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Titolo:
STRUCTURAL REMODELING IN HEART-FAILURE - GELATINASE INDUCTION
Autore:
ARMSTRONG PW; MOE GW; HOWARD RJ; GRIMA EA; CRUZ TF;
Indirizzi:
UNIV ALBERTA,2F1 30 WALTER C MACKENZIE HLTH SCI CTR,DEPT MED,8440-112ST EDMONTON T6G 2R7 AB CANADA
Titolo Testata:
Canadian journal of cardiology
fascicolo: 2, volume: 10, anno: 1994,
pagine: 214 - 220
SICI:
0828-282X(1994)10:2<214:SRIH-G>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Keywords:
HEART FAILURE; MATRIX METALLOPROTEINASE; REMODELING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
NO
Recensione:
Indirizzi per estratti:
Citazione:
P.W. Armstrong et al., "STRUCTURAL REMODELING IN HEART-FAILURE - GELATINASE INDUCTION", Canadian journal of cardiology, 10(2), 1994, pp. 214-220

Abstract

OBJECTIVE: Rapid ventricular pacing in the dog produces severe congestive cardiac failure in association with neurohumoral activation and marked depression of cardiac function. This syndrome is associated withleft ventricular dilation, significant wall thinning, assumption of amore globular shape and disruption of the cardiac collagen infrastructure, given that the fibrillar collagen network is a major determinantof cardiac architecture. The purpose of the present study was to investigate whether there was evidence of increased activity of matrix metalloproteinases. The authors speculated that it could play an important permissive role in myocyte realignment, thereby resulting in the changes in cardiac size and shape. DESIGN: Twenty-one male mongrel dogs underwent ventricular pacing and were allocated into one of three groups: early heart failure (n=6), severe heart failure (n=7) and recoveredheart failure (n=8). Measurements included echocardiographic and hemodynamic parameters, plasma noradrenaline levels, left ventricular noradrenaline levels and matrix metalloproteinase activity. RESULTS: The study showed gelatinase activity present in normal left ventricular tissue predominantly attributable to a 72 kDa gelatinase (85%) and, to a much lesser extent, by a 92 kDa gelatinase (15%). Levels of 92 kDa gelatinase increased slightly within one week and reached maximal levels with severe heart failure, where it represented over one-half of the total gelatinase activity. In animals allowed to recover for four weeks, 92 kDa gelatinase decreased significantly to approximately 50% of the levels observed at severe heart failure. The levels of 72 kDa gelatinase did not change significantly during any experimental condition. Significant correlations between 92 kDa percentage activity and systolic and diastolic left ventricular areas across all time-points were evident (r=0.59 and 0.63, respectively, P<0.05 for both). CONCLUSION: Theassociation of 92 kDa gelatinase with changes in left ventricular area suggests a possible modulating role for this matrix metalloproteinase in disruption of the fibrillar components of the left ventricular extracellular matrix.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 02:20:59