Literature DB >> 16463656

Effect of L-carnitine on cardiomyocyte apoptosis and cardiac function in patients undergoing heart valve replacement operation.

Daokang Xiang1, Zongquan Sun, Jiahong Xia, Nianguo Dong, Xinling Du, Xinzhong Chen.   

Abstract

The effects of L-carnitine, as an ingredient of cardioplegia solution, on cardiac function and cardiomyocyte apoptosis in patients undergoing heart valve replacement operation were investigated. Twenty-three cases undergoing heart valve replacement with cardiopulmonary bypass (CPB) were randomly allocated into two groups: L-carnitine group (n = 12, 12 g/L L-carnitine was put in the ST. Thomas cardioplegia) and control group (n = 11, identical to the L-carnitine group except that normal saline was administered instead of L-carnitine). Serum cardial troponin I (cTnI) levels, the left ventricular ejection fraction (LVEF), and cardiac index (CI) were measured perioperatively. A bit of myocardial tissue obtained from right atria was taken before CPB and by the end of intracardiac procedure to undergo electron microscopy examination and estimate apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL). From the end of CPB to 3 days after operation, the serum levels of cTnI in the L-carnitine group was significantly lower than that in the control group (P < 0.05). Heart color ultrasonogram showed that the CI index and LVEF at 7th day postoperatively in the L-carnitine group were significantly higher than in the control group (P < 0.05). Compared to the control group, L-carnitine significantly alleviated the morphologic changes of cardiac muscle cells (electron microscopy examination) and decreased the amounts of apoptotic cardiac muscle cells (TUNEL). Furthermore, the dosage of vasoactive drugs used after operation was significantly less in the L-carnitine group (P < 0.01). It was concluded that L-carnitine cardioplegia solution could improve cardiac function in patients undergoing heart valve replacement operation and alleviate CPB-mediated apoptosis of cardiac muscle cells.

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Year:  2005        PMID: 16463656     DOI: 10.1007/BF02895999

Source DB:  PubMed          Journal:  J Huazhong Univ Sci Technolog Med Sci        ISSN: 1672-0733


  12 in total

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Review 2.  Current experience in testing mitochondrial nutrients in disorders featuring oxidative stress and mitochondrial dysfunction: rational design of chemoprevention trials.

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