NO AND INFLAMMATION AS EFFECTORS OF CARDIAC MITOCHONDRIAL DYSFUNCTION AND ROS PRODUCTION IN LOW-GRADE AND SEVERE ENDOTOXEMIA.

VICO TAMARA; MARCHINI TIMOTEO; AREÁN JUAN SANTIAGO ADÁN; VALERIA CALABRÓ; GARCÉS MARIANA; CATUOGNO FRANCO; LOREZENTTI MARIO A; FERRERO MARIANA CRISTINA; GONZALEZ MAGLIO DANIEL; BALDI PABLO C; EVELSON PABLO; ALVAREZ SILVIA

Buenos Aires

Congreso; LXV Reunión anual de la Sociedad Argentina de Inmunología; 2017

Sociedad Argentina de Inmunología

Myocardial dysfunction is a complication of severe sepsis and endotoxemia.Previously, we described cardiac mitochondrial dysfunction in this syndrome. Mechanisms of how systemic inflammation could damage heart function remains still unknown. Cytokines, NO and bioenergetics derangements are thought to be involved. The aim was to analyse systemic NO and ROS in a model of low-grade and severe endotoxemia. Female Sprague-Dawley rats (55 days) were injected i.p. with a single dose of LPS 0.5 mg/kg, 8 mg/kg or vehicle (control), 6h later animals were sacrificed. White blood cells (WBC) and differential count were analysed. DFC-DA and DAF-2-DA were used to estimate intracellular ROS and NO concentration by polymorphonuclear cells (PMN), respectively. Nitrite/nitrate content and proinflammatory cytokines levels (TNFα and IL-6) were analysed in plasma samples. Mitochondrial H2O2 production was measured using Amplex Red probe. WBC count showed difference between groups: control 2638 cells/mm3 (N:17%/L:77%/M:5%/E:1%/B:0%), LPS 0.5: 6771 cells/mm3 (N:61%/L:28%/M:7%/E:0%/B:4%) and LPS 8: 1021 cells/mm3 (N:58%/L:40%/M:2%/E:0%/B:0%). PMN cells from LPS-treated animals increased intracellular NO by 147% (LPS 0.5) and 164% (LPS 8) compared with control (p