Abstract:
Excessive alcohol consumption, which is observed in many patients, causes cardiovascular diseases, in particular alcoholic cardiomyopathy, but the role of changes in H2S metabolism in heart damage in this pathology remains understudied. Therefore, the study aimed to determine the role of hydrogen sulphide in the mechanism of heart damage
in alcoholic myocardial injury in rats. The study was carried out on 35 white male Wistar rats weighing 260-290 g, divided into two groups. The study determined that the development of alcoholic cardiomyopathy in rats is accompanied by the development of pathobiochemical processes, including cardiomyocyte apoptosis, inflammation, development of oxidative and nitrosative stress, as evidenced by a significant increase in the content of caspase-3 (5.23 times) of tumour necrosis factor α (70.2%), malondialdehyde of carbonyl groups of proteins (2.7 and 2.5 times), respectively, as well as imbalance in the system of nitric oxide synthases (increase in inducible and decrease in endothelial isoform (+94.4 and -40.0%, respectively, p<0.05). All these changes were associated with a decrease in myocardial hydrogen sulphide content (-36.0%,
p< 0.05). The correlation and permutation analysis confirmed the relationship between the content of hydrogen sulphide
and markers of cardiac damage in alcoholic cardiomyopathy, namely, a low content of the gas transmitter was associated
with more severe disorders, while a higher level of hydrogen sulphide, on the contrary, was associated with moderate or minimal signs of cardiac damage under conditions of chronic alcoholism in animals. Assessment of the level of hydrogen sulphide in the body can predict the development of alcohol-induced heart damage and is an experimental basis for the
development of H2S-releasing drugs to improve the pharmacological management of patients
