Relevant bibliographies by topics / Molsidomine

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Molsidomine'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Molsidomine"

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Reden, J. "Molsidomine." Journal of Vascular Research 27, no. 2-5 (1990): 282–94. http://dx.doi.org/10.1159/000158820.

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Sardina, Marco, and Jacques Mizrahi. "Molsidomine." Lancet 344, no. 8921 (1994): 539. http://dx.doi.org/10.1016/s0140-6736(94)91925-9.

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Lopez-Ruiz, Arnaldo F., Radu Iliescu, and Jane F. Reckelhoff. "Refractory blood pressure in female SHR to increased oxidative stress is not mediated by NO or by upregulation of renal antioxidant enzymes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 2 (2010): R266—R271. http://dx.doi.org/10.1152/ajpregu.00471.2009.

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There is a sex difference in the blood pressure (BP) responses to prooxidants and antioxidants in the spontaneously hypertensive rat (SHR). In contrast to males, BP in female SHR does not decrease in response to antioxidants, such as tempol or apocynin, or increase in response to the prooxidant, molsidomine. Molsidomine decreases BP and increases expression of antioxidants in male Wistar-Kyoto rats (WKY), but not male SHR. The present study tested the hypothesis that the mechanism responsible for the lack of a pressor response to molsidomine in females is due to higher endogenous nitric oxide (NO) or to compensatory upregulation of renal antioxidant enzymes. Female SHR were treated with molsidomine in the presence or absence of nitro-l-arginine methyl ester (l-NAME) for 2 wk. Molsidomine increased nitrate/nitrite (NOx) and F2-isoprostane (F2-IsoP) excretion, whereas l-NAME reduced NOx but increased F-Isop. Molsidomine and l-NAME together further reduced NOx and increased F2-IsoP. Molsidomine alone had no effect on BP; l-NAME alone increased BP. The combination of molsidomine and l-NAME did not increase BP above l-NAME alone levels. Whole body and renal oxidative stress increased, while renal cortical Cu,Zn-SOD expression was downregulated and catalase was upregulated by molsidomine; glutathione peroxidase expression was unaffected. These data support our previous studies suggesting that BP in female SHR is independent of either increases or decreases in oxidative stress. The mechanisms responsible for the sex difference in BP response to increase or decrease of oxidative stress are not due to increased NO in females or to compensatory upregulation of antioxidant enzymes in response to increases in oxidants.
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Fournier, Claude. "Molsidomine dosage." American Heart Journal 122, no. 6 (1991): 1796. http://dx.doi.org/10.1016/0002-8703(91)90322-9.

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Basista, M., L. Grodzińska, and J. święs. "The Influence of Molsidomine and Its Active Metabolite SIN-1 on Fibrinolysis and Platelet Aggregation." Thrombosis and Haemostasis 54, no. 04 (1985): 746–49. http://dx.doi.org/10.1055/s-0038-1660124.

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SummaryMolsidomine and its active metabolite SIN-1 were examined in humans and animals for platelet suppressant and fibrinolytic activities.Following oral administration of molsidomine at doses of 6 or 15 mg/kg to rabbits, their blood platelets in PRP ex vivo required higher threshold concentrations of ADP, AA and thrombin to be aggregated. Unlike molsidomine, SIN-1 when infused (10 and 20 μg/kg i.v.) into anaesthetized cats caused a release of a substance disaggregating platelet clumps which had adhered to blood superfused collagen strip. The appearance of this unstable disaggregating substance was prevented by the pretreatment of cats with aspirin (50 mg/kg i.v.). It is suggested that SIN-1 may promote formation of a PGI2-like substance.In humans shortening of euglobulin clot lysis time was observed 60 min after a single ingestion of 2 mg of molsidomine. This fibrinolytic effect of molsidomine was not abolished by the pretreatment of patients with aspirin. Neither molsidomine nor SIN-1 activated fibrinolysis in preformed euglobulin clots in vitro.
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Koeners, Maarten P., Branko Braam, Dionne M. van der Giezen, Roel Goldschmeding, and Jaap A. Joles. "A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 6 (2008): R1847—R1855. http://dx.doi.org/10.1152/ajpregu.00073.2008.

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Enhancing perinatal nitric oxide (NO) availability persistently reduces blood pressure in spontaneously hypertensive rats. We hypothesize that this approach can be generalized to other models of genetic hypertension, for instance those associated with renal injury. Perinatal exposure to the NO donor molsidomine was studied in fawn-hooded hypertensive (FHH) rats, a model of mild hypertension, impaired preglomerular resistance, and progressive renal injury. Perinatal molsidomine increased urinary NO metabolite excretion at 8 wk of age, i.e., 4 wk after treatment was stopped ( P < 0.05). Systolic blood pressure was persistently reduced after molsidomine (42-wk females: 118 ± 3 vs. 141 ± 5 and 36-wk males: 139 ± 4 vs. 158 ± 4 mmHg; both P < 0.001). Perinatal treatment decreased glomerular filtration rate ( P < 0.05) and renal blood flow ( P < 0.01) and increased renal vascular resistance ( P < 0.05), without affecting filtration fraction, suggesting persistently increased preglomerular resistance. At 4 wk of age natriuresis was transiently increased by molsidomine ( P < 0.05). Molsidomine decreased glomerulosclerosis ( P < 0.05). Renal blood flow correlated positively with glomerulosclerosis in control ( P < 0.001) but not in perinatally treated FHH rats. NO dependency of renal vascular resistance was increased by perinatal molsidomine. Perinatal enhancement of NO availability can ameliorate development of hypertension and renal injury in FHH rats. Paradoxically, glomerular protection by perinatal exposure to the NO donor molsidomine may be due to persistently increased preglomerular resistance. The mechanisms by which increased perinatal NO availability can persistently reprogram kidney function and ameliorate hypertension deserve further study.
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Bezrukov, Vladislav, Liana Kuprush, Nina Sykalo, Tetyana Panteleymonova, Ludmila Sharabura, and Vitaliy Olar. "Effect of ATP and molsidomine combination on contractile function of isolated adult and old rat hearts during adequate coronary perfusion, at ischemia and reperfusion." Ageing & Longevity, no. 2 (July 7, 2021): 8–17. http://dx.doi.org/10.47855/jal9020-2021-2-2.

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Abstract. Pathology of the cardiovascular system occupies a major place in the structure of diseases of the elderly and old patients. Metabolic disturbances are very important in ischemic damages of myocardium in the elderly and old people. So, drugі with metabolic mechanism of action is very ppromising in the treatment of elderly patients with cardiovascular diseases. The relevance of this study is determined by the feasibility of using drugs of metabolic action, which have a beneficial effect on the metabolism of cardiomyocytes, improve blood supply to the myocardium, increase its contractile function. The effect of ATP-molsidomine combination on myocardial contractility in different age animals was stuiesy in vitro experiments. The experiments on the isolated hearts from adult and old rats have shown that combined use of ATP and molsidomine did not significantly affect the contractility of the isolated hearts of adult rats under different perfusion regimes. In old rats, the use of ATP-molsidomine combination had a positive effect on the contractile function of the myocardium under the influence of damaging factors (ischemia, reperfusion): prevented a decrease of left ventricular developing pressure and its first derivative (velocity of pressure rise and velocity of pressure decline) and accelerated its growth during reperfusion. Co-administration of ATP and molsidomine during ischemia had a positive effect on the heart rhythm and restored heart rate at the reperfusion period in adult and old rats. The results of the study indicate a positive effect of the ATP-molsidomine combination on the myocardial contractility in old rats. Combined use of ATP and molsidomine exerted a favourable influence on the heart rhythm under damaging factors both in the adult and old animals. Key words: ATP; molsidomine; isolated rat heart; myocardial contractility; ageing
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Ehlert, Angelika, Christoph Schmidt, Johannes Wölfer, et al. "Molsidomine for the prevention of vasospasm-related delayed ischemic neurological deficits and delayed brain infarction and the improvement of clinical outcome after subarachnoid hemorrhage: a single-center clinical observational study." Journal of Neurosurgery 124, no. 1 (2016): 51–58. http://dx.doi.org/10.3171/2014.12.jns13846.

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OBJECT Delayed ischemic neurological deficits (DINDs) and cerebral vasospasm (CVS) are responsible fora poor outcome in patients with aneurysmal subarachnoid hemorrhage (SAH), most likely because of a decreased availability of nitric oxide (NO) in the cerebral microcirculation. In this study, the authors examined the effects of treatment with the NO donor molsidomine with regard to decreasing the incidence of spasm-related delayed brain infarctions and improving clinical outcome in patients with SAH. METHODS Seventy-four patients with spontaneous aneurysmal SAH were included in this post hoc analysis. Twenty-nine patients with SAH and proven CVS received molsidomine in addition to oral or intravenous nimodipine. Control groups consisted of 25 SAH patients with proven vasospasm and 20 SAH patients without. These patients received nimodipine therapy alone. Cranial computed tomography (CCT) before and after treatment was analyzed for CVS-related infarcts. A modified National Institutes of Health Stroke Scale (mNIHSS) and the modified Rankin Scale (mRS) were used to assess outcomes at a 3-month clinical follow-up. RESULTS Four of the 29 (13.8%) patients receiving molsidomine plus nimodipine and 22 of the 45 (48%) patients receiving nimodipine therapy alone developed vasospasm-associated brain infarcts (p < 0.01). Follow-up revealed a median mNIHSS score of 3.0 and a median mRS score of 2.5 in the molsidomine group compared with scores of 11.5 and 5.0, respectively, in the nimodipine group with CVS (p < 0.001). One patient in the molsidomine treatment group died, and 12 patients in the standard care group died (p < 0.01). CONCLUSIONS In this post hoc analysis, patients with CVS who were treated with intravenous molsidomine had a significant improvement in clinical outcome and less cerebral infarction. Molsidomine offers a promising therapeutic option in patients with severe SAH and CVS and should be assessed in a prospective study.
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Fortepiani, Lourdes A., and Jane F. Reckelhoff. "Increasing oxidative stress with molsidomine increases blood pressure in genetically hypertensive rats but not normotensive controls." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 3 (2005): R763—R770. http://dx.doi.org/10.1152/ajpregu.00526.2004.

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Spontaneously hypertensive rats (SHR) have a higher level of oxidative stress and exhibit a greater depressor response to a superoxide scavenger, tempol, than normotensive Wistar-Kyoto rats (WKY). This study determined whether an increase in oxidative stress with a superoxide/NO donor, molsidomine, would amplify the blood pressure in SHR. Male SHR and WKY were given molsidomine (30 mg·kg−1·day−1) or vehicle (0.01% ethanol) for 1 wk, and blood pressure, renal hemodynamics, nitrate and nitrite excretion (NOx), renal superoxide production, and expression of renal antioxidant enzymes, Mn- and Cu,Zn-SOD, catalase, and glutathione peroxidase (GPx), were measured. Renal superoxide and NOx were higher in control SHR than in WKY. Molsidomine increased superoxide by ∼35% and NOx by 250% in both SHR and WKY. Mean arterial blood pressure (MAP) was also higher in control SHR than WKY. Molsidomine increased MAP by 14% and caused renal vasoconstriction in SHR but reduced MAP by 16%, with no effect on renal hemodynamics, in WKY. Renal expression of Mn- and Cu,Zn-SOD was not different between SHR and WKY, but expression of catalase and GPx were ∼30% lower in kidney of SHR than WKY. The levels of Mn- and Cu,Zn-SOD were not increased with molsidomine in either WKY or SHR. Renal catalase and GPx expression was increased by 300–400% with molsidomine in WKY, but there was no effect in SHR. Increasing oxidative stress elevated blood pressure further in SHR but not WKY. WKY are likely protected because of higher bioavailable levels of NO and the ability to upregulate catalase and GPx.
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Ganapathy, Hullathy Subban, Min Young Lee, Min Hee Woo, Yeong Tae Jeong, and Kwon Taek Lim. "Hydrophobically Modified Amphiphilic Cylodextrins as Novel Carriers for Controlled Delivery of Water-Soluble Drugs." Key Engineering Materials 342-343 (July 2007): 493–96. http://dx.doi.org/10.4028/www.scientific.net/kem.342-343.493.

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Hydrophobically modified derivative of a γ-cyclodextrin, functionalized with perfluoro alkyl ester group, was prepared and investigated for its potential use as a sustained release carrier for water-soluble drug molsidomine, a peripheral nitrovasodilator used in the treatment of angina pectoris. The molecular encapsulation of molsidomine by the amphiphilic cyclodextrin, octakis(6-O-perfluorobutanoyl)-γ-cyclodextrin (γ-CyD-F), was confirmed by DSC and XRD studies. The in-vitro release of molsidomine from peanut oil suspensions into aqueous phase was found to be significantly retarded by the complexation with γ-CyD-F, mainly due to the hydrophobic properties of the γ-CyD-F.
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Dissertations / Theses on the topic "Molsidomine"

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Hacmoun, Jean Pierre. "Les sydnonimines : la molsidomine et les dérivés apparentes, anti-angoreux." Paris 5, 1988. http://www.theses.fr/1988PA05P081.

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Monnin, Jean-Luc. "Etude de l'effet de la molsidomine et du propanolol sur le flux portal du cirrhotique mesuré par écho-doppler pulsé : étude randomisée chez 30 patients cirrhotiques." Montpellier 1, 1989. http://www.theses.fr/1989MON11071.

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COMBIS, FLORENCE. "Etude des effets hemodynamiques systemiques et splanchniques de l'association molsidomine - propranolol." Toulouse 3, 1993. http://www.theses.fr/1993TOU31016.

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Combis, Jean-Marc. "Effets des vasodilatateurs dans l'hypertension portale : étude des actions hémodynamiques systémiques et splanchniques du vérapamil et de la molsidomine." Toulouse 3, 1989. http://www.theses.fr/1989TOU31220.

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COAT, DESMORAT HELENE. "Effets hemodynamiques systemiques et splanchniques d'un vasodilatateur, la molsidomine, dans un modele d'hypertension portale chez le rat cirrhotique." Toulouse 3, 1990. http://www.theses.fr/1990TOU31176.

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Pfäffli, Daniel. "Molsidomine, a new drug for the treatment of coronary heart disease enhances PGI2 and PGE2 and inhibits thromoxane synthesis of cultured human skin fibroblasts /." [S.l : s.n.], 1985. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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CONTI, VALENTINA. "Embryonic Vessel-Associated Progenitors in Skeletal Muscle Development and in Tissue Repair." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/46756.

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Regeneration of skeletal muscle is sustained by production of new myofibers and satellite cells are indispensable for this process. However, a variety of non-satellite cell types can also participate in skeletal muscle regeneration in the adult. There is much interest in understanding the biology of these progenitors because of their potential use in clinical applications for degenerative diseases such as muscular dystrophies (MD). At the moment the best candidates are mesoangioblasts (MABs). Understanding the basic biology of these cells is mandatory to develop treatment to improve their regenerative potential. To unveil their native identity and physiological role, we used a lineage tracing strategy to label embryonic endothelial progenitors and we demonstrated that haemogenic endothelium harbors a population of progenitors that physiologically contributes to several mesodermal lineages during development, representing the in vivo counterpart of MABs. By following the fate of these cells until adulthood we showed that these cells contribute to subset of myogenic progenitors and take part in muscle regeneration. By using the same genetic system, we analyzed the effects of a pharmacological treatment based on a nitric oxide-donor on the fate of these cells during embryogenesis and during adult regeneration, showing an increased endothelial contribution to myogenesis in both cases. Moreover, combining current pre-clinical protocols for MABs transplantation with genetic manipulation, we demonstrated that over-expression of the MAGE protein Necdin promotes their survival and myogenic differentiation, resulting in an improved therapeutic efficacy.
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Mandíková, Petra. "Úloha oxidu dusnatého v kardioprotektivním působení chronické hypoxie." Master's thesis, 2010. http://www.nusl.cz/ntk/nusl-285199.

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The aim of present project was to uncover the effect of pharmacological increase in acute and chronic nitric oxide (NO) production on cardioprotective effect of chronic hypoxia. We studied the effect of NO donor molsidomine on hemodynamic conditions and ischemia - induced myocardium injury. Male Wistar rats were exposed to continual hypoxia in a normobaric chamber (10 % O2, 4 weeks). Rats received molsidomine either chronically (15 mg/kg/day) in drinking water or acutely (10 mg/kg) in saline infused 30 min before ischemia. Control rats were kept under normoxia and treated in a corresponding manner. Adaptation to chronic hypoxia resulted in development of pulmonary hypertension. Chronic treatment with molsidomine slightly reduced these consequences of chronic hypoxia but it had no effect on increased cardiac ischemic tolerance in chronically hypoxic rats. On the other hand acute treatment with molsidomine significantly reduced infarct size and increased the number of arrhythmias in both normoxic and chronically hypoxic animals. In conclusion, our data suggests that acute increase in availability of NO is cardioprotective in both normoxic and chronically hypoxic rats contrary to its chronic increase which seems to have no protective contribution.
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Guo-YuanHe and 何國淵. "Sustained transdermal delivery of molsidomine using PLGA microparticles for primary osteoporosis treatment." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/jxp6c4.

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碩士<br>國立成功大學<br>化學工程學系<br>106<br>In postmenopausal women, estrogen deficiency causes rebound of thymus, over-activation of T cell and osteoclasts, thus inducing osteoporosis. Appropriate concentrations of nitric oxide (NO) have been shown to promote the growth and differentiation of osteoblasts and suppress bone resorption through regulating thymocytes and T cells for the treatment of osteoporosis. In this study, we use cardiovascular drug, molsidomine, as a NO donor, and find its optimal oral dosage for osteoporosis. Based on this dosage, we develop microparticles (MPs) for sustained transdermal delivery of the NO donor and evaluate its feasibility in ovariectomized (OVX) mice, a model of postmenopausal osteoporosis. Oral administration of low-, medium-, or high-dose molsidomine started on the fifth month after OVX for a period of 3 months. We observed that the administration of low-dose (2 μg/day) molsidomine significantly reduced TNF-α levels and bone marrow adiposity in the tibia compared to the untreated OVX group. These results demonstrated that long-term low-dose molsidomine therapy has the therapeutic potential to improve bone mass. To improve convenience of administration and reduce dosing frequency, poly(lactic-co-glycolic acid) (PLGA) MPs were developed for sustained delivery of low-dose molsidomine. In vitro drug release study showed that the PLGA particles fabricated at pH 5.2 (LOW-P) have an approximate zero-order release up to 70 days. After subcutaneous injection of MPs to the mice, serum concentration of molsidomine reached a steady-state value at day 14 and can be sustained for at least 56 days. The fact indicates the PLGA MPs can control drug release and maintain the blood drug concentration within a specific interval. The OVX mice were randomly assigned to the following groups: OVX-control, OVX-empty (drug-free MPs), OVX-low dose (5 mg MPs), OVX-medium dose (15 mg MPs), or OVX-high dose (30 mg MPs). Compared to the OVX-control group, all drug-loaded MP groups increased bone volume (BV/TV) and bone mineral density (BMD). Notably, the OVX-medium dose group showed the strongest effects on BV/TV, BMD, and TNF-α levels. This study demonstrates that using the PLGA MPs for sustained release of molsidomine could be a potential therapeutic strategy for the treatment and prevention of postmenopausal bone loss.
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Kibbel, Thomas [Verfasser]. "Akute Veränderungen des neurovegetativen Tonus' bei intravenöser Molsidomin- oder Nitroglycerin-Applikation : randomisierte doppelblinde Crossover-Studie mittels Herzfrequenzvariabilitäts-Analyse und Plasma-Katecholaminbestimmung / vorgelegt von Thomas Kibbel." 2007. http://d-nb.info/98341050X/34.

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Books on the topic "Molsidomine"

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International, Symposium on Molsidomine (1984 Düsseldorf Germany). Ischemic heart disease and heart failure: Advances in treatment with molsidomine. Urban & Schwarzenberg, 1986.

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Bing, Richard J., and Martin Stauch. Ischemic Heart Disease and Heart Failure. Urban & Schwarzenberg,Germany, 1986.

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Book chapters on the topic "Molsidomine"

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Scholtholt, J. "Molsidomine." In Handbook of Experimental Pharmacology. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69524-7_11.

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Gryglewski, R. J., and J. Swies. "Cardioprotection by Molsidomine and Iloprost in Myocardial Ischaemia in Anaesthetized Cats." In Prostaglandins in the Cardiovascular System. Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7262-1_37.

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Piel, G., L. Pochet, L. Delattre, and J. Delarge. "Study of the Influence of γ-Cyclodextrin on the Molsidomine Photostability." In Proceedings of the Eighth International Symposium on Cyclodextrins. Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-5448-2_64.

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Beyer, Karl-Heinz. "Molsidomin." In Biotransformation der Arzneimittel. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74386-3_213.

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Ganapathy, Hullathy Subban, Min Hee Woo, Seong Soo Hong, and Kwon Taek Lim. "Supercritical Carbon Dioxide Assisted Impregnation of Molsidomine into Poly(DL-Lactide-co-Glycolide) for Sustained Release Applications." In Advanced Biomaterials VII. Trans Tech Publications Ltd., 2007. http://dx.doi.org/10.4028/0-87849-436-7.501.

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Matteo, Vincenzo, Massimo Pierucci, Arcangelo Benigno, et al. "Electrophysiological and Neurochemical Characterization of 7-Nitroindazole and Molsidomine Acute and Sub-Chronic Administration Effects in the Dopaminergic Nigrostrial System in Rats." In Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-92660-4_14.

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"Molsidomine." In Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/01414-5.

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Chevrel, Guillaume, and Virginie Dessus. "molsidomine." In 300 médicaments injectables. Elsevier, 2009. http://dx.doi.org/10.1016/b978-2-294-70698-1.50032-5.

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"Molsidomine." In Meyler's Side Effects of Drugs. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.01101-x.

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Laurent, Stéphane. "Pharmacology of vasodilators." In ESC CardioMed. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0034.

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Antihypertensive and antianginal agents are differentially able to vasodilate small resistance arteries, large conducting arteries, and epicardial coronary arteries. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and alpha-adrenergic antagonists are not addressed here, since they are discussed in specific chapters. This chapter discusses the pharmacology of calcium channel blockers, nitrovasodilators, and direct-acting vasodilators. Dihydropyridines, such as nifedipine and amlodipine, are compared to the non-dihydropyridine agents verapamil and diltiazem. Organic nitrates, such as nitroglycerine and isosorbide dinitrate, are compared to inorganic nitrates, such as sodium nitroprusside. Molsidomine and nicorandil are also discussed. Finally, the pharmacology of direct-acting vasodilators focuses on minoxidil and hydralazine. Pharmacology of mechanisms of action is detailed to better understand therapeutic indications and side effects.
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Conference papers on the topic "Molsidomine"

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Lulinski, Piotr, and Dorota Maciejewska. "Preliminary Evaluation of Molsidomine Imprinted Polymers." In The 12th International Electronic Conference on Synthetic Organic Chemistry. MDPI, 2008. http://dx.doi.org/10.3390/ecsoc-12-01269.

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Levy-Toledano, D., D. Weill, J. Maclouf, F. Rendu, and C. Soria. "INHIBITORY EFFECT OF SIN 1 ON PLATELET FUNCTION:POSSIBLE INTEREFRENCE WITH PHOSPHOLIPASE C AND FIBRINOGEN BINDING." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643424.

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The mode of action of SIN 1, the main metabolite of an antianginal drug (Molsidomine) was investigated in vitro on huma platelet functions. SIN 1 inhibited dose dependently platelet activation as reflected by aggregation and release of serotonin induced by arachidonic acid, prostaglandin endoperoxydes analogues (U 46619, U 44069), collagen, and ADP (figst and second wave). The maximal inhibition was reached at 10−5 M. The thromboxane (TX) synthesis was inconsis^antly impaired even at high concentrations of SIN 1 (104 M) suggesting a discrepancy between the inhibitory effect on platelet activation and TX formation. The main cofactor of ADP-stimulated aggregation is fibrinogen ; SIN 1 dose-dependently inhibited the fibrinogen binding to platelets thereby explaining it antiaggregatory properties.In order to further investigate the mechanism of action of this drug on platelet activation we tested SIN 1 on the thrombin-induced phg^phosinositide metabolism and protein phosphorylation on 32P-prelabelled isolated platelets.P-phosphatidate (PA) formation was greatly inhibited. Phosphorylations of the myosin light chain (P20) and of 43 kDa protein (P43) were also reduced. These effects were accompanied by an inhibition of serotoninrelease, TXB2 synthsei^, and platelet aggregation.SIN rl_would seem to act on early biochemical events and more especially at thelevel of the membrane phospholipase C.
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SIMON, M. F., H. CHAP, and L. DOUSTE-BLAZY. "EFFECTS OF SIN 1 ON PLATELET ACTIVATION INDUCED BY THROMBIN IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643423.

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The mechanism of platelet activation is well known. The interaction of agonist such as thrombin, on specific membrane receptor induces phosphatidylinositol-specific phospholipase C activation, with a concomitant formation of two second messengers (from PIP2): inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 is able to induce a rapid discharge of Ca2+ from internal stores and Ca2+ influx through plasma membrane by unidentified Ca2+ channels linked to receptor activation. The increase of cytoplasmic free calcium concentration leads to the activation of the calcium calmodulin dependent myosine light chain kinase which phosphoryla-tes 20 kD proteins (myosine light chain). DAG is a potent activator of protein kinase C, which phosphorylates 40 kD proteins. These different pathways act in synergism.Sin 1 is a platelet aggregating inhibitor. This compound is an active metabolite of molsidomine, which activates platelet guany-late cyclase, inducing a rapid rise in cyclic GMP level. The precise role of cyclic GMP in platelet activation is not yet known. In order to study the mechanism of action of this drug, we tried to determine the effect of Sin 1 on the different steps described above. We measured Ca2+ fluxes and phospholipase C activation in thrombin (0,5 U/ml) stimulated platelets in the presence of different doses of Sin 1 (10™7-10™3M). Serotonin secretion was inhibited by 30 % with Sin 1 (10™4M-10™5m). A parallel inhibition of phospholipase C was detected by measurement of [32P)-PA level. Platelets loaded with Quin 2 and stimulated by thrombin showed a 70 % inhibition of external Ca2+ influx as soon as a concentration of 10™7M of Sin 1 was added. A study on platelet loaded with [45Ca2+) and Quin 2 confirmed these results. On the contrary, discharge of internal Ca2+ store seemed to be unaffected.In conclusion, the major effect of Sin 1 on platelet phospholipase C pathway is an inhibition of Ca2+ influx through plasma membrane. Some further experiments are necessary to shown whether this inhibition is correlated with cyclic GMP formation (the major effect of Sin 1) and try to establish a relation between this inhibition and that exerted on phospholipase C.Sin 1 was a generous gift of Hoechst.
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4

Maurice, D. H., and R. J. Haslam. "ROLES OF cAMP AND cGMP IN THE SYNERGISTIC INHIBITORY EFFECTS OF NITROVASODILATORS AND PGE1 ON PLATELET AGGREGATION AND DEGRANULATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644533.

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Washed rabbit platelets labelled with [14C]5-HT and suspended in a modified Tyrode’s solution were used in this study. Incubation of the platelets with 0.1, 1 and 10 μM sodium nitro-prusside (SNP) for 30 s inhibited aggregation induced by 10 nM platelet-activating factor by 7, 13 and 45% and the release of [14C]5-HT by 16, 30 and 45%, respectively. In combination with 0.02 μM PGE1, which had little effect alone (7% inhibitions), these concentrations of SNP caused 58, 90 and 100% inhibitions of aggregation and 60, 73 and 81% inhibitions of [14C]5-HT release. Thus, SNP and PGE1 acted synergisti-cally. The changes in [3H]cGMP and [3H]cAMP caused by these compounds were measured in platelets labelled by preincubation with [3H]guanine and [3H]adenine. [3H]cGMP (initially 0.01% of platelet [3H]GTP) increased by amounts equivalent to 0.02, 0.10 and 0.63% of [3H]GTP with 0.1, 1 and 10 μM SNP. PGE1 had no effects on platelet [3H]cGMP. The above SNP concentrations also increased [3H]cAMP by amounts equivalent to 0.01, 0.02 and 0.04% of platelet [3H]ATP (basal value 0.02%). However, in the presence of 0.02 μM PGE1, 0.1, 1 and 10 μM SNP increased [3H]cAMP by amounts equivalent to 0.13, 0.26 and 0.39% of platelet [3H]ATP. Both with and without PGE1, 10 μM SIN-1 (the active metabolite of molsidomine) had effects similar to those of 1 μM SNP. Thus, the synergistic actions of PGE-, and SNP or SIN-1 on platelet function correlated with increases in [3H]cAMP, not [3H]cGMP. Preincubation of the platelets for 30 s with 200 μM 2∲,5∲-dideoxy-adenosine (an inhibitor of adenylate cyclase) reduced the above increases in [3H]cAMP and inhibitions of platelet reactions by about 60%, without affecting [3H]cGMP levels. Addition of specific inhibitors of platelet cAMP phosphodiesterase (e.g. cilostamide) enhanced the actions of PGE1 in a manner similar to SNP but had little effect on the actions of SNP. The results show that the nitrovasodilators studied have effects on platelet function and [3H]cAMP similar to those of inhibitors of cAMP phosphodiesterase, suggesting that their actions may be mediated by increases in cAMP caused by an effect of cGMP on the platelet cGMP-inhibited cAMP phosphodiesterase. (HSFO Grant T443H)
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Calancea, V., E. Terna, C. Martiniuc, et al. "Effects of Molsidomin upon pulmonary hemodynamics and oxygen transport by arterial blood in chronic obstructive pulmonary disease (COPD) and decompensated cor pulmonale." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3804.

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