Introduction: The coexistence of obesity and sepsis has become frequent in clinical practice. However, the influence of obesity on the outcomes of sepsis are still unclear. Therefore, we hypothesized that previous obesity harms the morbi-mortality of sepsis survivors mice which can be associated to impaired vascular function. Thus, the aim of this study was to evaluate the morbi-mortality and vascular alterations in obese mice that survived to sepsis. Methods: Male Balb/c mice (8 weeks old) were divided in four groups: (1)Control, (2)CLP, (3)CAF, and (4)CAF-CLP. The control groups received standard diet while the CAF groups received cafeteria diet for 30 days. On the 15th day of diet, CLP and CAF-CLP groups were submitted to cecal ligation and puncture to sublethal sepsis induction, while Control and CAF groups were submitted only to cecal exposition. Survival curve, sepsis clinical score and vascular reactivity of thoracic aorta were performed (CEUA: 383/2016). Results: The survival (~60%) and sepsis clinical score of CLP and CAF-CLP groups were similar over time after sepsis induction. Despite that, phenylephrine-induced vasoconstriction was significantly diminished in the CAF-CLP (Emax: 2.00±0.14,n=12), which demonstrated hyporeactivity compared to the others groups (Controle-Emax:3.33±0.19,n=6; CLP-Emax:3.04±0.10,n=8; CAF-Emax:2.60±0.15,n=10; p<0.05). The CAF-CLP hyporeactivity was completely restored by the endothelium mechanical removing. L-NAME incubation partially reversed the aortic hyporeactivity, while the Captopril, Catalase, TEA, 1400W incubations were not able to alter this vascular response. The Ibuprofen incubation, in turn, reduced the vasoconstriction of other groups at level found in CAF-CLP, which suggests that CAF-CLP presents reduced levels of vasoconstrictors derived from COX. Conclusion: CAF diet-induced obesity do not impair morbi-mortality of mice that survived sepsis; however, it significantly alter the vascular function. CAF-CLP animals show an aortic hiporeactivity caused essentially by endothelial mediators. Among them, NOS activation is partially involved and the COX-derived vasoconstrictors levels seem to be reduced.
Comissão Organizadora
José Wilson do Nascimento Corrêa
Simone Potje
Gabriel Tavares do Vale
Stêfany Cau
Roger Lyrio
Simone R Potje
Alice Valença Araújo
Ruth Cristina Albuquerque Santos
Lara Caroline Amaro
Ana Dária Cassoli da Silva
Pollyana Peixoto
Izabela Moreira Bonfim
Jocimar José Pitol
Sunamita Vaz Martins
Izabela Moreira Bonfim
Palloma Emanuelle Dornelas de Melo
Daniella Bonaventura
Tagana Rosa
Sarah Victory Santana Gomes
Priscila Cruz
André Lucas Borges
Jéssyca Aparecida Soares Giesen
Leticia Tinoco Gonçalves
Silvia Maria Luna Alves
NAYANA YARED BATISTA
Wellington Francisco Pereira da Silva
Natália Ferreira de Araújo
Leandro de Carvalho Gomes
Comissão Científica