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Articles in PresS, published online ahead of print July 11, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00305.2002
Submitted on April 8, 2002
Accepted on July 8, 2002
1 Cardiovascular and Metabolic Diseases, Pharmacia Corporation, St. Louis, MO, USA
2 Investigative Toxicology, Pharmacia Corporation, St. Louis, MO, USA
3 Global Medical Affairs, Pharmacia Corporation, Peapack, NJ, USA
4 Veterinary Pathobiology, Purdue University, West Lafeyette, IN, USA
5 Biotechnology, Pharmacia Corporation, St. Louis, MO, USA
* To whom correspondence should be addressed. E-mail: jonathan.r.heyen{at}pharmacia.com.
Heart failure is a complex multifactorial disease resulting in a myriad of progressive changes at the molecular, cellular, and physiological level. To better understand the mechanisms associated with the development of congestive heart failure, a comprehensive examination of the aging lean male spontaneously hypertensive heart failure-prone rat (SHHF) was conducted. Myocardial function and structural integrity progressively diminished as evidenced by decreased ejection fraction and increased left ventricular volume measured using echocardiography. Functional and structural changes were accompanied by elevations in circulating inflammatory markers including tumor necrosis factor alpha (TNF-
), interleukin-6 (IL-6), and TNF receptors type 1 and 2 (TNFR1 and TNFR2). Increased systemic inflammatory marker levels were consistent with age-dependent changes in the expression pattern of genes that contribute to stress, inflammation, and the extracellular matrix in SHHF animals analyzed from age 4 to 18 months. In summary, the SHHF rat shares many hallmark features of the human disease state and represents a key experimental model for the dissection of complex human heart failure pathophysiology.
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