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. Author manuscript; available in PMC: 2018 Sep 2.

Published in final edited form as: Exp Physiol. 2012 Nov 23;98(3):734–745. doi: 10.1113/expphysiol.2012.069831

Following coronary artery ligation surgery, mice treated with the control antibody (AB) had a significant enlargement of the left and right ventricles (left ventricular end-diastolic diameter [LVEDD], left ventricular end-systolic diameter [LVESD] and right ventricular end-diastolic area [RVEDA]) and a significant reduction in left and right ventricular function (left ventricular ejection fraction [LVEF], myocardial performance index [MPI] and tricuspidal annular plane systolic exercusion [TAPSE]). Administration of the antibody directed towards Interleukin-1β (IL-1β-AB) immediately after coronary ligation (10 mg/kg i.p.) significantly limited the cardiac enlargement and dysfunction without affecting the extent of infarct size measured as akynetic segments or as % area fibrosis at pathology. N=10 for sham; N=17 for control-AB; N=14 for IL-1β-AB.

Following coronary artery ligation surgery, mice treated with the control antibody (AB) had a significant enlargement of the left and right ventricles (left ventricular end-diastolic diameter [LVEDD], left ventricular end-systolic diameter [LVESD] and right ventricular end-diastolic area [RVEDA]) and a significant reduction in left and right ventricular function (left ventricular ejection fraction [LVEF], myocardial performance index [MPI] and tricuspidal annular plane systolic exercusion [TAPSE]). Administration of the antibody directed towards Interleukin-1β (IL-1β-AB) immediately after coronary ligation (10 mg/kg i.p.) significantly limited the cardiac enlargement and dysfunction without affecting the extent of infarct size measured as akynetic segments or as % area fibrosis at pathology. N=10 for sham; N=17 for control-AB; N=14 for IL-1β-AB.