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  • Articles: DFG German National Licenses  (2)
  • 1990-1994  (2)
  • 1965-1969
  • 1915-1919
  • 1993  (2)
  • cardiac hypertrophy  (2)
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  • Articles: DFG German National Licenses  (2)
Material
Years
  • 1990-1994  (2)
  • 1965-1969
  • 1915-1919
Year
  • 1993  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 129 (1993), S. 101-120 
    ISSN: 1573-4919
    Keywords: collagen ; cardiac hypertrophy ; heart failure ; diabetic cardiomyopathy ; myocardial infarction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The cardiac interstitium is populated by nonmyocyte cell types including transcriptionally active cardiac fibroblasts and endothelial cells. Since these cells are the source of many components of the cardiac extracellular matrix, and because changes in cardiac extracellular matrix are suspected of contributing to the genesis of cardiovascular complications in disease states such as diabetes, hypertension, cardiac hypertrophy and congestive heart failure, interest in the mechanisms of activation of fibroblasts and endothelial cells has led to progress in understanding these processes. Recent work provides evidence for the role of the renin-angiotensin-aldosterone system in the pathogenesis of abnormal deposition of extracellular matrix in the cardiac interstitium during the development of inappropriate cardiac hypertrophy and failure. The cardiac extracellular matrix is also known to change in response to altered cardiac performance associated with post-natal aging, and in response to environmental stimuli including intermittent hypoxia and abnormal nutrition. It is becoming clear that the extracellular matrix mainly consists of molecules of collagen types I and III; they form fibrils and provide most of the connective material for tying together myocytes and other structures in the myocardium and thus is involved in the transmission of developed mechanical force. The data available in the literature support the view that the extracellular matrix is a dynamic entity and alterations in this structure result in the development of heart dysfunction.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cardiovascular drugs and therapy 7 (1993), S. 611-619 
    ISSN: 1573-7241
    Keywords: transient outward current ; cardiac hypertrophy ; whole-cell voltage clamp ; cardiac myocytes ; right ventricular hypertrophy ; Ito regulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cardiac hypertrophy can decrease myocardial contractility and alter the electrophysiological activity of the heart. It is well documented that action potentials recorded from hypertrophied feline ventricular cells can exhibit depressed plateau voltages and prolonged durations. Similar findings have been made by others in rabbit, rat, guinea pig, and human heart. Whole-cell patch voltage-clamp studies designed to explain these changes in the action potential suggest that the only component of the membrane current recorded from feline right ventricular (RV) myocytes found to be substantially different from normal is the 4-aminopyridine-sensitive transient outward current (Ito). However, it was not clear if the change in Ito could explain the changes in the action potential of hypertrophied cardiocytes, nor was it clear if these changes reflect an alteration in the electrophysiological character of the channels underlying Ito. A kinetic comparison of Ito elicited by hypertrophied RV myocytes with that elicited by comparable normal RV myocytes previously revealed no differences, suggesting that the increased magnitude of the peak Ito recorded from hypertrophied myocytes arises because the current density increases and not because of any alteration in the kinetic parameters governing the current. This finding suggests that in hypertrophy additional normal channels are expressed rather than a kinetically different channel subtype emerging. Investigations designed to determine if enhancement of Ito could explain the hypertrophy-induced changes in plateau voltage and action potential duration suggest that a change in Ito density can indeed explain the entire effect of hypertrophy on RV action potentials. If this notion is correct, the likelihood of “sudden death” in patients with myocardial hypertrophy might be decreased by a blocker selective for cardiac Ito.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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