Investigation of the effect of sulfur dioxide on isoproterenol induced cardiac injury by electrophysiological parameters

Cardiac hypertrophy is an initial adaptive response to several types of cardiovascular stress and can precede the decompensatory phase of heart failure. Excitation-contraction coupling in cardiac muscle of hypertrophic cardiomyopathy (HCM) remains poorly understood, despite the fact that the genetic alterations are well defined. In this sense, many intracellular signaling molecules and pathways has been tested. Among these, the most interesting ones are gasotransmitters referred to as the carbon monoxide (CO), nitrogen monoxide (NO) and hydrogen sulfide (H2S) respectively. These molecules have been identified as primary contaminants of the environment, but the understanding of the production pathways and mechanisms physiological role draw the attention. In addition to these substances, sulfur dioxide (SO2) is the one that still investigated in the same way. SO2 is toxic and allergic agent and metabolic removal processes is also known for a long time. Recent studies regarding the heart muscle beside other organs, SO2 is endogenously produced and possible intercellular signaling molecule. However, several articles were discussing that subsidence of SO2 is histologically effective in the formation of hypertrophic signal. However, the influence on heart's electrical and mechanical functions is unknown. Based on these reasoning, the study designed to investigate the effect of SO2 on cardiomyocytes' excitation-contraction coupling in HCM model. This study was designed to uncover the potential role of SO2 in rat model of HCM generated by excessive ?-adrenergic stimulation was used. Single cells have been obtained by enzimatically from hearts of rats given ?-adrenergic agonist isoproterenol subcutaneously to generate HCM and/or SO2 donor sodium metabisulfite (i.p) for 7 days. It has been found that SO2 and antioxidant mixture do not effect that isoprotenol application caused hypertrophy by examining heart weight/tibia length ratio. It is observed that appeared pathology model caused lengthening at repolarization phase of action potential and SO2 application reversed this process. Moreover, antioxidant mixture does have an parallel effect on this lengthening. In other studies, this lengthening explained as it took place due to the INa-L currents. Although isoprotenol reduced Ca2+ current, Ca2+ current was lessened to control levels with application of SO2. It have been noticed that antioxidant mixture does not have any effect on the Ca2+ currents. Apart from this information, it is noticed that leads to adverse changes in mechanical parameters, even though SO2 causes improvement in the electrophysiological parameters. A number of studies showed that diastolic dysfunction appeared because of occurred Ca2+ sensitivity. The main reason of this interpretation is that shortening in the resting sarcomere length along with decreasing contraction amplitude. In order to understand that the relation between antioxidant system and effects of SO2 molecule mentioned above, biochemical parameters are also studied. As a result of this study, it is found that cardiac damage did not caused protein oxidation and lipid peroxidation and it is emphasized that possible effects of SO2 molecules cannot be out of this system. However, it is determined that SO2 application does not increase protein carbonyl values. In this context, while SO2 molecule creates oxidative stress in physiological conditions, different effects on the system can be revealed depending on the changing conditions Consequently, the obtained data have implications for the understanding of cardiovascular system pathology and positive effect of SO2 molecule. In order to fully understand of this effect, detailed studies should required