Effects of puerarin on lipopolysaccharide-induced myocardial dysfunction in isolated rat hearts

Myocardial dysfunction is a serious complication induced by sepsis. Puerarin is an oriental medicine that possesses therapeutic benefits for cardiovascular diseases. The aim of this study was to evaluate the anti-myocardial dysfunction effects of puerarin in isolated rat hearts induced iby lipopolysaccharide- and compare the myocardial protective effects between the different concentrations of puerarin. Isolated hearts were attached to a Langendorff apparatus and perfused with lipopolysaccharide [LPS] and different concentrations of puerarin. The hemodynamic parameters of heart rate [HR], left ventricular end systolic pressure [LVESP], +dp/dt[max], and -dp/dt[max] were recorded. The biochemical indexes of lactic dehydrogenase [LDH], tumor necrosis factor alpha [TNF-alpha], and creatine kinase [CK] in the coronary effluent were measured at 40, 90, and 120 min of perfusion. TNF-a in myocardial tissues was measured after perfusion was completed. As a result, puerarin [0.24 mmol/L-0.48 mmol/L] significantly increased LVESP, +dp/dt[max], -dp/dt[max], and HR in isolated rat hearts that were declined by LPS during perfusion periods. Puerarin could protect against increased LDH, CK, and TNF-alpha in coronary effluent of isolated rat hearts by LPS during perfusion periods. Treatment of 0.48 mmol/L puerarin significantly decreased the TNF-alpha in coronary effluent of isolated rat hearts compared with the treatment of 0.12 and 0.24 mmol/L puerarin, but the TNF-a values were not reverted to baseline levels. However, the difference of TNF-alpha in myocardial tissue in the three puerarin-combined groups was statistically significant. This study confirms that puerarin can improve LPS-induced contractile dysfunction in isolated heart and inhibit LPS-stimulated myocardial TNF-a production

Severe infective endocarditis with systemic embolism due to community associated methicillin-resistant Staphylococcus aureus ST630

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) are increasingly causing infective endocarditis over the past decade. Here we report a healthy man who developed a severe acute infective endocarditis with systemic embolism caused by CA- MRSA. The strain was recovered from repeated blood cultures and was characterized using molecular detection and genotyping. The S. aureus isolate was typed as ST630 SCCmecV with spa-type t4549, agrI/IV and was PVL-negative. This is the only case report, to our knowledge, of CA-MRSA infective endocarditis in China. This case highlights the emergence and geographical spread of life-threatening CA-MRSA infection within China.