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尼普地洛可预防大鼠心肌梗死后左心室收缩和舒张功能障碍。

Nipradilol can prevent left ventricular systolic and diastolic dysfunction after myocardial infarction in rats.

作者信息

Izutani Satoru, Yoshiyama Minoru, Omura Takashi, Yoshida Ken, Nakamura Yasuhiro, Kim Shokei, Takeuchi Kazuhide, Yoshikawa Junichi

机构信息

Department of Internal Medicine, Graduate School of Medicine, Osaka City University, Japan.

出版信息

Circ J. 2002 Mar;66(3):289-93. doi: 10.1253/circj.66.289.

DOI:10.1253/circj.66.289
PMID:11922280
Abstract

The purpose of this study was to examine the effects of nipradilol on the cardiac function and mRNA expression in Wistar rats with a myocardial infarction (MI) that was created by ligation of the anterior descending coronary. Ten mg x kg(-1) x day(-1) of nipradilol were administrated to the rats in random order, and hemodynamic and Doppler-echocardiographic findings and myocardial mRNA expression were analyzed at 4 weeks after MI. Although left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) were increased in the MI rats, nipradilol significantly reduced the degree of the increase in both parameters. MI also significantly increased the weight of the left and right ventricles, and increased the left ventricular end-diastolic dimension (LVDd), effects that were attenuated by nipradilol. The MI rats showed decreased fractional shortening as systolic dysfunction and decreased E wave deceleration rate as diastolic dysfunction, and nipradilol significantly prevented these. Nipradilol significantly suppressed the increase in the non-infarcted myocardial mRNA expression of atrial natriuretic peptide, brain natriuretic peptide and collagen I and III. In conclusions, nipradilol prevents the cardiac remodeling that is accompanied by systolic and diastolic dysfunction, and inhibits abnormal myocardial gene expression after MI.

摘要

本研究的目的是研究尼普地洛对通过结扎冠状动脉前降支造成心肌梗死(MI)的Wistar大鼠心脏功能和mRNA表达的影响。将10 mg·kg⁻¹·d⁻¹的尼普地洛随机给予大鼠,并在心肌梗死后4周分析血流动力学和多普勒超声心动图结果以及心肌mRNA表达。虽然心肌梗死大鼠的左心室舒张末期压力(LVEDP)和中心静脉压(CVP)升高,但尼普地洛显著降低了这两个参数的升高程度。心肌梗死还显著增加了左、右心室重量,并增加了左心室舒张末期内径(LVDd),尼普地洛减轻了这些影响。心肌梗死大鼠表现出射血分数缩短降低作为收缩功能障碍,E波减速速率降低作为舒张功能障碍,尼普地洛显著预防了这些情况。尼普地洛显著抑制了心房利钠肽、脑利钠肽以及I型和III型胶原在非梗死心肌中的mRNA表达增加。总之,尼普地洛可预防伴有收缩和舒张功能障碍的心脏重塑,并抑制心肌梗死后异常的心肌基因表达。

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Circ J. 2002 Mar;66(3):289-93. doi: 10.1253/circj.66.289.
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