P135Sulfur dioxide derivative prevents isoproterenol induced electrophysiological alterations.

Cardiovascular Research

PubMedID: 25020555

Yaras N, Ozdemir S, Dalaman U, Ozdogan H. P135Sulfur dioxide derivative prevents isoproterenol induced electrophysiological alterations. Cardiovasc Res. 2014;103 Suppl 1S23-4.
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 carbon monoxide (CO), nitrogen monoxide (NO) and hydrogen sulfide (H2S) referred to as the gasotransmitters. These molecules have been identified primarly as contaminants of the environment. In addition to these substances, sulfur dioxide (SO2) is the one that still investigated in the same way. Recent studies regarding the heart muscle beside other organs, SO2 is endogenously produced and possible intercellular signaling molecule. However, the influence on heart's electrical and mechanical functions is unknown. This study was designed to uncover the potential role of SO2 in rat model of HCM generated by excessive ß-adrenergic stimulation was used. Single cells have been obtained by enzymatically from hearts of wistar rats given ß-adrenergic agonist isoproterenol (25 mg per kg body weight per day) subcutaneously to generate HCM and/or SO2 donor sodium metabisulfite (85 mg per kg body weight per day) for 7 days (i.p). It has been found that SO2 had no effect on isoproterenol induced hypertrophy via examining heart weight/tibia length ratio. It is observed that lengthening at repolarization phase of action potential in the animal model and SO2 application reversed this process. Moreover, isoproterenol treatment reduced L-type Ca2+ current, it was returned to control levels by application of SO2. Experimental HCM model leads to adverse changes in mechanical parameters, even though SO2 causes improvement in the electrophysiological parameters. Also shortening in the resting sarcomere length along with decreasing contraction amplitude in isoproterenol and SO2 applied animals would interpret diastolic dysfunction due to increased Ca2+ sensitivity. Also isoproterenol induced cardiac damage were not caused by oxidation since no difference observed on protein oxidation and lipid peroxidation measurements. However, it is determined that SO2 application alone does increase protein carbonyl values. In this context, while SO2 molecule creates oxidative stress in physiological condition, different effects on the organism can be revealed depending on the physiological conditions. Consequently, the data have implied that SO2 molecule has possible effect on cardiovascular system pathology and on electrophysiology of heart. In order to fully understand of this effect, detailed studies are required.