Literature DB >> 6213304

Effect of volume-overload hypertrophy on the coronary circulation awake dogs.

J A Gascho, T M Mueller, C Eastham, M L Marcus.   

Abstract

Inadequate coronary reserve is present in left ventricular hypertrophy secondary to hypertension. Since this abnormality might be due in part to vascular hypertrophy of coronary resistance vessels in response to chronic hypertension, we studied a model of ventricular hypertrophy without hypertension. Volume-overload hypertrophy was produced by creating complete heart block in mongrel dogs; 6 to 7 weeks later the dogs were studied in the awake state. The thirteen dogs with chronic heart block had a 49% increase (P less than 0.05) in left ventricular mass compared with eight control dogs. The major findings in this study were: 1) at rest, coronary blood flow (microsphere technique) per unit weight of left ventricle was not increased in dogs with hypertrophy; and 2) the minimal coronary vascular resistance per unit weight of left ventricle calculated during iv adenosine infusion at a rate that produced maximal vasodilatation was not significantly higher in dogs with left ventricular hypertrophy than in controls (16.4 +/- 1.0 vs 14.7 +/- 1.5 kPa . litre-1 . min . 100 g, respectively). Minimal coronary vascular resistance of the entire left ventricle was significantly less in dogs with hypertrophy than controls (13.0 +/- 0.8 vs 17.3 +/- 1.7 kPa . litre-1 . min, respectively). This data suggests that vascular hypertrophy of coronary resistance vessels related to chronic hypertension may be the cause of the increased minimal coronary vascular resistance seen in dogs with pressure-overload left ventricular hypertrophy.

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Year:  1982        PMID: 6213304     DOI: 10.1093/cvr/16.5.288

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  3 in total

1.  Myocardial characteristics of thyroxine stimulated hypertrophy. A structural and functional study.

Authors:  E A Breisch; F C White; H K Hammond; S Flynn; C M Bloor
Journal:  Basic Res Cardiol       Date:  1989 Jul-Aug       Impact factor: 17.165

2.  Chronic nitric oxide inhibition as a model of hypertensive heart muscle disease.

Authors:  H Moreno; K Metze; A C Bento; E Antunes; R Zatz; G de Nucci
Journal:  Basic Res Cardiol       Date:  1996 May-Jun       Impact factor: 17.165

Review 3.  Growth factor activation in myocardial vascularization: therapeutic implications.

Authors:  Robert J Tomanek; Wei Zheng; Xinping Yue
Journal:  Mol Cell Biochem       Date:  2004-09       Impact factor: 3.396

  3 in total

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