COLLAGEN CHARACTERIZATION IN VOLUME-OVERLOAD-INDUCED AND PRESSURE-OVERLOAD-INDUCED CARDIAC-HYPERTROPHY IN MINIPIGS

Citation
J. Harper et al., COLLAGEN CHARACTERIZATION IN VOLUME-OVERLOAD-INDUCED AND PRESSURE-OVERLOAD-INDUCED CARDIAC-HYPERTROPHY IN MINIPIGS, The American journal of physiology, 265(2), 1993, pp. 80000434-80000438
Citations number
32
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
265
Issue
2
Year of publication
1993
Part
2
Pages
80000434 - 80000438
Database
ISI
SICI code
0002-9513(1993)265:2<80000434:CCIVAP>2.0.ZU;2-N
Abstract
Previous studies in several different species have shown reduced extra ctability of collagens in some types of cardiac hypertrophy (volume ov erload) but not others (pressure overload). The objective of the prese nt study was to examine collagen proteins from the same species (minip igs) with both pressure-overload- and volume-overload-induced cardiac hypertrophy. Hypertrophy was induced by two methods: thoracic banding of the aorta to create pressure overload and arteriovenous shunt to ca use volume overload in a porcine model. Collagen types I, III, IV, and V were isolated by pepsin digestion from normal and hypertrophied pig left ventricle tissues. Types I and III collagens from normal and hyp ertrophied samples, when separated from types IV and V, were digested with cyanogen bromide (CB), and the peptides were examined. Collagen c oncentration was increased in myocardium removed from hearts subjected to volume overload and unchanged in hearts subjected to pressure over load. The extractability of total collagen was unaffected in pressure- overloaded left ventricles but lower in samples from volume-overloaded hearts. CB digestion cleaved all of the types I and III collagens int o similar smaller CB peptides with the exception of a 100-kDa peptide that was observed in both control and hypertrophied hearts. This pepti de corresponds to one of the high-molecular-weight peptides found in c anine heart tissue. The. mature collagen cross-link hydroxylysylpyridi noline (HP) was identified in normal and hypertrophied types I and III collagen from porcine sources. Pressure-overload- and volume-overload -induced cardiac hypertrophy in the pig produced different alterations in the extracellular matrix. Collagen concentration was increased in hearts from arteriovenous fistula animals but not pressure-overload an imals. Reductions in extraction of collagens were also observed in the fistula model but not in the pressure overload of animals.