| ObjectiveTo observe the influences of phenoprolamine hydrochloride (DDPH) on heart functional indices, myocardial infarct size, myocardial enzyme, myocardial ultrastructure and reperfusion arrhythmia against ischemia-reperfusion injury (I/R) in isolated rat hearts and investigate the cardioprotective effect of DDPH against I/R injury and the mechanism of its myocardial protection.Methods72 male Sprague-Dawley rats were divided into six groups:control group, I/R group, verapamil treated group, and three DDPH treated groups (3,7 and 15μmol/L, respectively). Myocardial I/R mode was established by 40 min ischemia and 120 min reperfusion induced by the ligation of left descending coronary artery in isolated rat hearts. The recorded heart functional indices were left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), the maximal rate of increase and decrease of left ventricular pressure (±dp/dtmax) and coronary flow (CF) at different time points. The arrhythmic quantification during myocardial ischemia-reperfusion period was examined according to Curtis and Walker's scoring method. The activities of superoxide dismutase and glutathione peroxidase and the content of malondialdehyde (MDA) in myocardium were determined. Myocardial infarct size and the ultrastructural changes of myocardial cells were observed.Results1. Before ischemia, heart functional indices and basic values of each group had no significant difference. Compared with control group, I/R significantly decreased LVSP, LVDP,+dp/dtmax,-dp/dtmax, increased LVEDP, and reduced CF (P< 0.05, P < 0.01). Compared with I/R group, DDPH 7,15μmol/L significantly increased LVSP, LVDP,+dp/dtmax,-dp/dtmax, decreased LVEDP, increased CF, and heart functions recovered obviously (P< 0.05, P< 0.01). Heart functional indices in DDPH 3μmol/L treated group and Verapamil treated group had no obvious improvement (P> 0.05).2. Compared with control group, the incidence rate of reperfusion arrhythmia in I/R group was 100%, and arrhythmia score was 3.83±0.39 (P< 0.05, P< 0.01). Compared with I/R group, DDPH 3,7,15μmol/L and Verapamil treated groups had lower incidence rate of reperfusion arrhythmia and arrhythmia score (P< 0.05, P< 0.01).3. Compared with control group, I/R significantly increased myocardial infarct size (39.86%), and had serious ultrastructural injury in myocardial cells (P< 0.05, P< 0.01). Compared with I/R group, myocardial infarct sizes in DDPH 7,15μmol/L and Verapamil treated groups were significantly diminished (26.33%,23.94%,30.70%, respectively), and the degree of ultrastructure injury in myocardial cells were slighter (P< 0.05, P< 0.01). Myocardial infarct size in DDPH 3μmol/L treated group diminished disobviously fewer (34.79%), and ultrastructure injury in myocardial cells was serious (P> 0.05).4. Compared with control group, the content of MDA was significantly decreased, and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were significantly increased in I/R group (P< 0.05, P< 0.01). Compared with I/R group, the content of MDA was significantly decreased in DDPH 3,7,15μmol/L and Verapamil treated groups (P< 0.05, P< 0.01). The activities of SOD and GSH-Px were significantly increased in DDPH 7,15μmol/L and Verapamil treated groups (P< 0.05, P< 0.01), however, DDPH 3μmol/L treated group had no obvious increase (P> 0.05).Conclusions1. DDPH has a significantly protective effect against ischemia-reperfusion injury in isolated rat heart; it lightens myocardial contraction and diastole functional disturbance.2. DDPH significantly decreases the incidence rate of reperfusion arrhythmia and arrhythmia score, diminishes myocardial infarct size, and lightens the degree of ultrastructure injury in myocardial cells.3. The cardioprotective effect of DDPH may be related to blocking intracellular calcium influx and inhibiting the formation of the oxygen free radical and subsequent peroxidation of lipid. |
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