[Role of homocysteine in the pathogenesis of alcoholic cardiomyopathy].

OBJECTIVE: To explore the role of homocysteine in the pathogenesis of alcoholic cardiomyopathy. METHODS: A total of 69 male Wistar rats were randomly assigned into two groups: alcohol-fed group and the control. Cardiac function was assessed by pulse Doppler. Plasma Hcy levels were examined using automatic biochemical instrument (chemiluminescence). The protein expression of MMP-9 was evaluated using immunohistochemical method, and collagen fiber of myocardium was quantitative analyzed by Masson stain. RESULTS: After heavy drinking, the LVEDd of alcohol-fed group were larger than the control group [(7.0±0.6) mm vs (5.0±0.4) mm, P<0.05], the LVEF and FS were lower in the 4th month (52%±8% vs 78%±4%, 31%±3% vs 47%±2%, P<0.05), the data changed more significantly (P<0.01) in the 6th month. The level of plasma Hcy from alcohol-fed group was significantly higher from the 2nd month than that before the experiment [(18.1±3.1) µmol/L vs (9.8±2.1) µmol/L, P<0.01], and it was higher in 4th month than that in 2nd month [(26.3±4.0) µmol/L vs (18.1±3.1) µmol/L, P<0.05], it was highest in 6 months. After 4-month and 6-month drinking, the expression of MMP-9 protein from alcohol group was higher than before the experiment (0.161%±0.019%, 0.263%±0.014% vs 0.050%±0.008%, P<0.01). Masson staining showed myocardial collagen of alcohol group was more after 4-month and 6-month drinking than those before the experiment (10.23%±1.20% vs 0.50%±0.09%; 22.41%±2.57% vs 0.50%±0.09%, P<0.01). Plasma Hcy and cardiac tissue MMP-9 is a significant positive correlation (r=0.848, P<0.01). CONCLUSION: Long-term and large drink liquor can lead to plasma Hcy levels significantly increased, and participate cardiac remodeling and the pathogenesis of ACM through increasing the expression of myocardial tissue MMP-9 protein.

Hemodynamic effect of apelin in a canine model of acute pulmonary thromboembolism.

The peptide apelin is expressed in the pulmonary vasculature and is involved in the pathogenesis of many cardiovascular diseases. It has a biphasic role in the regulation of vasomotor tone related to the vascular endothelium. In this study, we induced acute pulmonary embolism (APE) in dogs with autologous blood clots to assess the effect of apelin on pulmonary and systemic circulation in the acute phase of APE. The expression of apelin mRNA was found to be upregulated in the lung tissue in the early several hours after APE induction and decreased at 24 h. The expression of apelin protein in the pulmonary arteries did not change within 24 h after APE, but significantly increased in the bronchial epithelial cells as early as 1h and decreased at 24 h. In normal anesthetized dogs, intravenous bolus administration of apelin significantly reduced the mean arterial pressure (MAP), but did not significantly affect the mean pulmonary arterial pressure (MPAP). In the dogs with APE, apelin decreased MPAP, whereas its impact on MAP was not significantly different from that in the control group. Taken together, the level of endogenous apelin did not change significantly in the pulmonary arterial wall, whereas its expression in the bronchial epithelium was upregulated in the early stage of APE. The effect of exogenous apelin on vasomotor tone was complicated: it resulted in differential changes in the pulmonary and systemic arterial pressures under different physiological and pathological conditions.