Cardioprotective effect of lithium chloride on a rat model of myocardial infarction
<p><strong>Aim.</strong> To investigate the cardioprotective effect of lithium chloride in vivo on a rat model of myocardial infarction.<br /><strong>Methods.</strong> Twelve male Sprague-Dawley rats were randomly divided into two groups of six, with both groups modelling cardiac ischaemia and subsequent reperfusion. At the start of reperfusion, 30 mg/kg of 4.2% lithium chloride solution was intravenously administered via a catheter to the test group and 0.5 ml/kg of saline solution was administered to the comparison group. A control group comprised sham-operated rats that were not injected with any drugs other than anaesthesia during making skin incision. At the end of each experiment, the total area of the risk zone and areas of the infarction zone and left ventricle were calculated for each animal using a double-staining technique with 2% methylene blue and 1% triphenyltetrazolium chloride. A further series of experiments using 15 male Sprague-Dawley rats (third group) was performed to assess the protein content of glycogen synthase-3β in myocardial tissue. The method was similar to that for the earlier experiments; however, at the end of the experiments, the hearts were removed and homogenised, following which the concentration of glycogen synthase-3β was determined using electrophoresis.<br /><strong>Results.</strong> The group treated with lithium chloride showed a significant decrease in the area of the infarction zone compared with the group treated with saline. The difference in the indices between the two groups was >26% (p < 0.05).<br /><strong>Conclusion.</strong> This study demonstrated that 30 mg/kg of 4.2% lithium chloride solution, administered at the onset of reperfusion, exerted a protective effect on cardiomyocytes in a rat model of myocardial infarction by reducing the area of the infarction zone compared with that in the control group. This effect was probably mediated by an almost two-fold increase in the content of the phosphorylated form of glycogen synthase-3β in the myocardium.</p><p>Received 23 June 2019. Revised 6 August 2019. Accepted 7 August 2019.</p><p><strong>Funding:</strong> The study did not have sponsorship.</p><p><strong>Conflict of interest:</strong> Authors declare no conflict of interest.</p><p><strong>Author contributions</strong> <br />Conception and study design: A.N. Kuzovlev<br />Data collection and analysis: O.A. Grebenchikov<br />Statistical analysis: A.V. Ershov<br />Drafting the article: A.V. Lobanov, E.R. Shayhutdinova<br />Critical revision of the article: V.V. Likhvantsev<br />All authors approved final version to be published.<br /><br /></p>