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Cardiovascular and inflamatory effects of insulin, glucose and potassium therapy in an experimental model of sepsis

Grant number: 14/05357-7
Support type:Regular Research Grants
Duration: October 01, 2014 - September 30, 2016
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal researcher:Luciano Cesar Pontes de Azevedo
Grantee:Luciano Cesar Pontes de Azevedo
Home Institution: Hospital Sírio-Libanês. Sociedade Beneficente de Senhoras (SBSHSL). São Paulo , SP, Brazil
Assoc. researchers:Eduardo Leite Vieira Costa ; Marcelo Park

Abstract

Sepsis is a clinical condition with high morbidity and mortality, often complicated with cardiac dysfunction. Cardiac dysfunction in sepsis occurs by the release of inflammatory mediators generating reduction of myocardial contractility. There are no established treatments for myocardial failure during sepsis, besides the usual support with vasoactive drugs. Previous studies suggest that insulin might be beneficial for myocardial contractile function under low oxygen supply conditions such as heart failure due to coronary heart disease and sepsis cardiomyopathy. However, the mechanisms by which insulin exert these benefits are unclear. Thus, this experimental intervention study aims to compare cardiac function and inflammatory response between two groups of pigs with septic shock induced by fecal peritonitis: one treatment group treated with insulin, glucose and potassium and other control group who receives only conventional treatment. Insulin will be administered by continuous infusion after hemodynamic stabilization with fluid replacement and norepinephrine infusion and the animals will be monitored for 24 hours from the induction of peritonitis. The main parameters measured over time will be cardiac output, mean arterial pressure, ejection fraction, end systolic and diastolic pressure volume relationship, maximum change of pressure with time, inflammatory mediators (IL-1±, IL-1², IL-1ra, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, TNF-±, IFN³, GM-CSF) and troponin-I. (AU)

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