Metoprolol, attenuates cardiomyocyte apoptosis in left ventricular (LV) myocardium of dogs with heart failure (HF). Metoprolol induces the expression of Bcl-2 independent of heart failure (HF) and that this independently confers protection. [1]

Metoprolol partly reverses the depressed left ventricular (LV) systolic pressure, positive and negative rates of changes in pressure development, ejection fraction, fractional shortening and cardiac output, as well as increased LV end-diastolic pressure in 20 weeks myocardial infarction (MI) rats. Metoprolol partially reverses the elevated levels of plasma norepinephrine and dopamine without affecting the elevated levels of epinephrine. [2] Metoprolol treatment attenuates the development of cardiac dysfunction in streptozotocin (STZ)-diabetic rats. Metoprolol leads to reduced rates of palmitate oxidation, stimulation of glucose oxidation, and increases tissue ATP levels. Metoprolol leads to decreased maximum activity and decreased sensitivity of carnitine palmitoyltransferase I to malonyl-CoA. Metoprolol also increases sarco(endo) plasmic reticulum Ca(2+)-ATPase expression and prevents the reexpression of atrial natriuretic peptide in diabetic hearts of in streptozotocin (STZ)-diabetic rats. [3] Metoprolol, attenuates the increase in collagen content in noninfarcted regions and prevents the increase in right ventricular weight/body weight, and its effect is similar to captopril in rat model with myocardial infarction (MI). Metoprolol treatment tends to increase right ventricular weight and heart weight. [4]