RESUMEN
Myocardial ischemia/reperfusion (I/R) injury is a growing concern for global public health. This study seeks to explore the potential protective effects of L-carnitine (LC) against heart ischemia-reperfusion injury in rats. To induce I/R injury, the rat hearts underwent a 30-min ligation of the left anterior descending coronary artery, followed by 24 h of reperfusion. We evaluated cardiac function through electrocardiography and heart rate variability (HRV) and conducted pathological examinations of myocardial structure. Additionally, the study investigated the influence of LC on myocardial apoptosis, inflammation, and oxidative stress in the context of I/R injury. The results show that pretreatment with LC led to improvements in the observed alterations in ECG waveforms and HRV parameters in the nontreated ischemic reperfusion model group, although most of these changes did not reach statistical significance. Similarly, although without a significant difference, LC reduced the levels of proinflammatory cytokines when compared to the values in the nontreated ischemic rat group. Furthermore, LC restored the reduced expressions of SOD1, SOD2, and SOD3. Additionally, LC significantly reduced the elevated Bax expressions and showed a nonsignificant increase in Bcl-2 expression, resulting in a favorable adjustment of the Bcl-2/Bax ratio. We also observed a significant enhancement in the histological appearance of cardiac muscles, a substantial reduction in myocardial fibrosis, and suppressed CD3 + cell proliferation in the ischemic myocardium. This small-scale, experimental, in vivo study indicates that LC was associated with enhancements in the pathological findings in the ischemic myocardium in the context of ischemia/reperfusion injury in this rat model. Although statistical significance was not achieved, LC exhibits potential and beneficial protective effects against I/R injury. It does so by modulating the expression of antioxidative and antiapoptotic genes, inhibiting the inflammatory response, and enhancing autonomic balance, particularly by increasing vagal tone in the heart. Further studies are necessary to confirm and elaborate on these findings.