ISSN : 1301-5680
e-ISSN : 2149-8156
Turkish Journal of Thoracic and Cardiovascular Surgery     
THE EFFECTS OF L CARNITINE AS AN ADDITIVE IN CARDIOPLEGIC SOLUTIONS FOR MYOCARDIAL PROTECTION
Eyüp Hazan Baran Uğurlu, Nurten Saydam Erdem Silistireli, Mehmet Ateş *, Gül Güner Ünal Açıkel
Dokuz Eylül Üniversitesi Tıp Fakültesi, Göğüs Kalp Damar Cerrahisi Ana Bilim Dalı, İzmir
*Dokuz Eylül Üniversitesi Tıp Fakültesi, Biyokimya Ana Bilim Dalı, İzmir
**Dokuz Eylül Üniversitesi Tıp Fakültesi, Tıbbi Farmakoloji Ana Bilim Dalı, İzmir
Background: The purpose of this study was to determine the effects of carnitine supplementation of a crystalloid cardioplegic solution on postischemic functional recovery, oxygen free radical production and ischemic injury.

Methods: New Zealand White rabbits (n = 10 control group, n = 10 carnitine group) were used for isolated heart, Langendorff perfusion. Isolated hearts were arrested with cold cardioplegic solution for 90 minutes and the cardioplegic solution (St Thomas) was repeated every 20 minutes. In the study group carnitine was added into the cardioplegic solution at a concentration of 6 mM/L. Ventricular function was determined by measurements of peak developed pressure and heart rate. Oxygen free radical production was determined by measuring postischemic tissue levels of malondialdehyde, GSH / GSSG ratio, glutathione reductase and peroxidase enzyme levels. Tissue injury was detected by measuring levels of creatin phosphokinase, aspartate transaminase and lactic dehydrogenase levels in the perfusate.

Results: Ischemic injury resulted in a drop in peak developed pressure of 23% in the control and 14% in the carnitine group (p = 0.124). Post ischemic heart rates were similar in the control (130 + 9 / min) and the carnitine (130 ± 6 / min) groups (p = 0.82). Post ischemic peak systolic pressure-heart rate product also did not differ (p = 0.198). Post ischemic tissue levels of malondialdehyde was 0.970 + 0.1 4 nmol/mg protem in the control group and 0.974 + 0.l nmol/mg protein in the carnitine group (p = 0.519). Postischemic tissue levels of glutathione reductase (p = 0.004) and GSH (p = 0.035) were significantly higher in the carnitine group but post ischemic tissue levels of glutathione peroxidase (p = 0.82), and GSH / GSSG ratio (p = 0.733) did not differ. Post ischemic perfusate concentrations of creatin phosphokinase (p = 0.495), aspartate transaminase (p = 0.73), and lactic dehydrogenase (p = 0.788) were similar in both groups.

Conclusion: Carnitine supplementation of a standard crystalloid cardioplegic solution do not effect functional recovery, oxygen free radical production and biochemical markers of injury in the isolated heart model.

Keywords : Carnitine, ischemia, reperfusion, oxygen free radical
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