Key result
Nebivolol therapy reduced ventricular remodeling in rats after myocardial infarction, with less decrease in ejection fraction and fractional shortening compared to controls.
Why the study?
Does nebivolol prevent ventricular remodeling in a rat myocardial infarction model?
Does nebivolol prevent ventricular remodeling in a rat myocardial infarction model?
Nebivolol therapy reduces ventricular remodeling and improves hemodynamics in a rat model of myocardial infarction, potentially mediated by nitric oxide regulation.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in rat MI model; human trials needed before any clinical consideration.
OBJECTIVE: Ventricular remodeling (VR) which develops after myocardial infarction (MI) plays an important role in progressive left ventricular dysfunction. We aimed to investigate the role of nebivolol treatment on VR after a MI in a rat ischemia-reperfusion model. METHODS: Rats were divided into 3 groups of 12 each: sham operated (sham-control), MI-induced (MI-control) and nebivolol treated (MI-nebivolol). Left ventricular (LV) diameters, volumes, and diastolic filling parameters were evaluated by echocardiography. On the 28th day, after recording the systemic and LV pressures and determining the plasma nitric oxide (NO) and peroxynitrite (ONOO-) levels , animals were sacrificed and heart, body and LV weights (HW, BW, LVW) were measured and infarct sizes were determined. Results were evaluated statistically by ANOVA for repeated measurements 3x3 factorial design with post-hoc Bonferroni test. RESULTS: After MI, while VR (an increase in LV diameters and volumes associated with a decrease in EF, FS and posterior wall thickness change (LWPc) was significant in MI-control rats (p<0.05 for; all comparisons) these changes were significantly less in MI-nebivolol group (p=0.08 and p=0.06 for EF and FS respectively). LV end diastolic pressure (LVEDP) was lower (p<0.005) and Delta+/- dp/dt's (p<0.05) were higher in MI-nebivolol group compared to MI-control animals. Although infarct sizes were similar in MI-induced groups (p=0.79); LVW/HW and HW/BW's were significantly greater in the MI-control group compared to sham-control (p<0.01 for all comparisons), these changes were not statistically significant in MI-nebivolol group. The increase in plasma NO and ONOO- levels were also prevented with nebivolol. CONCLUSION: Nebivolol therapy reduced the effects of VR in rats after MI. These beneficial effects were not related to its heart rate and blood pressure reducing effects. Nitric oxide regulatory action of this compound may contribute these beneficial effects on VR developed after MI.
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Mercanoğlu et al. (2010) studied Myocardial infarction (n=36). Nebivolol vs. MI-control and sham-control was evaluated on Ventricular remodeling (LV diameters, volumes, EF, FS, and posterior wall thickness change) (p=p=0.08 and p=0.06 for EF and FS respectively). Nebivolol therapy reduced ventricular remodeling in rats after myocardial infarction, with less decrease in ejection fraction and fractional shortening compared to controls.
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