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  • Articles: DFG German National Licenses  (3)
  • Prostaglandins  (2)
  • Antiplatelet actions  (1)
Source
  • Articles: DFG German National Licenses  (3)
Material
Years
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 64 (1986), S. 545-551 
    ISSN: 1432-1440
    Keywords: Iloprost ; Antiplatelet actions ; Blood pressure ; Regional perfusion ; Peripheral arterial obliterative disease (PAOD) ; Dose-response study ; Controlled trial
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The dose-dependent inhibition of platelet aggregation by the chemically stable, prostacyclin-mimetic, iloprost, was studied in patients suffering from stage II–III peripheral arterial obliterative disease (PAOD). The study was designed as a randomized placebo-controlled cross-over trial. Iloprost was administered i.v. to six patients at doses of 0.5, 1.0, 2.0 or 3.0 ng/kg×min for 4 h, with an interval of 2–3 days between the infusions. During iloprost infusion, systolic and diastolic arterial blood pressure, heart rate and blood flow in the affected limb remained unchanged. In contrast, there was a considerable, dose-dependent inhibition of ADP- and thrombin-induced platelet aggregation and secretion ex vivo at doses of 0.5–2.0 ng/kg×min iloprost, indicating that iloprost reduced platelet stimulation by 50%–70%. The antiplatelet action of iloprost remained unchanged during infusion but ceased with 2 h after administration had ended. The agent was tolerated by the patients without unacceptable side-effects at doses up to 2 ng/kg × min. It is concluded that iloprost administered i.v. at doses of 1–2 ng/kg×min in patients with stage II–III PAOD does not involve haemodynamic side-effects and might be considered an effective antiplatelet agent.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 18 (1980), S. 391-394 
    ISSN: 1432-0428
    Keywords: Prostaglandins ; prostacyclin ; PGE2 ; perfused rat heart ; prostaglandin endoperoxides ; coronary flow ; platelet aggregation ; streptozotocin diabetes ; bioassay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The release of prostacyclin and PGE2 from the isolated perfused hearts of acutely diabetic (streptozotocin 100 mg/kg) rats was studied and compared with hearts from control animals. Prostacyclin and PGE2 were measured by a differential bioassay technique. No basal release of either prostaglandin was detected. However, after addition of arachidonic acid, a dose dependent release of prostacyclin and PGE2 was noted. Prostacyclin was identified as the major prostaglandin. Release of prostacyclin and PGE2 from acutely diabetic rat hearts was increased 2–3 times compared to control hearts. No release of prostaglandin endoperoxides was observed in either group of hearts.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Basic research in cardiology 87 (1992), S. 2-11 
    ISSN: 1435-1803
    Keywords: Prostaglandins ; leukotrienes ; thromboxanes ; myocardialcontraction ; intracellularsignaling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eicosanoids (prostaglandins, leukotrienes, thromboxane A2 and other metabolites of C-20 polyunsaturated fatty acids) have numerous effects in the cardiovascular system. Direct inotropic actions have been repeatedly described, but appear in only very few cases to be due to direct modification of the inotropic state of the heart. Specific eicosanoid receptors have been identified on the surface of the sarcolemmal membrane. Signal transduction pathways in the cardiac myocyte involve the adenylate cyclase/cAMP system or stimulation of the phospholipase C/IP3 pathway. In general, concentrations of eicosanoids which affect myocardial contractility are higher as the response is less predictable than the effects on platelet function or vessel tone. Therefore, eicosanoid-induced extracardiac effects may be superimposed to more direct changes in the contractile state of the intact heart in vitro or in vivo. In contrast to non-failing hearts, there is a significant improvement of the contractile function in contractile failure (“stunning”, ischemia, congestive heart failure) by vasodilating prostaglandins (e.g., PGI2). The mechanism of this action is still unknown.
    Type of Medium: Electronic Resource
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