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  • Key words Diabetes mellitus  (1)
  • Myocardial ischemia  (1)
  • 1
    Electronic Resource
    Electronic Resource
    The ACE-inhibitor captopril improves myocardial perfusion in spontaneously diabetic (BB) rats (1995)
    Springer
    Diabetologia 38 (1995), S. 509-517 
    Details
    ISSN: 1432-0428
    Keywords: Key words Diabetes mellitus ; cardiopathy ; ACE-inhibition ; captopril ; BB rats ; regional perfusion ; myocardial function.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this study was to examine the influence of inhibition on angiotensin converting enzyme (ACE) of myocardial function and perfusion of the rat impaired by diabetes. Spontaneously diabetic rats were treated with the ACE-inhibitor captopril for 4 months. Cardiac performance was analysed in the isolated heart perfused at constant volume. Epicardial perfusion was determined by measuring changes in epicardial fluorescence after injection of a bolus of fluoresceinisothiocyanate-dextrane (3 kDa) as described previously. As compared to untreated diabetic controls, captopril prevented the increase of end diastolic pressure, coronary perfusion pressure and vascular resistance. The intravascular volume was enlarged and the epicardial perfusion rate increased in hearts of diabetic rats treated with captopril as compared to diabetic controls. Treatment of diabetic rats with the ACE-inhibitor captopril (1) increases the number of perfused capillaries, and (2) can partly prevent the development of cardiac dysfunction in diabetes. Together with morphological data demonstrating an inhibition of interstitial and perivascular fibrosis in hearts of diabetic rats treated with captopril, our data suggest that ACE-inhibition is cardioprotective in diabetes. These observations are also compatible with the assumption that an accelerated generation of angiotensin II may be involved in the pathophysiological chain of events leading to diabetic cardiopathy. [Diabetologia (1995) 38: 509–517]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400718
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Free radical scavenging properties of β-adrenoceptor blockers are not relevant for cardioprotection in isolated rabbit hearts (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 431-434 
    Details
    ISSN: 1432-1912
    Keywords: Myocardial ischemia ; Cardioprotection - ; NADH-fluorescence ; SOD ; β-adrenoceptor blockers ; Propranolol ; Pindolol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Several β-adrenoceptor-blocking agents have been shown to possess free radical scavenging properties. Therefore, the direct cardioprotective properties of propranolol or pindolol were investigated in comparison to superoxide dismutase (SOD). We used isolated rabbit hearts paced at a constant rate (Langendorff, constant pressure: 70 cm H2O, Tyrode solution, Ca2+ 1.8 mmol/l). Acute regional myocardial ischemia (MI) was induced by left coronary artery branch occlusion and quantitated from epicardial NADH-fluorescence photography. Propranolol (10−8 mol/l), pindolol (10−6 mol/l) or SOD (48 I.U./ml) had no significant influence on left ventricular pressure, pressure-rate product or global coronary flow (p 〉 0.05). Whereas epicardial NADH-fluorescence area after repetitive coronary occlusions was significantly diminished by SOD-treatment (−25%) (p 〈 0.05), MI size was not significantly affected by either propranolol or pindolol (p 〉 0.05). Conclusion: Oxygen-derived free radicals contribute to tissue injury during myocardial ischemia, and propranolol or pindolol do not possess free radical scavenging properties relevant for cardioprotection in a repetitive coronary occlusion model in isolated rabbit hearts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171344
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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