Mice Surviving Sepsis Show Impaired Cardiac Function And Increased Vascular Resistance Aortic

Mice Surviving Sepsis Show Impaired Cardiac Function And Increased Vascular Resistance Aortic

• Autor
• Natália Nóbrega
• Co-autores
• Daniela Reis , Natália Araújo , Naiara Assis , Marcos Barrouin Melo , José Evaldo Filho , Alexandre Santos Bruno , Robson Santos , Jader Cruz , Stefany Bruno , Daniella Bonaventura
• Resumo

• Introduction: Cardiovascular diseases (CVDs) are considered the leading cause of death in the world. Recent studies have shown that there is an increase in the incidence of CVD in patients with acute infection, such as sepsis, in which it involves important circulatory changes, mainly vasodilation and increased vascular permeability, both contributing to relative hypovolemia and reduced blood pressure. Survivors of sepsis show an increase in the development of CVD between 1 and 5 years after the previous infection. Objective: evaluate the cardiovascular parameters in animals surviving sepsis. Methods: In male Balb/c mice (8 weeks old) was performed cecal ligation and a puncture (26-gauge needle) to induce sepsis. After 15 days, in survivor animals, we performed electrocardiogram and echocardiogram, blood pressure measurements by tail-cuff plethysmography, langendorff experiments, and vascular reactivity in thoracic aorta (CEUA: 383/2016). Results: The echocardiogram showed a significant reduction in systolic volume, ejection fraction and cardiac output in the sepsis-survivor group (SSG). Besides that, the electrocardiogram showed an increase in time to initiate ventricular repolarization in SSG. Also, the Langendorff experiments showed that pressure developed by the left ventricle, as well as pressure derived from time derived, both are reduced in SSG when compared to animals in the control group. Evaluate the function of this heart when subjected to stress, we confirm the cardiac damage since there was no reestablishment of the response. About vasomotor tonus, the contractile effect induced by phenylephrine in thoracic aortas from SSG was significantly higher than that in the control group (Sham: Emax 3.13±0.24 and pD2 6.80±0.17 (n=15); Sepsis- survivor: Emax 3.99±0.23 and pD2 7.16±0.11 (n=13)) by AT1 receptors activation, anions superoxide and COX-derived. Conclusion: The sepsis-surviving mice showed contractility enhancement in the aorta, afterload increase, and consequently heart failure. Propranolol treatment was able to reverse the increased vascular resistance triggered by sepsis.

• Palavras-chave
• Sepsis, Vascular Reactivity, Aorta, Cardiac Function.
• Modalidade
• Comunicação oral
• Área Temática
• Inflamação e doenças vasculares