Metoprolol prevents ischemia-reperfusion injury by reducing lipid peroxidation

Myocardial ischemia and reperfusion result in endothelial and ventricular d ysfunction. Beta-blockers protect the myocytes from injury by acting as ant i-ischemia agents. These anti-ischemic effects of the beta-blockers are due not only to their negative inotropic/chronotropic effects but also to a li pid peroxidation reducing mechanism. Thus, beta-blockers enhance myocardial recovery. In the present study 20 isolated guinea-pig hearts were perfused with Krebs-Henseleit buffer (KHB) using a Langendorff apparatus. The anima ls were allocated into 2 groups. In the study group (Group I), metoprolol, as the beta-blocker agent, was added into the KHB and in the control group (Group II) perfusion was performed without metoprolol. The percentage chang e (%change) of heart rate, developed pressure and dP/dtmax; malondialdehyde (MDA) and glutathione (GSH) levels of the perfusate and heart tissue were obtained as data. The %change of heart rate was 70.5+/-9.2 in the study gro up and 87.3+/-8.2 in the control (p=0.003). The %change of developed pressu re was 68.7+/-14.4 and 55.9+/-8.6 in the study group and control group, res pectively (p=0.04). The % change of dP/dt was 63.3+/-10.0 in the study grou p and 54.4+/-5.3 in the control group (p=0.01). The tissue MDA level was 31 .0+/-5.5 nmol/g tissue in the study group and 53.5+/-4.2 nmol/g tissue in t he control group (p=0.0002). The tissue GSH levels were 1.08+/-0.20 and 0.8 0+/-0.07 (mol/g tissue) in Groups I and TI, respectively (p=0.001). The lev els of the perfusate MDA decreased and the levels of the perfusate GSH incr eased significantly in the metoprolol group in the postreperfusion period i n comparison with the preischemia term (p=0.003 and p=0.03, respectively). Metoprolol reduces ischemic injury via prevention of lipid peroxidation and reduces the myocardial energy demand by decreasing the heart rate.