Myocardial dysfunction with increased ventricular compliance in volume overload hypertrophy
Myocardial dysfunction with increased ventricular compliance in volume overload hypertrophy
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DOI：
10.1016/j.ejheart.2006.02.005
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发表时间：
2006-12-01
影响因子：
18.2
通讯作者：
Matsubara, Beatriz Bojikian
中科院分区：
文献类型：
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作者：
De Stefano, Laercio Martins;Matsubara, Luiz Shiguero;Matsubara, Beatriz Bojikian
为探讨容量超负荷性心肌肥厚大鼠的收缩和舒张功能，本研究采用肾下动静脉瘘（AVF）建立容量超负荷性心肌肥厚大鼠模型。结果与SHAM手术组（n = 11）进行了比较。术后8周，记录尾袖血压，然后处死大鼠进行Langendorffs离体心脏研究，AVF大鼠左心室和右心室重量与对照组相比增加。AVF组标准化心室容积增加（V0/LVW，0.141 +/- 0.035 mL/g vs. 0.267 +/- 0.071 mL/g，P < 0.001）表明心室扩张。心肌羟脯氨酸浓度保持不变。+dP/dt显著降低（3318 +/- 352 mm Hg s（-1）vs. 2769 +/- 399 mm Hg s（-1）; P= 0，002），收缩末期压力-容积关系（246 +/- 56 mm Hg mL（-1）vs. 114 +/- 63 mm Hg mL（-1）;，P <0.001），和-dP/dt AVF组（1746 +/- 240 mm Hg s（-1）vs. 1361 +/- 217 mm Hg s（-1），P < 0.001），心室顺应性增加（Delta V-25：假手术=0.172 +/- 0.05 mL vs. AVF=0.321 +/- 0.072 mL，P < 0.001），心肌被动僵硬度保留（应变（25）：SHAM=13.5 +/-3. 0% vs. AVF=12.3 +/-1.9%，P > 0.05）。我们得出结论：容量超负荷诱导的心肌肥厚导致心肌收缩和舒张功能障碍，心室顺应性增加。这些血流动力学特征有助于解释慢性容量超负荷在转变为明显充血性心力衰竭之前的长期代偿期。(c)2006年欧洲心脏病学会。Elsevier B. V.出版，保留所有权利。
The aim this study was to evaluate systolic and diastolic function in volume overload induced myocardial hypertrophy in rats.Volume overload myocardial hypertrophy was induced in thirteen male Wistar rats by creating infrarenal arteriovenous fistula (AVF). The results were compared with a SHAM operated group (n = 11). Eight weeks after surgery, tail-cuff blood pressure was recorded, then rats were sacrificed for isolated heart studies using Langendorffs preparation.AVF rats presented increased left and right ventricular weights, compared to controls. The increased normalized ventricular volume (V0/LVW, 0.141 +/- 0.035 mL/g vs. 0.267 +/- 0.071 mL/g, P < 0.001) in the AVF group indicated chamber dilation. Myocardial hydroxyproline concentration remained unchanged. There was a significant decrease in +dP/dt (3318 +/- 352 mm Hg s(-1) vs. 2769 +/- 399 mm Hg s(-1); P=0,002), end-systolic pressure-volume relation (246 +/- 56 mm Hg mL(-1) vs. 114 +/- 63 mm Hg mL(-1);, P < 0,001), and -dP/dt (1746 +/- 240 min Hg s(-1) vs. 1361 +/- 217 mm Hg s(-1), P < 0.001) in the AVF group, which presented increased ventricular compliance (Delta V-25: SHAM=0.172 +/- 0.05 mL vs. AVF=0.321 +/- 0.072 mL, P < 0.001) with preserved myocardial passive stiffness (Strain(25): SHAM=13.5 +/- 3.0% vs. AVF=12.3 +/- 1.9%, P > 0.05).We conclude that volume-overload induced hypertrophy causes myocardial systolic and diastolic dysfunction with increased ventricular compliance. These haemodynamic features help to explain the long-term compensatory phase of chronic volume overload before transition to overt congestive heart failure. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.