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通过高分辨率多普勒超声对1型心肾综合征小鼠模型的特征描述。

Characterization of a murine model of cardiorenal syndrome type 1 by high-resolution Doppler sonography.

作者信息

Pesce P, Cecchetto L, Brocco S, Bolognesi M, Sodhi K, Abraham N G, Sacerdoti D

机构信息

Department of Medicine (DIMED), University of Padova, Padua, Italy.

Department of Medicine, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755 USA.

出版信息

J Ultrasound. 2014 Sep 20;18(3):229-35. doi: 10.1007/s40477-014-0129-y. eCollection 2015 Sep.

Abstract

ABSTRACT

Cardiorenal syndrome type 1 (CRS-1) is the acute kidney disfunction caused by an acute worsening of cardiac function. CRS-1 is the consequence of renal vasoconstriction secondary to renin-angiotensin system (RAS) activation. No animal models of CRS-1 are described in literature.

PURPOSE

To characterize a murine model of CRS-1 by using a high-resolution ultrasound echo-color Doppler system (VEVO2100).

MATERIALS

Post-ischemic heart failure was induced by coronary artery ligation (LAD) in seven CD1 mice. Fifteen and thirty days after surgery, mice underwent cardiac and renal echo-color Doppler. Serum creatinine and plasma renin activity were measured after killing. Animals were compared to seven CD1 control mice.

RESULTS

Heart failure with left ventricle dilatation (end diastolic area, p < 0.05 vs. controls) and significantly reduced ejection fraction (EF; p < 0.01 vs. controls) was evident 15 days after LAD. We measured a significant renal vasoconstriction in infarcted mice characterized by increased renal pulsatility index (PI; p < 0.05 vs. controls) associated to increased creatinine and renin levels (p < 0.05 vs. controls).

CONCLUSIONS

The mice model of LAD is a good model of CRS-1 evaluable by Doppler sonography and characterized by renal vasoconstriction due to the activation of the renin-angiotensin system secondary to heart failure.

摘要

摘要

1型心肾综合征(CRS-1)是由心功能急性恶化引起的急性肾功能障碍。CRS-1是肾素-血管紧张素系统(RAS)激活继发肾血管收缩的结果。文献中未描述CRS-1的动物模型。

目的

通过使用高分辨率超声回声彩色多普勒系统(VEVO2100)来表征CRS-1的小鼠模型。

材料

对7只CD1小鼠进行冠状动脉结扎(左前降支,LAD)诱导缺血后心力衰竭。术后15天和30天,对小鼠进行心脏和肾脏回声彩色多普勒检查。处死小鼠后测量血清肌酐和血浆肾素活性。将这些动物与7只CD1对照小鼠进行比较。

结果

LAD术后15天,明显出现伴有左心室扩张(舒张末期面积,与对照组相比p<0.05)和射血分数显著降低(EF;与对照组相比p<0.01)的心力衰竭。我们在梗死小鼠中测量到明显的肾血管收缩,其特征为肾搏动指数(PI)增加(与对照组相比p<0.05),同时肌酐和肾素水平升高(与对照组相比p<0.05)。

结论

LAD小鼠模型是一种可通过多普勒超声评估的CRS-1良好模型,其特征是由于心力衰竭继发肾素-血管紧张素系统激活而导致肾血管收缩。

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本文引用的文献

1
HO-1 induction improves the type-1 cardiorenal syndrome in mice with impaired angiotensin II-induced lymphocyte activation.
Hypertension. 2013 Aug;62(2):310-6. doi: 10.1161/HYPERTENSIONAHA.111.00495. Epub 2013 Jun 10.
2
Acute Kidney Injury (AKI) biomarker.
Acta Med Indones. 2012 Jul;44(3):246-55.
3
Analyzing left ventricular function in mice with Doppler echocardiography.
Heart Fail Rev. 2013 Jul;18(4):511-6. doi: 10.1007/s10741-012-9345-8.
6
Angiotensin II and oxidative stress in the failing heart.
Antioxid Redox Signal. 2013 Oct 1;19(10):1095-109. doi: 10.1089/ars.2012.4588. Epub 2012 May 3.
7
Animal models of cardiorenal syndrome: a review.
Heart Fail Rev. 2012 May;17(3):411-20. doi: 10.1007/s10741-011-9279-6.
8
CXCR4 antagonism attenuates the cardiorenal consequences of mineralocorticoid excess.
Circ Heart Fail. 2011 Sep;4(5):651-8. doi: 10.1161/CIRCHEARTFAILURE.110.960831. Epub 2011 Jun 17.

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