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  • Cardiac anaphylaxis  (2)
  • 3-Morpholinosydnonimine (SIN-1)  (1)
  • 5,8,11,14-Eicosatetraynoic acid  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Effect of 3-morpholinosydnonimine (SIN-1) and NG-nitro-l-arginine (NNA) on isolated perfused anaphylactic guinea-pig hearts (1992)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 345 (1992), S. 93-99 
    Details
    ISSN: 1432-1912
    Keywords: Cardiac anaphylaxis ; Nitric oxide ; 3-Morpholinosydnonimine (SIN-1) ; NG-nitro-l-argi-nine (NNA) ; Eicosanoids
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The modulating effects of exogenous and endogenous nitric oxide (NO) on the cardiac anaphylactic reaction and eicosanoid release were investigated in isolated perfused sensitized guinea-pig hearts using 3-morpholinosydnonimine (SIN-1), the active metabolite of molsidomine, as NO-donor and NG-nitro-l-arginine (NNA) as an inhibitor of NO biosynthesis. Infusion of SIN-1 (final concentrations in the perfusates 0.3 or 1.0 mmol/l) elevated coronary flow under basal conditions as well as during cardiac anaphylaxis, while NNA (0.1 mmol/l) decreased basal coronary flow and aggravated the anaphylactic coronary constriction. Both drugs did not modify the characteristic biphasic profile of the coronary constriction after antigen challenge with an initial more severe phase followed by a less pronounced long-lasting flow reduction. Neither SIN-1 nor NNA affected spontaneous heart rate. However, while NNA tended to prolong the duration of antigen-induced arrhythmias, SIN-1 (1 mmol/l) had an inhibitory effect. This protection might be related to the increased coronary flow in the presence of SIN-1. SIN-1 inhibited anaphylactic release of cysteinyl-leukotrienes (LT) and 6-keto-prostaglandin (PG) F1α, but did not influence thromboxane (TX) B2 release. On the other hand, NNA (0.1 mmol/l) inhibited anaphylactic release of TXB2, but had only marginal effects on the release of cysteinyl-LT and 6-keto-PGF1α. The results suggest that exogenous and endogenous NO functionally antagonize the effects of vasoconstrictor mediators released after antigen challenge. Additional effects of high concentrations of SIN-1 and NNA on antigen-induced eicosanoid release could modulate the vascular actions of these drugs during cardiac anaphylaxis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175475
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    On the relation between release of prostaglandins and contractility of rabbit splenic capsular strips (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 292 (1976), S. 35-42 
    Details
    ISSN: 1432-1912
    Keywords: Prostaglandins ; α-Receptor agonists ; Smooth muscle contraction ; Indometacin ; 5,8,11,14-Eicosatetraynoic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rabbit splenic capsular strips release prostaglandins E and F when contracted by noradrenaline or methoxamine. Contractions and prostaglandin release are dose-dependent. Cocaine increases significantly the effect of noradrenaline, but not that of methoxamine, on contraction of the strips and release of prostaglandin E. Release of prostaglandin F was increased by the addition of cocaine not only when noradrenaline was used as an agonist but also at two of three dose levels of methoxamine. When indometacin is added to the bath fluid, it inhibits prostaglandin release and at the same time potentiates the contractile effects of noradrenaline and methoxamine on the rabbit splenic capsular strips. The prostaglandin-synthetase blocker 5,8,11,14-eicosatetraynoic acid also potentiates the contractions induced by noradrenaline and methoxamine. Both the effects on prostaglandin synthesis and on contraction exerted by indometacin can be reversed, when indometacin is washed out. Exogenous prostaglandins E1, E2 and F2α in concentrations up to 150 ng/ml do not influence contractions of the strips induced by either noradrenaline or methoxamine. At higher concentrations prostaglandin E1 decreases, but prostaglandins E2 and F2α increase the contractions induced by both agonists. The potentiation of the effects of noradrenaline and methoxamine on rabbit splenic strips by indometacin and 5,8,11,14-eicosatetraynoic acid cannot be explained by inhibition of uptake1 or uptake2, release of endogenous noradrenaline or inhibition of metabolism of the agonists. It is suggested that the potentiation is caused by inhibition of synthesis of endogenous prostaglandins, although an undefined sensitizing effect of indometacin and 5,8,11,14-eicosatetraynoic acid cannot be completely excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00506487
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of exogenous prostaglandins on the release of leukotriene C4-like immunoreactivity and on coronary flow in indomethacin-treated anaphylactic guinea-pig hearts (1984)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 326 (1984), S. 368-374 
    Details
    ISSN: 1432-1912
    Keywords: Cardiac anaphylaxis ; Coronary constriction ; Leukotrienes ; Prostaglandins ; Indomethacin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is known that both vasoconstrictor cyclooxygenase products and sulfidopeptide-containing leukotrienes (LT) contribute to the biphasic coronary constriction observed in isolated perfused anaphylactic guineapig hearts. We have now investigated the effects of the cyclooxygenase inhibitor indomethacin and of several exogenous prostaglandins (PG) on the release of LTC4-like immunoreactivity and on various symptoms of cardiac anaphylaxis. Indomethacin decreased basal coronary flow and delayed the onset of coronary vasoconstriction after antigenic challenge. Furthermore, indomethacin inhibited cardiac release of 6-keto-PGF1α and thromboxane (TX) B2 and simultaneously enhanced the antigen-induced release of LTC4-like immunoreactivity significantly. Neither the vasodilators PGE2 and PGI2 nor the vasoconstrictors PGF2α, PGD2 and 11,9-epoxymethano-PGH2, a compound with biological properties similar to TXA2, affected the anaphylactic release of immunoreactive LTC4 in the presence of indomethacin. These results suggest that the indomethacin-induced increase in LT release is not due to inhibition of synthesis of a cyclooxygenase product, which normally curbs anaphylactic release of immunoreactive LTC4. The indomethacin effect may rather be explained by diversion of arachidonic acid metabolism away from fatty acid cyclooxygenase towards the synthesis of lipoxygenase products. Although the various PG did not significantly affect cardiac release of LTC4-like immunoreactivity, they antagonized the anaphylactic coronary contriction. This antagonism may be due to direct effects of the PG on vascular smooth muscle tone as well as to indirect effects on the release of anaphylactic mediators not related to LT like histamine and platelet-activating factor. Antigen-induced arrhythmias were completely suppressed by PGF2α, while PGE2 and PGI2 tended to decrease the incidence of arrhythmias and the other PG had no consistent effect. It is concluded that the pharmacological effects of the PG used on coronary flow and arrhythmias during cardiac anaphylaxis are not mediated by inhibition of release of LTC4-like immunoreactivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501445
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    Paper (German National Licenses)
    Fulltext
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