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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 38 (1995), S. 509-517 
    ISSN: 1432-0428
    Keywords: 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.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 38 (1995), S. 509-517 
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Cardiovascular drug reviews 17 (1999), S. 0 
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 293 (1976), S. 39-47 
    ISSN: 1432-1912
    Keywords: Cardiac glycosides ; Membranes ; Lecithin ; Phase separation ; Spin-label
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The binding of digitoxigenin to lecithin model membranes was investigated by application of electron spin- and nuclear magnetic resonance methods. A digitoxigenin spin-label derivative was found to bind specifically to the pseudohexagonal rigid lattice of lecithin membranes. The binding is accomplished by some of the structural features which are required for the biological activity of cardiac glycosides. Digitoxigenin has a procooperative effect on dipalmitoyl-lecithin membranes. The induction of lipid phase separation is discussed as a hypothetic molecular mechanism of action of cardiac glycosides on biological membranes.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1912
    Keywords: Thromboxane A2 (TXA2) ; Prostacyclin (PGI2) ; Human platelets ; Bovine coronary artery ; Non-steroidal antiinflammatory drugs ; Prostaglandin-cyclooxygenase ; Bioassay ; RCS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The action of the non-steroidal antiinflammatory drugs indomethacin, tiaprofenic acid, diclofenac and meclofenamate on vascular and plateletcyclooxygenases was studied by measuring the arachidonic acid-induced thromboxane A2 (TXA2)-formation of washed human platelets and prostacyclin (PGI2)-formation of bovine coronary artery rings. TXA2 was bioassayed as RCS on rabbit aorta strips, PGI2 in terms of its antiaggregatory activity on ADP-induced aggregation of human platelet-rich plasma. All of the substances studied produced concentration-dependent inhibition of PGI2- and RCS-release. The IC50 [μM] in inhibition of RCS-formation was 0.019 for indomethacin, 0.070 for tiaprofenic acid but 44.9 for meclofenamate and 63.2 for diclofenac. The IC50 [μM] in inhibition of PGI2-release was 0.42 for diclofenac, 0.63 for indomethacin and 0.99 for tiaprofenic acid. The data suggest (1) high sensitivity of human platelet-cyclooxygenase against indomethacin and tiaprofenic acid, (2) different sequence of the substances studied in inhibiting arachidonic acid-induced TXA2- and PGI2-formation. The possible therapeutic value of selective inhibition of platelets and vascular cyclooxygenases in discussed.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 431-434 
    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
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 79 (1984), S. 59-67 
    ISSN: 1435-1803
    Keywords: isolated heart ; guinea pig ; regional perfusion ; NADH ; surface fluorescence ; local ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In Langendorff-perfused guinea pig hearts, local myocardial perfusion was evaluated by analysis of FITC-dextran-150 elution kinetics after bolus injection. Locally estimated half-times of the monoexponential elution curves showed good correlation with global undisturbed coronary flow. After ligation of the left anterior descending coronary artery indicator transit kineties in the ischemic area were only slightly affected (increase of t/2 by 30±19%), indicating a residual flow of 80% to the ligated area. The moderate increase (40±20%) of NADH-surface fluorescence in the same area confirms a high degree of residual flow. Indicator partition volume (signal peak height after bolus injections) was additionally enhanced. Moreover, indicator transit kinetics changed from monoexponential to composed kinetics. On reperfusion these effects were partially reversible. Ligation of the left coronary artery at its aortic root produced only moderate ischemia, indicating very effective mechanisms in the isolated guinea pig heart from the right coronary artery to support the left ventricle. Severe ischemia as evidenced from NADH-surface fluorescence could be observed only after “stopped flow” ischemia.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 76 (1981), S. 416-420 
    ISSN: 1435-1803
    Keywords: surface fluorescence ; regional perfusion ; isolated heart ; adenosine ; dipyridamol ; sodium nitrite ; verapamil
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In isolated guinea pig hearts epicardial perfusion was estimated by analysis of the transit profile of different fluorescence indicators. Several coronary dilating agents were tested with regard to their influence on local perfusion kinetics revealing distinct patterns of microcirculatory drug action.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 87 (1992), S. 452-460 
    ISSN: 1435-1803
    Keywords: EDRF ; methemoglobin ; nitric oxide ; nitrendipine ; vasorelaxation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recent studies suggest endothelium to be involved in the vasorelaxation of calcium antagonists of the 1,4-dihydropyridine type, which may at least in part be mediated by endothelium-derived relaxing factor (EDRF=NO). To study this effect further, the influence of L-NG-nitro arginine (L-NNA), a specific inhibitor of EDRF-synthesis, on nitrendipine-induced vasorelaxation was examined in different isolated porcine arteries. Coronary, basilary, and tail arteries were bathed in Krebs-Henseleit solution and endothelial function was verified by means of substance P, and EDRF releasing neuropeptide. Vasorelaxation of nitrendipine in PGF2α-precontracted arteries was studied in the presence and absence of L-NNA. Nitrendipine-induced vasorelaxation was markedly reduced by the addition of L-NNA in all vessels studied. Tachyphylactic effects of nitrendipine could be excluded. The obtained results may be explained by an enhancement of nitrendipine action by basally released EDRF, alternatively, by an increased EDRF-release induced by this calcium antagonist. Therefore, in a second series of experiments the release of EDRF was studied in isolated coronary arteries under cumulative application of nitrendipine. Using the nitric oxide scavenging properties of oxyhemoglobin, EDRF release was measured spectrophotometrically by means of methemoglobin formation. The application of nitrendipine resulted in a concentration-dependent increase in the extinction rate, indicating an increased release of NO which could be inhibited by preincubation with L-NNA. It may be concluded that, in functionally intact vessels, vasorelaxation induced by nitrendipine may additionally be mediated by an increased release of EDRF.
    Type of Medium: Electronic Resource
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