,但RBV可能通过横截面积的增加而恢复。鉴于正常条件下几乎最大的氧摄取,这种与肥大相关的重构可能对组织供应有害。

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