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Macrophage Depletion in Hypertensive Rats Accelerates Development of Cardiomyopathy

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands, University of California Irvine, School of Medicine, Irvine, California

Umesh C. Sharma, MD, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Sudhir Gupta, MD, PhD

University of California Irvine, School of Medicine, Irvine, California, sgupta{at}uci.edu

Johan W. H. Verjans, MD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands, University of California Irvine, School of Medicine, Irvine, California

Susanne van den Borne, MD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands, University of California Irvine, School of Medicine, Irvine, California

Saraswati Pokharel, MD, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Thomas van Brakel, MD, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Adriaan Duijvestijn, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Nico van Rooijen, PhD

Faculty of Medicine, Vrije Universiteit, Amsterdam, Netherlands

Jos G. Maessen, MD, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Chris Reutelingsperger, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Yigal M. Pinto, MD, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Jagat Narula, MD, PhD

University of California Irvine, School of Medicine, Irvine, California

Leo Hofstra, MD, PhD

University Hospital Maastricht and Cardiovascular Research Institute Maastricht, Maastricht, Netherlands

Inflammation contributes to the process of ventricular remodeling after acute myocardial injury. To investigate the role of macrophages in the chronic process of cardiac remodeling, they were selectively depleted by intravenous administration of liposomal clodronate in heart failure—prone hypertensive Ren-2 rats from the age of 7 until 13 weeks. Plain liposomes were used for comparison. Liposomal clodronate treatment reduced the number of blood monocytes and decreased the number of macrophages in the myocardium. Compared to plain liposomes, liposomal clodronate treatment rapidly worsened left ventricular ejection function in hypertensive rats. Liposomal clodronate— treated Ren-2 rat hearts showed areas of myocyte loss with abundant inflammatory cell infiltration, predominantly comprising CD4 positive T lymphocytes. The current study showed that lack of macrophages was associated with earlier development of myocardial dysfunction in hypertensive rats. Modulation of macrophage function may be of value in the evolution of cardiomyopathy.

Key Words: hypertension • inflammation • ventricular remodeling • heart failure

This version was published on March 1, 2009

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 14, No. 1, 68-75 (2009)
DOI: 10.1177/1074248408329860


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