Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Thelen, KI; Dembinska-Kiéc, A; Pallapies, D; Simmet, T; Peskar, BA.
Effect of 3-morpholinosydnonimine (SIN-1) and NG-nitro-L-arginine (NNA) on isolated perfused anaphylactic guinea-pig hearts.
Naunyn Schmiedebergs Arch Pharmacol. 1992; 345(1): 93-99.
Doi: 10.1007/BF00175475
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- Co-Autor*innen der Med Uni Graz
- Peskar Bernhard
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- Abstract:
- 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) F1 alpha, 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-PGF1 alpha. 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.
- Find related publications in this database (using NLM MeSH Indexing)
- 6-Ketoprostaglandin F1 alpha - metabolism
- Anaphylaxis - metabolism
- Animals - metabolism
- Antihypertensive Agents - pharmacology
- Arginine - analogs and derivatives
- Coronary Circulation - analogs and derivatives
- Guinea Pigs - analogs and derivatives
- Heart - drug effects
- Leukotriene B4 - metabolism
- Male - metabolism
- Molsidomine - analogs and derivatives
- Nitroarginine - analogs and derivatives
- Perfusion - analogs and derivatives
- Thromboxane B2 - metabolism
- Vasodilator Agents - pharmacology
- Find related publications in this database (Keywords)
- CARDIAC ANAPHYLAXIS
- NITRIC OXIDE
- 3-MORPHOLINOSYDNONIMINE (SIN-1)
- NG-NITRO-L-ARGININE (NNA)
- EICOSANOIDS