Genetic deletion of Galectin 3 reduced the infarct size and Preserved myocardial contractility in an experimental model of ischemia and reperfusion in mice

NAYA, NADIA L; DIAZ ÁVALOS, YAMILA; GONZÁLEZ, GERMÁN E.; CASSAGLIA, PABLO; CASANOVA, VERÓNICA; ARUANNO, MARÍA E; MORALES, CELINA

Mar del Plata, Buenos Aires

Congreso; LXI Reunión Científica Anual de la Sociedad Argentina de Investigación Clínica; 2016

Sociedad Argentina de Investigación Clínica

GENETIC DELETION OF GALECTIN 3 REDUCED THE INFARCT SIZE AND PREVESERVED MYOCARDIAL CONTRACTILITY IN AN EXPERIMENTAL MODEL OF ISCHEMIA AND REPERFUSION IN MICENadia Martínez Naya, Pablo Cassaglia, María Eugenia Aruanno, Celina Morales, Germán E. GonzálezIt has been previously shown that genetic deletion of Galectin 3 (Gal-3) reduces inflammation, oxidative stress and unfavorable modifies the ventricular remodeling after permanent coronary artery ligature in mice. Despite its active involvement in the inflammatory response, the role of Gal-3 in a model of myocardial ischemia and reperfusion has not been studied. Therefore, we hypothesize that genetic deletion of Gal-3 reduces myocardial infarct size and improves ventricular function after 2 hours of reperfusion in mice.Male C57 (n=6) and Gal-3KO (n=7) mice were subjected to 30 minutes of regional myocardial ischemia followed by 2 hours of reperfusion. Meanwhile, heart rate (HR, BPM), LV systolic pressure (LVSP, mmHg), LV +dP/dtmax (mmHg/sec) and LV end diastolic pressure (EDP, mmHg) were continuously monitored by cardiac catheterization. Once the protocol was finished, hearts were perfused with Evans blue to determine the area at risk. Then the infarct size was measured by using the triphenyltetrazolium chloride technique.The area at risk was similar between groups (C57: 38±4% vs Gal-3KO: 36±4%; p=NS) while the infarct size was significantly reduced in Gal-3KO mice (C57: 71±4% vs Gal3KO: 52±5%; p