Inhibition of nitric oxide aggravates pancreatic mitocondrial dysfunction during endotoxemia

ADÁN AREÁN JUAN SANTIAGO; EVELSON PABLO; VICO TAMARA; ORQUERA TAMARA; ALVAREZ SILVIA; VANASCO VIRGINIA; FERRERO, MARIANA CRISTINA; VACCARO MARÍA INÉS

Mar del plata

Congreso; LXIII Reunión Anual de la Sociedad Argentina de Investigaciones Clínicas; 2019

Sociedad Argentina de Investigaciones clínicas

Pancreas has been described to be early affected in endotoxemia. As mitochondria are the main source of ATP, it is essential to maintain mitochondrial bioenergetics during recovery from pancreatic cellular, tissue and organic damage in this syndrome. Moreover, high systemic NO levels observed during endotoxemia could be involved in pancreatic tissue damage, as well as initiating cellular recovery processes such as autophagy. The aim of this project was to analyze the relationship between the severity of the systemic inflammatory insult and pancreatic mitochondrial dysfunction during endotoxemia, focusing on NO as a possible damage modulator. Female Sprague Dawley rats (45 days) were i.p. injected with: vehicle (control); LPS 0.5 mg/kg (LPS 0.5) and LPS 8 mg/kg (LPS 8). Co-treatment with i.p. L-NAME 20 mg/kg was performed in all experimental groups. Blood NO levels (by EPR), as well as plasma nitrate/nitrite content increased 4-fold (LPS 0.5) and 7-fold (LPS 8) compared to control group (p