Sepsis is a systemic inflammatory syndrome associated to infection with high mortality. Recent data show that sepsis mortality rates can reach up to 80% depending on the severity (1). Cardiovascular dysfunction is associated with high mortality varying from 70% to 90% compared with 20% in patients without any cardiovascular damage (2). Despite the high number of cases, sepsis does not have an effective therapeutic option for mortality control, largely due to the still limited knowledge about cellular mechanisms and sub-cellular components involved in cardiovascular changes during the development of sepsis (3). This work proposes to investigate if there are changes in excitability and/or contractility at the cellular level that could be correlated with the heart dysfunction observed during sepsis. Balb C mice (8-12 weeks of age) were anesthetized (xylasine/ketamine 10/50 mg/kg) and submitted to cecal ligation and puncture (CLP) based on Baker et al. (1983). After, 6 and 24 hours (h) of CLP left ventricular cardiomyocytes were isolated from Sham and CLP operated mice as described by Shioya (2007). The cells were submitted to electrophysiological recordings to measure action potentials (AP). The same batch of isolated cells was used to determine contractile parameters. Experiments were performed in accordance with Ethics Committee in Animal Experimentation (CEUA) from Universidade Federal de Minas Gerais, Protocol Nr: 137/2012. In a non-lethal sepsis experimental set, we could not detect important differences between AP from the studied groups neither after 6 nor 24 h post CLP procedure. There were no significant differences among the experimental groups in the cardiac AP overshoot, time to peak, depolarization rate (dV/dt) and time to 10%, 50% and 90% of repolarization. Considering an experimental set of lethal sepsis, 6 h after CLP, it was observed changes in AP that suggests modification in Na+ channel function and/or expression, once we observed that the depolarization rate was significantly increased in AP measured from septic cells (263±12 V/s, SHAM, n=16 and 578±64 V/s, SEPTIC, n=5, *One way ANOVA p<0.05). Likewise, contractile parameters showed no significant changes in fractional shortening, shortening rate and diastolic length. Interestingly, the relaxation rate was significantly different (156±2 µm/s, SHAM and 108±19 µm/s, SEPTIC. One Way ANOVA *p<0.05, n=20). Based in our results, we can conclude that the heart failure developed during sepsis may be not related to a reduction in cardiac excitability nor contractility in general. These observations points to the notion that the circulatory disorder that occurs after 6 h of sepsis is not due to a global cardiac dysfunction but, instead, the heart acts in a compensatory way to balance the hypodynamic vascular dysfunction. Clearly further studies are needed.