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主动脉阻抗对大鼠压力超负荷性左心室肥厚发展的影响。

Influence of aortic impedance on the development of pressure-overload left ventricular hypertrophy in rats.

作者信息

Kobayashi S, Yano M, Kohno M, Obayashi M, Hisamatsu Y, Ryoke T, Ohkusa T, Yamakawa K, Matsuzaki M

机构信息

Second Department of Internal Medicine, Yamaguchi University School of Medicine, Japan.

出版信息

Circulation. 1996 Dec 15;94(12):3362-8. doi: 10.1161/01.cir.94.12.3362.

DOI:10.1161/01.cir.94.12.3362
PMID:8989152
Abstract

BACKGROUND

Aortic input impedance, which represents LV afterload, is considered to be a major determinant for the development of pressure-overload left ventricular (LV) hypertrophy.

METHODS AND RESULTS

To test whether the sustained change in aortic input impedance might affect the mode of development of LV hypertrophy, coarctation of either the ascending aorta (G1, n = 13) or suprarenal abdominal aorta (G2, n = 12) was performed over 4 weeks in 6-weeks-old Wistar rats. Although peak LV pressure and total systemic resistance were increased similarly in G1 and G2, time to peak LV pressure was decreased by 24% (P < .01) in G1 compared with G2. The aortic input impedance spectra revealed that the early systolic loading in G1 was characterized by an increase in characteristic impedance, whereas the late systolic loading in G2 was by an augmented arterial wave reflection. G1 showed a smaller increase (P < .01) in either the ratio of LV weight (mg) to body weight (g) or LV wall thickness than G2 after aortic banding. Myocyte diameter was also smaller (P < .05) in G1 (14.3 +/- 0.7 mm) than in G2 (16.1 +/- 1.2 mm). The ex vivo passive pressure-volume relation had a rightward shift in G1 compared with G2, suggesting less concentric LV hypertrophy in G1.

CONCLUSIONS

The sustained early systolic loading due to the increase in characteristic impedance was accompanied by less concentric, reduced hypertrophy, whereas the sustained late systolic loading due to the augmented arterial wave reflection was accompanied by concentric, adequate hypertrophy.

摘要

背景

主动脉输入阻抗代表左心室后负荷,被认为是压力负荷性左心室肥厚发生发展的主要决定因素。

方法与结果

为了检验主动脉输入阻抗的持续变化是否会影响左心室肥厚的发展模式,在6周龄的Wistar大鼠中进行了为期4周的升主动脉缩窄(G1组,n = 13)或肾动脉以上腹主动脉缩窄(G2组,n = 12)。尽管G1组和G2组的左心室峰值压力和总全身阻力同样升高,但与G2组相比,G1组的左心室压力达峰时间缩短了24%(P <.01)。主动脉输入阻抗谱显示,G1组收缩早期负荷的特征是特征阻抗增加,而G2组收缩晚期负荷的特征是动脉波反射增强。主动脉缩窄后,G1组的左心室重量(mg)与体重(g)之比或左心室壁厚度的增加幅度均小于G2组(P <.01)。G1组的心肌细胞直径(14.3±0.7μm)也小于G2组(16.1±1.2μm)(P <.05)。与G2组相比,G1组的离体被动压力-容积关系向右移位,提示G1组的左心室向心性肥厚程度较轻。

结论

特征阻抗增加导致的持续性收缩早期负荷伴有较轻的向心性、减轻的肥厚;而动脉波反射增强导致的持续性收缩晚期负荷伴有向心性、适度的肥厚。

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