Literature DB >> 2423210

Coronary capillaries during normal and pathological growth.

P Anversa, R Ricci, G Olivetti.   

Abstract

The adaptive capacity of the myocardium with respect to its capillary concentration and distribution has been measured morphometrically during the hypertrophic growth occurring physologically after birth and as a result of induced overload in the adult. In particular, the growth of the capillary network of the left ventricle was examined in rats from one to 150 days of age and in rats with spontaneous hypertension, aortic stenosis, two-kidney one-clip renal hypertension and myocardial infarction. The following quantitative structural parameters of the capillary microvasculature were analyzed: 1. Capillary luminal volume density; 2. Capillary luminal surface density; 3. The average diffusion distance for oxygen; and 4. The aggregate capillary length in the whole ventricle. The major conclusions of the present study are: 1. The postnatal growth of the heart is characterized by lengthening of the whole capillary network that is linearly related to the aging process; 2. The rate of capillary proliferation, measured by changes in capillary density, is greater in the first month of age; 3. In contrast to postnatal development, lengthening of the capillary microvasculature is not a consistent adaptive mechanism of induced cardiac hypertrophy; 4. Capillary luminal volume and surface densities and the diffusion distance for oxygen are essentially maintained in spontaneous, mechanical and renal hypertension; and 5. Cardiac hypertrophy in acute and healed myocardial infarction results in alterations of the capillary properties implicated in tissue oxygenation that may constitute the morphological counterpart of the greater vulnerability to ischemic episodes of the hypertrophied myocardium after infarction.

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Year:  1986        PMID: 2423210

Source DB:  PubMed          Journal:  Can J Cardiol        ISSN: 0828-282X            Impact factor:   5.223


  5 in total

1.  Myocyte cellular hypertrophy and hyperplasia contribute to ventricular wall remodeling in anemia-induced cardiac hypertrophy in rats.

Authors:  G Olivetti; F Quaini; C Lagrasta; R Ricci; G Tiberti; J M Capasso; P Anversa
Journal:  Am J Pathol       Date:  1992-07       Impact factor: 4.307

2.  Nerve growth factor promotes cardiac repair following myocardial infarction.

Authors:  Marco Meloni; Andrea Caporali; Gallia Graiani; Costanza Lagrasta; Rajesh Katare; Sophie Van Linthout; Frank Spillmann; Ilaria Campesi; Paolo Madeddu; Federico Quaini; Costanza Emanueli
Journal:  Circ Res       Date:  2010-04-01       Impact factor: 17.367

3.  Up-regulation of soluble vascular endothelial growth factor receptor-1 prevents angiogenesis in hypertrophied myocardium.

Authors:  Elisabeth Kaza; Klemens Ablasser; Dimitrios Poutias; Eric R Griffiths; Fawzy A Saad; Jochen G Hofstaetter; Pedro J del Nido; Ingeborg Friehs
Journal:  Cardiovasc Res       Date:  2010-10-08       Impact factor: 10.787

Review 4.  Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts.

Authors:  Sanford P Bishop; Jianyi Zhang; Lei Ye
Journal:  Biology (Basel)       Date:  2022-06-08

5.  Cardiac overexpression of human VEGF(165) by recombinant Semliki Forest virus leads to adverse effects in pressure-induced heart failure.

Authors:  A E Loot; A J M Roks; D Westermann; H-D Orzechowski; C Tschöpe; J C Wilschut; R A Tio; W H van Gilst; R H Henning
Journal:  Neth Heart J       Date:  2007       Impact factor: 2.380

  5 in total

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