Relationship between α-actinin and cardiac function in rats with myocardial ischemia-reperfusion / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the relationship between α-actinin content and cardiac function in rats during myocardial ischemia-reperfusion.</p><p><b>METHODS</b>Thirty-two rats were randomized equally into sham-operated group, 30 min ischemia group, 1 h ischemia group, and 1 h ischemia with 2 h reperfusion group. Acute myocardial ischemia was induced in the 3 ischemia groups by ligation of the left anterior descending coronary artery, and the cardiac functions were evaluated. The myocardial contents of α-actinin was measured by immunohistochemistry, and phospholipase C (PLC) and phosphatidylinositol-3-kinase (PI3K) contents were determined by ELISA after the operations.</p><p><b>RESULTS</b>The left ventricular systolic pressure (LVSP), +dp/dt max, and -dp/dt max tended to decrease during myocardial ischemia, and increased after reperfusion, and the left ventricular end-diastolic pressure (LVEDP) showed reverse changes. The levels of α-actinin decreased with prolonged ischemia, showing a significant difference in 1 h ischemia group from those in the other 3 groups. PI3K and PLC contents were significantly increased with prolonged myocardial ischemia. Stimulation by LY-294002 and U-73122 caused enhanced contraction of single cardiomyocytes, and also increased the fluorescence intensity of α-actinin in the cardiomyocytes compared with that in 1 h ischemia group.</p><p><b>CONCLUSIONS</b>The cardiac dysfunction during acute ischemia-reperfusion in rats may be related with the changes of myocardial α-actinin content, which are probably a result of increased PI3K and PLC contents in the ischemic myocardium.</p>

Role of Na(+)-K(+)-ATPase in lipopolysaccharide-induced cardiomyocyte hypertrophy in rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the possible mechanism of lipopolysaccharide (LPS)-induced cardiomyocyte hypertrophy in rats.</p><p><b>METHODS</b>Neonatal rat cardiomyocytes cultured in vitro were stimulated with 100 µg/L LPS for 1, 4 or 8 h and scanned by atomic force microscopy (AFM) for measurement of the two-dimensional area, three-dimensional surface area and volume of each cell. The total proteins and Na(+)-K(+)-ATPase activity in the cardiomyocytes were determined. The same measurements were also carried out in neonatal rat cardiomyocyte cultures stimulated by 0.5 µmol/L ouabain for 8 h and the total protein levels were measured.</p><p><b>RESULTS</b>Following a 8-hour stimulation with LPS, the two-dimensional area, three-dimensional surface area and volume of the single cardiomyocyte became enlarged and the total cellular proteins increased significantly as compared with those in the normal control cells (P < 0.05). LPS treatment for 4 and 8 h resulted in significantly decreased activity of Na(+)-K(+)-ATPase in the cardiomyocytes (P < 0.05). In the cells treated with ouabain for 8 h, the two-dimensional area, three-dimensional surface area, volume of the single cardiomyocyte and the total cellular proteins increased significantly in comparison with the normal control group (P < 0.05).</p><p><b>CONCLUSION</b>LPS can result in cardiomyocyte hypertrophy in rats possibly in relation to lowered Na(+)-K(+)-ATPase activity in the cardiomyocytes after LPS exposure.</p>