Journal articles: 'Molsidomine'

1

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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Żorniak, Michał, Katarzyna A. Mitręga, Maurycy Porc, and Tadeusz F. Krzemiński. "New approach to molsidomine active metabolites coming from the results of 2 models of experimental cardiology." Canadian Journal of Physiology and Pharmacology 95, no. 2 (2017): 111–21. http://dx.doi.org/10.1139/cjpp-2016-0251.

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Molsidomine is a well-known vasodilatating, antianginal drug. Despite earlier studies with its metabolites (3-morpholino-syndnonimine (SIN-1) and N-nitroso-N-morpholino-amino-acetonitrile (SIN-1A)), which indicated a potential favorable cardioprotective activity, a lot of controversy remains. The aim of our research was to compare molsidomine, SIN-1, SIN-1A, and lidocaine influence on arrhythmias and hemodynamic parameters in 2 experimental models in rats. In the Langendorff heart study, SIN-1A markedly elevated left ventricular systolic pressure, maximum rise and fall of the first pressure derivative, coronary flow, and myocardial oxygen consumption. In addition, SIN-1A more so than SIN-1 significantly lowered creatine kinase release. The antiarrhythmic action of SIN-1 was observed, while lidocaine significantly diminished ventricular arrhythmias duration in comparison with the control. In the ischemia–reperfusion-induced arrhythmias model, hypotensive action of molsidomine was observed as well as the reduction in pressure rate product. Molsidomine also prolonged ventricular tachycardia duration. On the other hand, no significant effects on hemodynamic parameters as well as on ventricular arrhythmias were found in any of the SIN-1 and SIN-1A groups. In conclusion, our research suggests a possible direct, cardioprotective action of SIN-1A. It seems worthwhile to further investigate molsidomine derivatives, especially SIN-1A, because of its potential use in invasive cardiology procedures such as percutaneous transluminal coronary angioplasty.

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Kuprash, Liana, Ludmila Sharabura, Tetyana Panteleymonova, Svitlana Hudarenko, Nina Sykalo, and Vladislav Bezrukov. "INFLUENCE OF ATP-LONG AND MOLSIDOMINE COMBINATION ON THE BIOELECTRIC ACTIVITY OF THE MYOCARDIAL OF YOUNG AND OLD RATS IN CHRONIC SOFT STRESS." JOURNAL OF THE NATIONAL ACADEMY OF MEDICAL SCIENCES OF UKRAINE, Issue 1; 2021 (May 26, 2021): 5–11. http://dx.doi.org/10.37621/jnamsu-2021-1-1.

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Introduction. Age-related changes in the cardiovascular system lead to a decrease in its reserve adaptive capabilities and an increase in the likelihood of developing diseases under stress and overstrain. A number of experiments have proven the significant role of emotional overstrain and stress in the development of cardiovascular diseases. The high incidence of the circulatory system, the long course and severity of diseases in elderly and old people determine the relevance of the search for treatment using effective and safe drugs. Aim: iinvestigate the effect of a combination of ATP-LONG and molsidomine on the functional state of the myocardium of young and old rats under chronic soft stress. Materials and methods. In experiments on young (10 months) and old (24 months) male Wistar rats, the cardiotropic and cardioprotective activity of the combination of the metabolic cardioprotector ATP-LONG and the vasodilator molsidomine was studied under conditions of chronic soft stress. Results. The negative impact of chronic soft stress on the bioelectrical activity of the myocardium – a violation of the processes of repolarization, conduction and contractility of the heart was found in young rats. The combination of ATP-LONG and molsidomine normalized the bioelectrical activity of the myocardium and increased its resistance to stress factors. In old rats under the influence of chronic stress, signs of impaired repolarization and electrical instability of the heart were more significant than in young animals. The combination ATP-LONG and molsidomine prevented the damaging effect of chronic stress and contributed to the normalization of the electrophysiological parameters of the myocardium of old rats. Conclusions. The results of experiments indicate the pharmacological cardiotropic activity of the combination of ATPLONG and molsidomine in young and old rats with chronic soft stress. Keywords: young rats, old rats, chronic soft stress, myocardium, electrocardiogram, bioelectrical activity of the heart, ATP-LONG, molsidomine, cardioprotective effect.

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Bezrukov, Vladislav, Liana Kuprash, Nina Sykalo, Tetyana Panteleymonova, Ludmila Sharabura, and Vitaliy Olar. "Age features of the influence of ATP-LONG and molsidomine on heart and vascular contractions." Ageing & Longevity, no. 1 2021 (May 5, 2021): 16–25. http://dx.doi.org/10.47855/jal9020-2021-1-1.

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The high incidence of cardiovascular discases, the long course and severity of diseases in the elderly and old patients determine the need to use effective and safe drugs for their treatment. The relevance of this study is determined by the feasibility of using drugs of metabolic action, which have a beneficial effect on the metabolism and energy metabolism of cardiomyocytes, improve vascular tone and blood supply to the myocardium, increase its contractile function. The effect of a combination of ATP-long and molsidomine on vascular and myocardial contractility in young and old rats was studied in in vitro experiments. In experiments on isolated segments of the thoracic aorta, it was found that combination of ATP-long and molsidomine has a vasodilating effect, which did not differ significantly from the action of acetylcholine in animals of both ages. Combined use of ATP-long and molsidomine did not significantly affect the contractility of the isolated heart of young rats under different perfusion regimens. In old rats, the use of a combination of ATP-long and molsidomine had a positive effect on the contractile function of the myocardium under the influence of damaging factors: prevented a decrease in left ventricular pressure during hypoxia and accelerated its growth during reperfusion. The results of the studies indicate a positive effect of the combination of ATP-long and molsidomine on the contractility of blood vessels and myocardium in older animals.

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Kuprash, Liana, Tetyana Panteleymonova, Ludmila Sharabura, Irina Labunets, Nina Sykalo, and Vitaliy Olar. "Protectoral action of molsidomin ATP combination in chronic stress in young and old rats." Ageing & Longevity, no. 2 (October 30, 2020): 50–64. http://dx.doi.org/10.47855/jal9020-2020-2-1.

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Adaptive reactions to chronic stress, reaching a certain intensity, can become harmful and be involved in any pathological process. Therefore, the search for new ways to increase the adaptive capacity reduced with age and the body's resistance to the negative effects of chronic stress remains relevant. The aim of the study was to experimentally study the age-related protective properties of the combination of molsidomine and ATP in chronic mild stress. The experiments were performed on young (6 months) and old (26 months) Wistar rats exposed to stressors that changed periodically at random for 8 weeks. During the 6-8th week of the experiment, against the background of stress, the animals were sublingually administered a pharmacological combination based on molsidomine - 2 mg / kg, ATP - 10 mg / kg. It was found that the adaptive reactions of young and old animals to chronic stress have qualitative and quantitative differences. Chronic stress in old rats caused changes in behavior and psycho-emotional state, deterioration of cognitive function, changes in lipoperoxidation. On the part of the immune system in old rats, against the background of a pronounced age involution of lymphoid organs, no significant changes in thymus mass and cellularity were observed during chronic stress, while the mass and cellularity of the spleen increased. The combination of molsidomine and ATP prevented post-stress changes in animal behavior, reduced anxiety, normalized social activity, restored the lost ability to recognize, improved cognitive function. The drug contributed to the preservation of the function of immunocompetent organs in young animals and to a lesser extent showed a protective effect in older animals against the background of involutional changes caused by both aging and chronic stress. The combination of molsidomine and ATP had an antioxidant effect. Thus, in chronic mild stress, older animals showed a different response from young animals to both stress and the administration of molsidomine with ATP. The applied pharmacological combination can be considered as a promising stress-protective agent that has a complex effect on various pathogenetic links of chronic stress due to its neuro- and immunomodulatory, energy-saving, antioxidant properties. Keywords: aging, chronic stress, anxiety, social activity, cellularity of the thymus and spleen, lipid peroxidation, combination of molsidomine and ATP, pharmacological action.

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NGUYEN, Loi, Ari KARJALAINEN, A. Elizabeth MILBOURNE, and L. Fyfe BYGRAVE. "Permeable analogues of cGMP promote hepatic calcium inflow induced by the synergistic action of glucagon and vasopressin but inhibit that induced by vasopressin alone." Biochemical Journal 330, no. 2 (1998): 877–80. http://dx.doi.org/10.1042/bj3300877.

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Treatment of perfused rat liver with the nitric oxide-generating reagent molsidomine led to substantial increases in cGMP without itself affecting basal Ca2+ fluxes. Under these conditions the ability of glucagon plus vasopressin to induce Ca2+ influx was greatly enhanced. The permeable analogue of cGMP (8-bromo-cGMP) enhanced glucagon plus vasopressin-induced Ca2+ influx to a similar extent as that with molsidomine. This suggests that the effect of the latter is attributable to the generation of cGMP which itself enhances the ability of the two hormones to induce synergistic Ca2+ influx. While 8-bromo-cGMP (or molsidomine) did not influence Ca2+ fluxes induced by glucagon, these agents strongly inhibited Ca2+ influx induced by vasopressin alone. These data show that while 8-bromo-cGMP has no effect on basal Ca2+ fluxes, it is able to modify the Ca2+ influx induced by glucagon and vasopressin action in hepatic tissue.

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Rosenkranz, Bernd, Bernhard R. Winkelmann, and Michael J. Parnham. "Clinical Pharmacokinetics of Molsidomine." Clinical Pharmacokinetics 30, no. 5 (1996): 372–84. http://dx.doi.org/10.2165/00003088-199630050-00004.

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Chassoux, G. "Molsidomine and Lipid Metabolism." Journal of Cardiovascular Pharmacology 14 (1989): S137–138. http://dx.doi.org/10.1097/00005344-198906152-00026.

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Chassoux, G. "Molsidomine and Lipid Metabolism." Journal of Cardiovascular Pharmacology 14 (1989): S137–138. http://dx.doi.org/10.1097/00005344-198914110-00026.

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&NA;. "Molsidomine disappoints in acute MI." Inpharma Weekly &NA;, no. 946 (1994): 15. http://dx.doi.org/10.2165/00128413-199409460-00032.

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&NA;. "Molsidomine may have hypolipaemic properties." Inpharma Weekly &NA;, no. 725 (1990): 1. http://dx.doi.org/10.2165/00128413-199007250-00002.

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Bentli, Recep, Hakan Parlakpinar, Alaadin Polat, Emine Samdanci, Mehmet Ediz Sarihan, and Mustafa Sagir. "Molsidomine Prevents Cisplatin-induced Hepatotoxicity." Archives of Medical Research 44, no. 7 (2013): 521–28. http://dx.doi.org/10.1016/j.arcmed.2013.09.013.

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Kukovetz, Walter R., and Sigrid Holzmann. "Mechanism of vasodilation by molsidomine." American Heart Journal 109, no. 3 (1985): 637–40. http://dx.doi.org/10.1016/0002-8703(85)90669-6.

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Ostrowski, J., and K. Resag. "Pharmacokinetics of molsidomine in humans." American Heart Journal 109, no. 3 (1985): 641–43. http://dx.doi.org/10.1016/0002-8703(85)90670-2.

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Freese, Tyll, Jan C. Namyslo, Martin Nieger, and Andreas Schmidt. "Sulfur, mercury, and boron adducts of sydnone imine derived anionic N-heterocyclic carbenes." RSC Advances 9, no. 9 (2019): 4781–88. http://dx.doi.org/10.1039/c9ra00294d.

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The sydnone imines (5-benzoylimino)-3-(2-methoxyphenyl)-sydnone imine and molsidomine were deprotonated at C4 to give sydnone imine anions which can be represented as anionic N-heterocyclic carbenes, respectively.

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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." Key Engineering Materials 342-343 (July 2007): 501–4. http://dx.doi.org/10.4028/www.scientific.net/kem.342-343.501.

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Supercritical carbon dioxide (scCO2) was used as a processing medium for the fabrication of drug encapsulated poly(DL-lactide-co-glycolide) (PLGA) monoliths for their potential application in the controlled release of water soluble drugs. Exposure of PLGA to scCO2 leads to effective plasticization and liquefaction due to the high solubility and interaction of the scCO2 in the copolymer. By exploiting this property, it was demonstrated that prolonged release formulations of molsidomine, a peripheral nitrovasodilator used to treat angina pectoris, can be prepared by chemical solvent-free, scCO2 assisted drug impregnation method. The in-vitro dissolution studies revealed that the release rates of drug from the porous polymer monoliths containing different amount of the drug samples were significantly retarded due to encapsulation of molsidomine into the PLGA matrix.

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&NA;. "Molsidomine pharmacokinetics are altered in cirrhosis." Inpharma Weekly &NA;, no. 806 (1991): 18. http://dx.doi.org/10.2165/00128413-199108060-00049.

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Vanhoutte, Paul M. "Molsidomine Is a Donor of EDRF." Journal of Cardiovascular Pharmacology 14 (1989): S139. http://dx.doi.org/10.1097/00005344-198906152-00027.

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Vanhoutte, Paul M. "Molsidomine Is a Donor of EDRF." Journal of Cardiovascular Pharmacology 14 (1989): S139. http://dx.doi.org/10.1097/00005344-198914110-00027.

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YAMADA, MASAYUKI, and YOSHIAKI UDA. "Enhancement of percutaneous absorption of molsidomine." CHEMICAL & PHARMACEUTICAL BULLETIN 35, no. 8 (1987): 3390–98. http://dx.doi.org/10.1248/cpb.35.3390.

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Mindlin deAptecar, Fanny R., Alberto Vazquez, and Moisés Aptecar. "Molsidomine – an Effective Antianginal Drug." Cardiology 72, no. 4 (1985): 185–92. http://dx.doi.org/10.1159/000173872.

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Fiedler, Volker B., and Trevor S. Abram. "Molsidomine on cardiovascular leukotriene D4 actions." Naunyn-Schmiedeberg's Archives of Pharmacology 329, no. 2 (1985): 152–57. http://dx.doi.org/10.1007/bf00501205.

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Herchuelz, Andr??, Fabienne Carreer-Bruhwyler, Jacques Crommen, et al. "Clinical Pharmacokinetics of Once-Daily Molsidomine." American Journal of Drug Delivery 2, no. 2 (2004): 131–41. http://dx.doi.org/10.2165/00137696-200402020-00005.

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Monnin, J. L., J. P. Vinel, J. P. Pascal, et al. "Pulsed doppler flowmetry assessment of molsidomine and Molsidomine + Propranolol effects on portal haemodynamics patients with cirrhosis." Journal of Hepatology 9 (January 1989): S192. http://dx.doi.org/10.1016/0168-8278(89)90560-6.

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Kuprash, Liana, Tetyana Panteleymonova, Ludmila Sharabura, et al. "Pharmacology-based toxicity assessment of molsidomine and ATP-LONG combination with singular and repetitive injections under experimental conditions." Ageing & Longevity 2, no. 3 2021 (2021): 1–13. http://dx.doi.org/10.47855/jal9020-2021-3-1.

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Abstract. The aim of the work was to study toxic properties of the new combined drug which comprise nitrovasodilator molsidomine and adenosine- 5’-triphosphate in a form of coordination compound with histidine, magnesium, and potassium (ATP-LONG). The drug was examined for its acute and subacute toxicity on Balb/c mice and Wistar rats of reproductive age with peroral (p/o) and sublingual (s/l) administrations. It has been established that LD50 of the substance contains over 10000 mg/kg (p/o) and 5010 mg/kg (s/l), which corresponds to the category of Practically non-toxic substances. The repetitive administrations within a 28 day period of the conditionally therapeutic dose of 260 mg/hg (s/l) did not cause any negative impact on physiological, biochemical, histological values in male and female rats. In doses 1300 and 2080 mg/kg, which exceed conditionally therapeutic doses by 5 and 8 times, the combination was not changing clinical laboratory urine and blood values but induced histological changes such as dilation and plethora of capillaries along with edema of smooth muscle cells of the brain, myocardium, liver, spleen, kidneys, and adrenal glands in rats. Additionally, the particular dosages of the combined substance provoked irritation of the mucous membrane of the tongue. Detected effects of the drug do not carry any pathological character and can be viewed as a specific reaction of the organism to high doses of nitrovasodilator. However, the duration and reversibility of unwanted consequences of molsidomine overdose, particularly in its combined form, need further investigation. Keywords: combination of molsidomine and ATP-LONG, acute and subacute toxicity

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Schmutzler, H. "Alternative Anti-Anginal Drugs: Amiodarone and Molsidomine." European Heart Journal 6, suppl F (1985): 77–82. http://dx.doi.org/10.1093/eurheartj/6.suppl_f.77.

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VANDENBOSSCHE, G. M. R., C. MUYNCK, F. COLARDYN, and J. P. REMON. "Light stability of molsidomine in infusion fluids." Journal of Pharmacy and Pharmacology 45, no. 5 (1993): 486–88. http://dx.doi.org/10.1111/j.2042-7158.1993.tb05583.x.

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LAICHER, A., H. JÜNGER, and F. H. KLEMM. "Stability Behaviour of Molsidomine-containing Pellet Formulations." Journal of Pharmacy and Pharmacology 49, no. 2 (1997): 131–34. http://dx.doi.org/10.1111/j.2042-7158.1997.tb06766.x.

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Watanabe, Sachiro, Hitoshi Matsuo, Akira Goto, et al. "Effects of molsidomine on right ventricular function." Current Therapeutic Research 52, no. 1 (1992): 70–80. http://dx.doi.org/10.1016/s0011-393x(05)80438-2.

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39

Bertel, O., and G. Noll. "Additional molsidomine in refractory unstable angina pectoris." Cardiovascular Drugs and Therapy 2, no. 1 (1988): 107–11. http://dx.doi.org/10.1007/bf00054260.

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40

Nitz, Rolf-Eberhard, and Volker B. Fiedler. "Molsidomine: Alternative Approaches To Treat Myocardial Ischemia." Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy 7, no. 1 (1987): 28–37. http://dx.doi.org/10.1002/j.1875-9114.1987.tb03503.x.

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41

&NA;. "Nifedipine and molsidomine suppress coronary artery spasm equally." Inpharma Weekly &NA;, no. 792 (1991): 18. http://dx.doi.org/10.2165/00128413-199107920-00053.

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Noack, Eike, and Martin Feelisch. "Molecular Aspects Underlying the Vasodilator Action of Molsidomine." Journal of Cardiovascular Pharmacology 14 (1989): S1–5. http://dx.doi.org/10.1097/00005344-198906152-00002.

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Noack, Eike, and Martin Feelisch. "Molecular Aspects Underlying the Vasodilator Action of Molsidomine." Journal of Cardiovascular Pharmacology 14 (1989): S1–5. http://dx.doi.org/10.1097/00005344-198914110-00002.

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Kisheva, Antoniya, Yoto Yotov, Sava Ognyanov, and Polina Nincheva. "Opportunities for molsidomine application in the clinical practice." Heart - Lung (Varna) 19, no. 3-4 (2013): 39. http://dx.doi.org/10.14748/hl.v19i3-4.3771.

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Weber, S. "La molsidomine dans le traitement de l'insuffisance coronaire." La Revue de Médecine Interne 8, no. 4 (1987): 437–43. http://dx.doi.org/10.1016/s0248-8663(87)80022-x.

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Darius, Harald, Andreas Mulfinger, Johannes Zander, Michael Spielberger, and J. Meyer. "No-releasing molsidomine augments aspirin — induced platelet inhibition." Journal of the American College of Cardiology 15, no. 2 (1990): A86. http://dx.doi.org/10.1016/0735-1097(90)92059-b.

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Cano, Jean-Paul, Jean-Claude Guillen, Rémy Jouve, et al. "Molsidomine prevents post-ischaemic ventricular fibrillation in dogs." British Journal of Pharmacology 88, no. 4 (1986): 779–89. http://dx.doi.org/10.1111/j.1476-5381.1986.tb16250.x.

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Kumins, Norman H., Julia Hunt, Richard L. Gamelli, and James P. Filkins. "MOLSIDOMINE INCREASES ENDOTOXIC SURVIVAL AND DECREASES CYTOKINE PRODUCTION." Shock 7, no. 3 (1997): 200–205. http://dx.doi.org/10.1097/00024382-199703000-00008.

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Karakoc, Habib, Ramazan Altintas, Hakan Parlakpinar, et al. "Protective Effects of Molsidomine Against Cisplatin-Induced Nephrototoxicity*." Advances in Clinical and Experimental Medicine 24, no. 4 (2015): 585–93. http://dx.doi.org/10.17219/acem/58970.

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Kwak, H. J., H. O. Pae, G. S. Oh, et al. "Molsidomine Ameliorates Experimental Allergic Encephalomyelitis in Lewis Rats." Immunopharmacology and Immunotoxicology 25, no. 1 (2003): 41–52. http://dx.doi.org/10.1081/iph-120018282.

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Journal articles on the topic 'Molsidomine'

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