Abstract
Lipopolysaccharide of bacterial origin (LPS) belongs to the group of PAMPs (pathogen-associated molecular patterns). LPS is a component of the outer membrane of gram-negative bacteria. As a pro-inflammatory factor, LPS binds to “toll-like receptors 4” (TLR4) and thus activates the production of cytokines. Cytokines are known to provoke the development of arrhythmia, disrupt the processes of electromechanical coupling and lead to the damage of myocardium during myocarditis. We have investigated the effects of the intraperitoneal administration of LPS (10µg/100g of body mass) on the electrocardiographic parameters of frogs’ heart, such as the heart rate (HR), the velocity of impulse transmission through the atrioventricular node to the ventricle (PR), amplitude (QRS), and the duration of the ventricular complex (QT). LPS induced a significant increase of heart rate and shortening of the duration of the ventricular complex, as compared with the control group. In addition, we have investigated the contraction amplitude (mechanical systole) of the isolated frog heart in the ex vivo conditions, where LPS was found to cause a negative inotropic effect. Based on these results, it can be assumed that the overactivation of the immune system as mimicked by the administration of LPS in vivo is responsible for the cross-talk between the altered heart functional activity (increase of pacemaker rhythm, decrease of the amplitude of contractions) and a rapid formation of the ventricular complex. These effects might be responsible for the decrease in cardiac output and chronic heart failure characteristic for myocarditis.
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