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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 306 (1979), S. 213-217 
    ISSN: 1432-1912
    Keywords: Dihydro-PGI2 ; Prostacyclin (PGI2) ; Bovine coronary artery ; Guinea pig heart ; Myocardial mechanics ; Coronary vascular tone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The action of the dihydro prostacyclins, (6R)-PGI1 and (6S)-PGI1, was studied on the isolated guinea pig heart and bovine coronary artery strips. PGE2 and PGI2 were used as standards. In the isolated guinea pig heart (6S)-PGI1 decreased the coronary perfusion pressure (CPP), myocardial force of contraction (MFC) and oxygen consumption (QO2). (6R)-PGI1 did not produce a significant change in these parameters. The ED50 (50% of maximum coronary dilation) was approximately 20 times higher for (6S)-PGI1 than for PGI2 or PGE2. Treatment of the hearts with reserpine + tyramine abolished the (6S)-PGI1-induced decrease in MFC but not the decrease in the CPP. The same pattern of responses was seen with PGE2. Bovine coronary artery strips were contracted by both (6S)-PGI1 and (6R)-PGI1, the ED50 (50% of maximum increase in tension) being 5 and 10 times higher than that for PGE2. The (6S)-PGI1-induced contraction was preceeded by a small relaxation, which, however, was much less than that seen after PGI2. It is concluded that the hydration of the 5,6 double bound in the PGI2-like activity and generates PGE-like activity. The same biological activity of both dihydro prostacyclins in the isolated coronary artery strip but not in the intact coronary vascular bed leads to suggest that the sites of action in these systems are different.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 307 (1979), S. 213-221 
    ISSN: 1432-1912
    Keywords: Prostacyclin (PGI2) ; Bradykinin ; Coronary artery ; Guinea pig heart ; Indomethacin ; Oxygen consumption ; Myocardial mechanics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The action of bradykinin on prostacyclin (PGI2) release and the coronary artery tone was studied in the isolated guinea pig heart and the bovine coronary artery. Myocardial force of concentration and oxygen consumption were monitored continuously. 2. Addition of bradykinin to the guinea pig heart was followed by a dose-dependent decrease in the coronary perfusion pressure, while myocardial contractile force and oxygen consumption remained unchanged, indicating a direct effect on the coronary vascular resistance. There was no evidence for tachyphylaxis. 3. Long-term treatment of the hearts with indomethacin at low concentrations (5×10−7 g/ml) did not influence the bradykinin-induced coronary dilation. Increasing the indomethacin (5×10−6 g/ml) produced a partial (repetitive application) or complete inhibition (cumulative dose-response curves). 4. Application of bradykinin to coronary artery strip also produced relaxation. Indomethacin (2×10−6 g/ml) did only attenuate this effect although it completely prevented the response to arachidonic acid. 5. The release of PGI2-like material from the heart by bradykinin was studied using the cascade-technique of Vane (1969). There was a dose-dependent release of a substance, which relaxed the bovine coronary artery. Pretreatment of the hearts with 15-hydroperoxy arachidonic acid or indomethacin (5×10−6 g/ml) produced a partial or complete inhibition of this response. However, there was no significant inhibition of the bradykinin-induced relaxation of the coronary vascular bed. 6. It is suggested that the inhibitory effect of high dose indomethacin is not due to inhibition of prostaglandin biosynthesis, which is already completely blocked at low doses. According to this, two different actions of indomethacin on the coronary vessels could be established. 7. The results indicate that bradykinin produces a pronounced release of PGI2 from the coronary vessels, which, however, can be blocked without abolition of the coronary relaxing activity. This provides evidence for an additional, PGI2-independent coronary action of this substance.
    Type of Medium: Electronic Resource
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  • 4
    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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