Synergistic effects of diabetes mellitus and renovascular hypertension on the rat heart - stereological investigations on papillary muscles View Full Text


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Article Info

DATE

1987-11

AUTHORS

G. Mall, K. Klingel, H. Baust, Ch. Hasslacher, J. Mann, T. Mattfeldt, R. Waldherr

ABSTRACT

The effects of combined renovascular hypertension and diabetes mellitus on the rat heart were investigated in order to detect possible synergistic effects of the two conditions. Hypertensive diabetic and hypertensive nondiabetic young male Wistar rats were compared with diabetic and nondiabetic controls. Since the normal body weight increase of the diabetic animals was markedly suppressed a weight-matched nondiabetic control group was introduced in addition. Hypertension was established for eight weeks by a surgical stenosis of the left renal artery, diabetes mellitus was maintained for four weeks after a single intraperitoneal injection of 75 mg/kg streptozotocin. Light and electron microscopic stereological parameters were obtained for the left ventricular papillary muscles. The whole hearts were also investigated histologically. Qualitative morphology failed to substantiate synergistic effects in the hypertensive diabetic rats. Vascular abnormalities were not observed. The stereological parameters, however, revealed microstructural reactions which were observed exclusively in the hypertensive diabetic group: the volume ratio of mitochondria-to-myofibrils was decreased, the surface-to-volume ratio of mitochondria was increased (reduction of mitochondrial size) and the mean cross sectional area of capillaries was decreased. Similar quantitative mitochondrial changes have been frequently described in long-standing hypertension, but in the present investigation, they were not found in the nondiabetic hypertensive group. It is therefore concluded that diabetes mellitus potentiates the effects of chronic pressure overload on myocardial cells. However, the myocardial fibrosis which has been found by other groups at later stages of hypertension and/or diabetes mellitus was not detected in the present study. The reduced mean cross sectional area of capillaries in hypertensive-diabetic rats may be correlated with early molecular changes of the myocardial interstitium or with early abnormalities of small arteries. Thus our stereological results support the hypothesis that a non-coronary hypertensive diabetic cardiomyopathy occurs in mammalian hearts. More... »

PAGES

531-542

References to SciGraph publications

  • 1983. Cardiac Adaptation to Hemodynamic Overload, Training and Stress in NONE
  • 1987-01. Ultrastructural alterations in cardiac muscle of diabetic BB Wistar rats in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 1978-09. An effective morphometric method for electron microscopic studies on papillary muscles in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 1983. Chronic reactions of myocardium at the myofibrillar level Reflections on “adaptation” and “disease” based on the biology of long-term cardiac overload in CARDIAC ADAPTATION TO HEMODYNAMIC OVERLOAD, TRAINING AND STRESS
  • 1968-03. Über das Verhältnis Mitochondrien: Myofibrillen in den Herzmuskelzellen der Ratte bei Druckhypertrophie des Herzens in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 1983-01. Hypertensive diabetic cardiomyopathy in the rat: ultrastructural features in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 1969-11. Die Feinstruktur des Herzmuskels der Ratte nach einmaligem und nach wiederholtem Schwimmtraining in CELL PATHOLOGY
  • 1974. Angewandte Statistik, Planung und Auswertung Methoden und Modelle in NONE
  • 1983-03. Connective tissue content and myocardial stiffness in pressure overload hypertrophy A combined study of morphologic, morphometric, biochemical, and mechanical parameters in BASIC RESEARCH IN CARDIOLOGY
  • 1986-07. Stereology of myocardial hypertrophy induced by physical exercise in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 1980-11. Ultrastructural morphometric study on the rat heart after chronic ethanol feeding in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 1962-01. Über das Volumenverhältnis von Mitochondrien zu Myofibrillen im chronisch überlasteten, hypertrophierten Herzen in THE SCIENCE OF NATURE
  • 1984-12. Morphometric studies on retinal microangiopathy and myocardiopathy in hypertensive rats (SHR) with induced diabetes in CELL PATHOLOGY
  • 1983-12. Cardiac hypertrophy in rats after supravalvular aortic constriction in CELL PATHOLOGY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/bf00713284

    DOI

    http://dx.doi.org/10.1007/bf00713284

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1001241205

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/2960073


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    33 schema:description The effects of combined renovascular hypertension and diabetes mellitus on the rat heart were investigated in order to detect possible synergistic effects of the two conditions. Hypertensive diabetic and hypertensive nondiabetic young male Wistar rats were compared with diabetic and nondiabetic controls. Since the normal body weight increase of the diabetic animals was markedly suppressed a weight-matched nondiabetic control group was introduced in addition. Hypertension was established for eight weeks by a surgical stenosis of the left renal artery, diabetes mellitus was maintained for four weeks after a single intraperitoneal injection of 75 mg/kg streptozotocin. Light and electron microscopic stereological parameters were obtained for the left ventricular papillary muscles. The whole hearts were also investigated histologically. Qualitative morphology failed to substantiate synergistic effects in the hypertensive diabetic rats. Vascular abnormalities were not observed. The stereological parameters, however, revealed microstructural reactions which were observed exclusively in the hypertensive diabetic group: the volume ratio of mitochondria-to-myofibrils was decreased, the surface-to-volume ratio of mitochondria was increased (reduction of mitochondrial size) and the mean cross sectional area of capillaries was decreased. Similar quantitative mitochondrial changes have been frequently described in long-standing hypertension, but in the present investigation, they were not found in the nondiabetic hypertensive group. It is therefore concluded that diabetes mellitus potentiates the effects of chronic pressure overload on myocardial cells. However, the myocardial fibrosis which has been found by other groups at later stages of hypertension and/or diabetes mellitus was not detected in the present study. The reduced mean cross sectional area of capillaries in hypertensive-diabetic rats may be correlated with early molecular changes of the myocardial interstitium or with early abnormalities of small arteries. Thus our stereological results support the hypothesis that a non-coronary hypertensive diabetic cardiomyopathy occurs in mammalian hearts.
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