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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Inorganic chemistry 6 (1967), S. 2259-2260 
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The relaxing response of dopamine (DA) was studied in the rabbit pulmonary artery. DA caused concentration-related relaxation in helically cut strips of the artery contracted with prostaglandin F2α in the presence of prazosin.2. The DA-induced relaxation in endothelium-denuded strips was reduced to about 40% compared with that in endothelium-intact strips.3. Methylene blue and haemoglobin, inhibitors of endothelium-dependent relaxation, reduced the DA-induced relaxations in endothelium-intact strips to the level of endothelium-denuded strips. These results indicate that the DA-induced relaxation is partially mediated or modified by the release of endothelium-derived relaxing factor (EDRF).4. Apomorphine, as a DA agonist, caused concentration-dependent relaxation in endothelium-intact strips. Bromocriptine, a DA2 agonist, produced only a little relaxation at higher concentration.5. In endothelium-intact strips, haloperidol, a DA antagonist, and the DA1 antagonists, fluphenazine and SCH 23390 inhibited DA-induced relaxations. On the other hand spiperone and domperidone, DA2 antagonists, were inactive.6. In endothelium-denuded strips, fluphenazine and SCH 23390 inhibited DA-induced relaxations, but domperidone was inactive.7. These results indicate that the DA-induced relaxation is mediated by DA receptors, and that DA1 receptors are involved in both endothelium-dependent and-independent relaxation in the rabbit pulmonary artery.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 27 (2000), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. To clarify the mechanism of the cardioprotective effect of nicorandil (2-nicotinamidoethyl-nitrate ester), the effects of nicorandil and nitric oxide (NO) donors on the release of ATP, ADP, AMP and adenosine from arterial segments and cultured endothelial cells of the porcine coronary artery were examined.2. Nicorandil significantly increased the release of total adenyl purines from arterial segments and from cultured endothelial cells.3. Cromakalim, an ATP-sensitive K+ channel opener, did not affect the release of total adenyl purines from coronary artery segments.4. S-Nitroso-N-acetyl- D, L-penicillamine and isosorbide dinitrate, NO donors, significantly increased the release of total adenyl purines from coronary artery segments.5. These results demonstrate that nicorandil stimulates ATP release from the coronary artery by acting not as an ATP-sensitive K+ channel opener, but as a nitrate, thus suggesting the cardioprotective properties of nicorandil.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2013
    Keywords: Key words Prostacyclin (PGI2) ; Endocardial endothelial cell (EEC) ; Vascular endothelial cell (VEC) ; Pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We assessed the effects of pressure on the release of prostacyclin (PGI2) from cultured endocardial endothelial cells (EECs) and vascular endothelial cells (VECs). EECs were harvested from the right ventricle (RV) and left ventricle (LV) of porcine hearts, and VECs from pulmonary artery (PA), aorta (Ao) and coronary artery (CA). Confluent EECs and VECs were incubated for 30 min under various pressures (0, 50, 100, 150 mmHg) and PGI2 release from each cell was measured. Pressure-induced PGI2 release from LV-EECs was larger than that from RV-EECs. Pressure also increased PGI2 release from both PA- and Ao-VECs, but not from CA-VECs. These findings suggest that endocardium can produce PGI2 in response to pressure and PGI2 released into the coronary blood from the ventricle may play an important role in the prevention of myocardial ischemia.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-4919
    Keywords: nicaraven ; reperfusion injury ; hydroxyl radical ; endothelium-derived relaxing factor ; pig coronary artery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Recently, we have reported that a new synthetic compound, 1,2bis(nicotinamido)-propane (nicaraven), improved cardiac function following preservation and reperfusion. In this study, we investigated the efficacy of nicaraven as a radical scavenger by using an in vitro model of oxidative stress, to clarify mechanisms of the protective effect of this new compound on reperfusion injury in rat heart. Ring segments of epicardial right coronary arteries (RCA) of pig were suspended in organ chambers and exposed to hydroxyl radicals (·OH), generated (by two different systems ) by 0.28 mM FeSO4/0.28 mM H2O2 and DHF/Fe3+-ADP (2.4 mM, 43 nM, and 1.56 uM, respectively) to the bathing solution for 60 min. Prior exposure of the coronary arteries to ·OH significantly produced right-ward shift of the dose-response curves of the bradykinin-induced endothelium-dependent relaxations (an increase in the ED50 value for bradykinin by 4.37 and 1.98 times than control in two different ·OH generating systems, respectively), but did not affect the maximum relaxation responses. The presence of nicaraven (10-4 and 10-5 M) in the ·OH generating system, shifted the dose-response curves to bradykinin to the control level, suggesting a significant hydroxyl radical scavenging effect of the drug. These results indicate that nicaraven, a new hydroxyl radical scavenger, exhibits a protective effect on hydroxyl radicalinduced endothelial dysfunctions of pig coronary artery.
    Type of Medium: Electronic Resource
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