Baroreceptor Sensitivity During the Compensatory Phase of Left Ventricular Overloading

Nishimura, Hiroshi; Yoshikawa, Tsutomu; Anzai, Toshihisa; Baba, Akira; Kobayashi, Noboru; Wainai, Yumiko; Ogawa, Satoshi

doi:10.1253/jcj.62.773

Cited by 1 publication

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References 41 publications

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“…20 Significant abnormalities of the adrenergic system have also been identified in humans and animals submitted to chronic volume overload. [2][3][4][5][6][7][8][9][10][11][12]21,22 Others have reported significant decreases in ␤-adrenoreceptor density in the LV of patients with chronic volume overload compared with pressure-overload and normal controls. 23 In subjects with clinical heart failure from severe AR, intense adrenergic activity is present, as in other causes of heart failure.…”

Section: Discussionmentioning

confidence: 99%

Effectiveness of β-Blockade in Experimental Chronic Aortic Regurgitation

et al. 2004

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Background-Past studies have suggested that the adrenergic system becomes abnormally activated in chronic volume overload, such as in severe aortic valve regurgitation (AR). However, the effectiveness of agents directed against this adrenergic activation has never been adequately tested in chronic AR. We therefore tested the effects of metoprolol treatment on the left ventricular (LV) function and remodeling in severe chronic AR in rats. Methods and Results-Severe AR was created in adult male Wistar rats by retrograde puncture of the aortic leaflets under echocardiographic guidance. Two weeks later, some animals received metoprolol treatment (25 mg/kg) orally for 24 weeks, and some were left untreated. LV dimensions, ejection fraction, and filling parameters were evaluated by echocardiography. Hearts were harvested at 1, 2, 14, and 180 days for the evaluation of hypertrophy, ␤-adrenergic receptor status, and extracellular matrix remodeling. We found that metoprolol treatment prevented LV dilatation and preserved the ejection fraction and filling parameters compared with untreated animals. Metoprolol increased the expression of ␤ 1 -adrenoreceptor mRNA and reduced G protein receptor kinase 2 levels. Collagen I and III mRNA levels were reduced. Cardiac myocyte hypertrophy was also prevented. Conclusions-In our experimental model of severe AR, metoprolol treatment had a significant beneficial global effect on LV remodeling and function. These results suggest that the adrenergic system is important in the development of volume-overload cardiomyopathy in AR and that adrenergic-blocking agents may play a role in the treatment of this disease.

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