Internal medicine: Effects of β-blocker on left ventricular remodeling in rats with volume overload cardiac failure

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  • KOBAYASHI Masayuki
    Department of Veterinary Clinical Oncology, Faculty of Agriculture, Tokyo University of Agriculture and Technology
  • MACHIDA Noboru
    Department of Veterinary Clinical Oncology, Faculty of Agriculture, Tokyo University of Agriculture and Technology
  • TANAKA Ryou
    Department of Veterinary Surgery, Faculty of Agriculture, Tokyo University of Agriculture and Technology
  • YAMANE Yoshihisa
    Department of Veterinary Surgery, Faculty of Agriculture, Tokyo University of Agriculture and Technology

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  • Effects of .BETA.-Blocker on Left Ventricular Remodeling in Rats with Volume Overload Cardiac Failure
  • Internal medicine Effects of v blocker on left ventricular remodeling in rats with volume overload cardiac failure

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The beneficial effects of β-blockers on left ventricular (LV) remodeling have been reported in association with several conditions that cause heart failure, but their effects on the volume overloaded heart failure have not been well defined. Fifty Wistar rats that survived aortocaval (AC) shunt creation were randomly allotted into the following two groups: untreated animals (ACS; n=26) and animals treated with 100 mg/kg/day metoprolol (MP; ACS+MP; n=24). The effects of MP were evaluated at 1, 4 and 12 weeks post-surgery through echocardiographic, hemodynamic and pathologic studies. At 12 weeks post-surgery, LV wall thinning associated with chamber dilatation was observed in ACS but not in ACS+MP. LV end-diastolic pressure and diastolic wall stress were lower in ACS+MP than in ACS. The increase in LV weight was similar in both ACS and ACS+MP at 1 and 4 weeks post-surgery, but at 12 weeks post-surgery, it was significantly greater in ACS+MP than in ACS. At the cellular level, although the cardiac myocyte length progressively increased to a similar extent in both groups, the mean cross-sectional diameter of these cells in ACS+MP was greater than in ACS. In conclusion, MP did not prevent early eccentric hypertrophy in response to volume overload. However, in the late phase of volume overload-induced heart failure, MP appears to allow for myocyte cross-sectional growth and thus prevents LV wall thinning, resulting in a net increase in LV mass. In this manner, MP might contribute to reduction of diastolic wall stress and thereby delay progression of heart failure.<br>

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