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Updated: Apr 27, 2026
A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
Interleukin-1β blockade improves left ventricular systolic/diastolic function and restores contractility reserve in
Stefano Toldo1, Eleonora Mezzaroma, Edoardo Bressi
1*Virginia Commonwealth University Pauley Heart Center, Virginia Commonwealth University, Richmond, VA; †Victoria Johnson Research Laboratories, Virginia Commonwealth University, Richmond, VA; and ‡Department of Pharmacotherapy and Outcome Studies, Virginia Commonwealth University, Richmond, VA.
Background:
Interleukin-1β (IL-1β) modulates the inflammatory response during acute myocardial infarction (AMI) and progression to ischemic cardiomyopathy. We investigated whether blockade of IL-1β after the onset of the cardiac dysfunction prevented left ventricular (LV) adverse remodeling in a mouse model of anterior nonreperfused AMI.
Methods:
Infarct size and LV systolic function were assessed by echocardiography 7 days after coronary artery ligation. Mice with large infarct size and LV ejection fraction (LVEF) <40% were randomly assigned to treatment with a monoclonal antibody directed toward IL-1β antibody (10 mg/kg IL-1β-AB) or with a cyclosporine directed antibody (10 mg/kg control-AB). Echocardiogram was repeated after 10 weeks, followed by assessment of contractile reserve using isoproterenol challenge and LV catheterization.
Results:
After 10 weeks, control-AB-treated mice showed significantly increased LV end-diastolic diameter (+15%, P < 0.001) and decreased LVEF (-18%, P = 0.050). IL-1β-AB had no significant effect on LV end-diastolic diameter (+10%, P = 0.25 vs. control-AB) but significantly prevented LVEF reduction (+7%, P = 0.031 vs. control-AB), enlargement of the right ventricle (P = 0.024), impairment in myocardial performance index (P = 0.028) and contractile reserve (P = 0.008), and increased LV end-diastolic pressure (P = 0.030).
Conclusions:
IL-1β blockade using a monoclonal antibody in mice with severe LV dysfunction after AMI prevents further deterioration in LV systolic and diastolic function and restores contractile reserve.
