Sepsis is a severe clinical syndrome in which a system-wide inflammatory response follows initial attempts to
eliminate pathogens. It is not novel that in sepsis the brain is one of the first organs affected which causes an increase in
morbidity and mortality and its consequences may be exacerbated when associated with a diagnosis of chronic inflammation,
such as in obesity. Thus, the aim of the present study is to evaluate the susceptibility to brain damage after sepsis in
obese rats. During two months, Wistar rats, 60 days, 250-300g received hypercaloric nutrition to induce obesity. Sepsis
was submitted to the cecal ligation and perforation (CLP) procedure and sham-operated rats was considered control group.
The experimental groups were divided into Sham + Eutrophic, Sham + Obesity, CLP + Eutrophic and CLP + Obesity.
Twelve and twenty four hours after surgery the blood brain barrier (BBB) permeability, nitrite/nitrate concentration, myeloperoxidase
(MPO) activity, oxidative damage to lipids and proteins and superoxide dismutase (SOD) and catalase
(CAT) activities were evaluated in the hippocampus, cortex and prefrontal cortex. The data indicate that in obese rats subjected
to sepsis occurs an increase of BBB permeability in different brain regions compared to eutrophic septic rats. This
alteration reflected an increase of MPO activity, concentration of nitrite/nitrate, oxidative damage to lipids and proteins
and an imbalance of SOD and CAT especially 24 hours after sepsis. It follows that obesity due to its pro-inflammatory
phenotype can aggravate or accelerate the sepsis-induced damage in rat brain.