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concentration is increased in pacing-induced heart failure in rabbits
1 Institute of Pathophysiology, University of Essen Medical School, Essen, Germany
* To whom correspondence should be addressed. E-mail: rainer_schulz{at}uni-essen.de.
In animals and patients with severe heart failure (HF) the serum tumor necrosis factor 
(TNF) concentration is increased. It is, however, still controversial whether or not such increased serum TNF originates from the heart itself or is of peripheral origin secondary to gastrointestinal congestion and increased endotoxin concentration. We therefore now examined TNF in serum, myocardium and liver of sham and HF rabbits.
In 9 rabbits, in which HF was induced by left ventricular (LV) pacing at 400 bpm for 3 weeks, LV end-diastolic diameter was increased and systolic shortening fraction (9.4±1.0 vs. 28.5±1.3%, echocardiography, p<0.05) reduced. Serum TNF was higher in HF than in sham rabbits (240±24 vs. 150±22 U/ml, WEHI-cell assay, p<0.05). In the heart, TNF was located mainly in the vascular endothelium (immunohistochemistry) and TNF protein (920±160 vs. 900±95 U/g) did not differ between groups. In the liver of HF rabbits, hepatocytes expressed TNF, and TNF protein was increased compared to sham rabbits (2,390±310 vs. 1,220±135 U/g, p<0.05) and correlated to the number of hepatic leukocytes (r=0.85) and serum TNF (r=0.69). The intestinal endotoxin concentration was 24.5±1.2 vs. 17.0±3.1 EU/g wet weight (p<0.05) in HF compared to sham rabbits.
In this HF model, serum but not myocardial TNF is increased. The increased serum TNF originates from peripheral sources.
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