Minoxidil-induced cardiac hypertrophy in guinea pigs

To investigate whether during cardiac hypertrophy changes occur in contractile protein composition and in mechanical and energetic properties of the myocardium, contractile protein composition, isometric force and adenosine triphosphate (ATP) consumption were studied in control and hypertrophied guinea-pig hearts. Cardiac hypertrophy was induced by adding minoxidil (120 or 200 mg/l) to the drinking water. Protein analysis was performed by one-dimensional gel electrophoresis. The myosin heavy-chain (MHC) composition was determined in an enzyme-linked immunosorbent assay (ELISA). ATP consumption and force development were simultaneously measured during isometric contraction in chemically skinned trabeculae. Histochemical analysis of cross-sectional area of cardiomyocytes and interstitial space was performed on the left ventricular tissue of 200 mg/l minoxidil-treated and control guinea pigs. Minoxidil treatment (120 and 200 mg/l) significantly increased left ventricular dry weight normalized for body weight by 19 ± 4 and 24 ± 4%, respectively. No significant differences were found in the cellular cross-sectional area, while interstitial space was slightly decreased in minoxidil-treated hearts. In left ventricular trabeculae of 200 mg/l minoxidil-treated guinea pigs, ATPase activity was slightly less than in those of control guinea pigs, whereas force did not differ significantly. Calcium sensitivity of force and ATPase activity were not affected by minoxidil treatment. Gel electrophoresis revealed no difference in contractile protein composition, but a tendency towards a lower amount of α-MHC in the minoxidil-treated hearts was found in ELISA. Received 1 February 1999; accepted 15 March 1999     

Ethanol inhibition of audiogenic stress induced cardiac hypertrophy

Zusammenfassung Gruppen weiblicher jungfräulicher Albinoratten wurden 2 Wochen lang periodischem Lärm-und Geräuschhintergrund ausgesetzt, während welcher Zeit sie entweder Leitungswasser oder Äthanol trinken durften. Kontrollgruppen wurden bei Abwesenheit des Lärmhintergrunds geprüft. Herzhypertrophie konnte in den Kontrollgruppen mit Äthanol und bei den Ratten (mit Lärmhintergrund) beobachtet werden. Nach Behandlung mit Äthanol war die Herzhypertrophie nicht mehr vorhanden.

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This study was supported by grants from the South Dakota Heart Association and USPHS No. HE-6488. The authors wish to express their appreciation toJ. A. Richardson, P. L. Mayclin andN. L. Burns for invaluable assistance in the technical and construction phases of the present study.     

Failure of cortisone and ACTH to regulate cardiac hypertrophy

Résumé L'hypertrophie cardiaque provoquée chez des rats mâles par un exercice forcé n'a été régularisée ni par la cortisone ni par l'ACTH utilisées chacune à 2 doses différentes.

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Supported by a grant from the West Virginia Heart Association.     

A pharmacological investigation of the influence of suxamethonium on cardiac function in the horse

Résumé Les auteurs étudient les différences quantitatives et qualitatives de l'effet du suxamethonium sur la fonction cardiaque chez des chevaux concients et des chevaux soumis à une anesthésie générale. Ils ont aussi contrôlé l'efficacité du propranolol, agent d'arrêt de transmission-adrénergique, empêchant tout changement dans les fonctions du cur.     

Methimazole treatment reduces cardiac hypertrophy and mortality without a concomitant reduction in blood pressure in established Goldblatt two-kidney one clip hypertension

The effects of methimazole, and antithyroid drug, on blood pressure and other parameters were evaluated in the established phase of Goldblatt two-kidney one clip (G2K-1C) hypertension. Methimazole was administered via drinking water for five weeks, starting five weeks after hypertension had been induced. After this period of treatment, similarly high blood pressures were observed in methimazole-treated and non-treated G2K-1C rats, despite the fact that a hypothyroid state had been achieved in methimazole-treated rats. Methimazole-treated G2K-1C rats showed reductions in heart rate, ventricular weight, ventricular/body weight ratio and mortality in comparison with rats not treated with methimazole. These results clearly demonstrate that hypothyroidism induced by methimazole: a) does not reverse G2K-1C hypertension, but b) improves the rate of survival and c) reduces relative cardiac hypertrophy, possibly by the reduction in cardiac work observed in Goldblatt hypothyroid rats.     

The effect of monoamine synthesis-inhibitors on the ovarian compensatory hypertrophy

Resumen La administración continuada de-metilpara-tirosina, un inhibidor de la síntesis de catecolaminas, impide la hipertrofia compensadora del ovario en ratas. Este efecto es prevenido por la simultânea injección de DOPA, un. precursor de las catecolaminas. El grado de la hipertrofia compensadora del ovario no fue modificado por lap-cloro-fenilalanina, un inhibidor de la síntesis de serotonina. El estudio histológico de los ovarios de los animales tratados con MPT sugiere que ésta bloquea la ovulación, no modificando aparentemente la secreción tonica de las gonadotrofinas FSH y LH.

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A grant from the Consejo Nacional de Investigaciones Científicas y Tecnicas of Argentina supported this research.-methylp-Tyrosine was a gift from Dr.Karl Pfister of Merck Sharp & Dohme Research Laboratories.     

Methimazole treatment reduces cardiac hypertrophy and mortality without a concomitant reduction in blood pressure in established Goldblatt two-kidney one clip hypertension.

The effects of methimazole, an antithyroid drug, on blood pressure and other parameters were evaluated in the established phase of Goldblatt two-kidney one clip (G2K-1C) hypertension. Methimazole was administered via drinking water for five weeks, starting five weeks after hypertension had been induced. After this period of treatment, similarly high blood pressures were observed in methimazole-treated and non-treated G2K-1 C rats, despite the fact that a hypothyroid state had been achieved in methimazole-treated rats. Methimazole-treated G2K-1 C rats showed reductions in heart rate, ventricular weight, ventricular/body weight ratio and mortality in comparison with rats not treated with methimazole. These results clearly demonstrate that hypothyroidism induced by methimazole: a) does not reverse G2K-1 C hypertension, but b) improves the rate of survival and c) reduces relative cardiac hypertrophy, possibly by the reduction in cardiac work observed in Goldblatt hypothyroid rats.     

The pathogenesis of cardiac fibrosis

Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins, and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression, and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.     

Numerical hyperplasia in human heart hypertrophy

Zusammenfassung Mit Hilfe kombinierter biochemischer und zytophotometrischer DNS-Messungen wurde die Anzahl der Herzmuskelzellen in Menschenherzen bestimmt. Normale Menschenherzen (330 g) haben nach dieser Berechnung 2×10⁹ Muskelzellen. In hypertrophierten Herzen (500–900 g) nimmt die Zellzahl bis auf 4 × 10⁹ Muskelzellen zu.     

Bilateral ovarian hypertrophy in pituitary-grafted rats

Summary Large masses that looked like tumours were found in place of the ovaries in rats with isotransplants of pituitaries, 11 months after this procedure. They were interpreted as being due to massive bilateral cystic hyperplasia and hypertrophy of both ovaries.Acknowledgments. This work was supported by research grants from the Fundación Cherny and from The Consejo Nacional de Investigaciones Científícas y Técnicas.     

Palliative effect of gelatine in benign prostatic hypertrophy

Résumé. La consommation journalière de 25 g de gélatine soulage rapiderment les symptomes urinaires accompagnant l'hypertrophie prostatique bénigne. La gélatine peut être trés utile dans le traitement de ce désordre.     

The experimental induction of ultrastructural damage in cardiac muscle

Experimentally-induced rises in intracellular calcium ([Ca2+]i) promote rapid myofilament degradation in amphibian and mammalian cardiac muscle strips. The relevance of these studies to the subcellular injury produced by ischaemia, the possible involvement of lysosomal enzymes and similarities with skeletal muscle are discussed.     

The influence of salt intake on glomerular count in compensatory kidney hypertrophy in rats of different ages

Summary Drinking saline instead of water elevated the glomerular count in hypertrophied kidneys of rats uninephrectomized as adults. No changes occurred in glomerular concentration in kideny tissue indicating a more marked increase of other kidney structures. This procedure was ineffective in immature animals.     

On the mechanism of compensatory hypertrophy in skeletal muscles

Riassunto L'ipertrofia compensatoria dei muscoli soleo e plantare di ratto in seguito a tenotomia del sinergista gastrocnemio non appare mediata dall'innervazione, ma è verosimilmente legata a un effetto diretto della accresciuta tensione meccanica sui muscoli interessati.     

Effects of thyroidectomy on ovarian compensatory hypertrophy in rats

Résumé Le nombre de corps jaunes dans l'ovaire de rates intactes, hémicastrées, hémicastrées et thyroïprivées fut déterminé. Les corps jaunes de l'animal thyroïprivé et hémicastré furent sensiblement plus petits que ceux de l'animal hémicastré. Cette diminution des corps jaunes se traduit par une diminution concomitante du poids ovarien et pourrait expliquer le blocage partiel de l'hypertrophie compensatrice du reste de l'ovaire.