title: Chronic cardiac reactions. III. Factors involved in the development of structural dilatation.
abstract: The significance of various factors for the development of structural dilatation in the chronically pressure-loaded and failing heart were evaluated. The investigations were performed on male rats with renal (Goldblatt II) and spontaneous (Aoki-Okamoto) hypertension at different stages of haemodynamic overload. Two groups of SHR were submitted to intermittent feeding (SHR IF); one group received additionally the beta-blocking agent atenolol (50 mg/kg b.w.; SHR IF + beta Bl.). Haemodynamic measurements were carried out under open chest conditions. Myosin isoenzyme pattern, hydroxyproline concentration and circulating blood volume were determined. Transformation to slower myocardium per se, induced by IF, did not lead to significant change in ventricular configuration. After additional blockade of beta-adrenergic receptors there were indications of unfavourable development of left ventricular configuration. Inhibition of hypertrophic mass increase due to curtailed adrenergic stimulation could be an influential factor in the development of dilatation. Further investigations, however, are required to establish the relationship between the adrenergic system, on the one hand, and degree of hypertrophy as well as structural dilatation of the ventricle, on the other hand. The established marked increase in hydroxyproline concentration of the dilated ventricle of SHR in congestive failure is consistent with the assumption of a causal link between the degree of fibrosis and structural dilatation. Observations on rats with aorto-caval shunt and Goldblatt II rats with eccentric hypertrophy and corresponding increase in filling potential or circulating blood volume indicate a correlation between the latter and ventricular size. Thus, we assume that curtailed protein synthesis, fibrosis and regulatory processes related to water and electrolyte balance, but not myocardial transformation per se, play a role in the development of structural dilatation. The relative contribution of each factor, however, may depend on the experimental model that is used.
authors: Physiologisches Institut II, Universität Tübingen, F.R.G.
authors: M
authors: M
authors: Vogt
authors: R
authors: R
authors: Jacob
authors: K
authors: K
authors: Noma
authors: B
authors: B
authors: Onegi
authors: H
authors: H
authors: Rupp
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D008297:Male; D014176:Protein Biosynthesis; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains