Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Progression of heart failure: a role for interstitial fibrosis.
H N Sabbah; V G Sharov; M Lesch; S Goldstein (Profiled Author: Hani N Sabbah)
Department of Medicine, Henry Ford Heart and Vascular Institute, Detroit, Michigan, USA.
Molecular and cellular biochemistry 1995;147(1-2):29-34.
Progressive deterioration of left ventricular (LV) function is a characteristic feature of the heart failure (HF) state. The mechanism or mechanisms responsible for this hemodynamic deterioration are not known but may be related to progressive intrinsic dysfunction, degeneration and loss of viable cardiocytes. In the present study, we tested the hypothesis that accumulation of collagen in the cardiac interstitium (reactive interstitial fibrosis, RIF), known to occur in HF, results in reduced capillary density (CD = capillary/fiber ratio) and increased oxygen diffusion distance (ODD) which can lead to hypoxia and dysfunction of the collagen encircled myocyte. Studies were performed in LV tissue obtained from 10 dogs with chronic HF (LV ejection fraction 26 +/- 1%) produced by multiple sequential intracoronary microembolizations. In each dog, CD and ODD were evaluated in LV regions that manifested severe RIF (volume fraction 16 +/- 2%) and in LV regions of little or no RIF (volume fraction 4 +/- 1%). In regions of severe RIF, CD was significantly decreased compared to regions of no RIF (0.92 +/- 0.02 vs. 1.05 +/- 0.03) (P < 0.003). Similarly, ODD was significantly increased in regions of severe RIF compared to regions of no RIF (15.3 +/- 0.4 vs. 12.2 +/- 0.3 microns) (P < 0.001). These data suggest that in dogs with chronic HF, constituent myocytes of LV regions which manifest severe RIF may be subjected to chronic hypoxia; a condition that can adversely impact the function and viability of the collagen encircled cardiocyte.
1 Originating Grant
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1.
Sabbah, Hani N
1 April 1994 - 31 December 2003
NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Total Funding: $ 2,329,997
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
Sabbah, Hani N
1 April 1994 - 31 December 2003
NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
Total Funding: $ 2,329,997
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2.
FRANK, ROBERT N
RETINAL CELLS: TISSUE CULTURE AND CELL BIOLOGY
30 September 1976 - 30 November 1994
NATIONAL EYE INSTITUTE
Total Funding: $ 2,189,726
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3.
ZHANG, KEZHONG
Hepatic Steatosis and ER Stress-Inducible Transcription Factor CREBH
1 January 2011 - 31 December 2015
NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES
Total Funding: $ 975,080
Related Publications
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1.
1997Y H Liu; X P Yang; O Nass; H N Sabbah; E Peterson; O A Carretero
Chronic heart failure induced by coronary artery ligation in Lewis inbred rats.
The American journal of physiology 1997;272(2 Pt 2):H722-7. -
2.
2002George Suzuki; Hideaki Morita; Takayuki Mishima; Victor G Sharov; Anastassia Todor; Elaine J Tanhehco; Amy E Rudolph; Ellen G McMahon; Sidney Goldstein; Hani N Sabbah
Circulation 2002;106(23):2967-72. -
3.
2000H N Sabbah; V G Sharov; S Goldstein
Cell death, tissue hypoxia and the progression of heart failure.
Heart failure reviews 2000;5(2):131-8.
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