Relevant bibliographies by topics / Levosimendan

Academic literature on the topic 'Levosimendan'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Levosimendan"

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Efentakis, Panagiotis, Aimilia Varela, Evangelia Chavdoula, Fragiska Sigala, Despina Sanoudou, Roxane Tenta, Katerina Gioti, et al. "Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy." Cardiovascular Research 116, no. 3 (June 22, 2019): 576–91. http://dx.doi.org/10.1093/cvr/cvz163.

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Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxide synthase (eNOS), and protein kinase-A and G (PKA/PKG) pathways emerged as contributors to the cardioprotection, converging onto phospholamban (PLN). To verify the contribution of PLN, phospholamban knockout (PLN−/−) mice were assigned to PLN−/−/Control (N/S-0.9%), PLN−/−/DXR (18 mg/kg), and PLN−/−/DXR+LEVO (ac) for 14 days. Furthermore, female breast cancer-bearing (BC) mice were divided into: Control (normal saline 0.9%, N/S 0.9%), DXR (18 mg/kg), LEVO, and DXR+LEVO (LEVO, 24 μg/kg-bolus) for 28 days. Echocardiography was performed in all protocols. To elucidate levosimendan’s cardioprotective mechanism, primary cardiomyocytes were treated with doxorubicin or/and levosimendan and with N omega-nitro-L-arginine methyl ester (L-NAME), DT-2, and H-89 (eNOS, PKG, and PKA inhibitors, respectively); cardiomyocyte-toxicity was assessed. Single bolus administration of levosimendan abrogated DXR-induced cardiotoxicity and activated Akt/eNOS and cAMP-PKA/cGMP-PKG/PLN pathways but failed to exert cardioprotection in PLN−/− mice. Levosimendan’s cardioprotection was also evident in the BC model. Finally, in vitro PKA inhibition abrogated levosimendan-mediated cardioprotection, indicating that its cardioprotection is cAMP-PKA dependent, while levosimendan preponderated over milrinone and dobutamine, by ameliorating calcium overload. Conclusion Single dose levosimendan prevented doxorubicin cardiotoxicity through a cAMP-PKA-PLN pathway, highlighting the role of inotropy in doxorubicin cardiotoxicity.
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&NA;. "Levosimendan." Reactions Weekly &NA;, no. 1272 (October 2009): 21–22. http://dx.doi.org/10.2165/00128415-200912720-00073.

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&NA;. "Levosimendan." Reactions Weekly &NA;, no. 1314 (August 2010): 27. http://dx.doi.org/10.2165/00128415-201013140-00086.

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Figgitt, David P., Peter S. Gillies, and Karen L. Goa. "Levosimendan." Drugs 61, no. 5 (2001): 613–27. http://dx.doi.org/10.2165/00003495-200161050-00006.

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Aronow, Wilbert S. "Levosimendan." Drugs 61, no. 5 (2001): 628–29. http://dx.doi.org/10.2165/00003495-200161050-00007.

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Nieminen, Markku S. "Levosimendan." Drugs 61, no. 5 (2001): 628–29. http://dx.doi.org/10.2165/00003495-200161050-00008.

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Innes, Carmen A., and Antona J. Wagstaff. "Levosimendan." Drugs 63, no. 23 (2003): 2651–71. http://dx.doi.org/10.2165/00003495-200363230-00009.

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&NA;. "Levosimendan." Inpharma Weekly &NA;, no. 1136 (May 1998): 7. http://dx.doi.org/10.2165/00128413-199811360-00013.

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Mason, Paula. "Levosimendan." Intensive and Critical Care Nursing 19, no. 6 (December 2003): 370–71. http://dx.doi.org/10.1016/s0964-3397(03)00074-0.

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Levin, Asher, and Gideon Paret. "Levosimendan." Journal of Pediatric Intensive Care 02, no. 03 (July 28, 2015): 095–103. http://dx.doi.org/10.3233/pic-13057.

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Dissertations / Theses on the topic "Levosimendan"

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Cavalcanti, Ruben Lundgren. "Efeitos da dobutamina ou levosimendana nas variáveis cardiopulmonares após a dexmedetomidina em pôneis submetidos à hipotensão pelo isoflurano." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/150240.

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Isoflurano reduz o débito cardíaco e produz vasodilatação periférica resultando em hipotensão sistêmica. Hipotensão pode contribuir para morbidade e mortalidade em equinos. Queda na pressão sanguínea pode ser tratada com inotrópicos e/ou vasopressores. Levosimendana é um inotrópico sensibilizador de cálcio que produz aumento na contratilidade e diminuição na resistência vascular periférica. Dexmedetomidina é um agonista de receptor adrenérgico α2 que aumenta a resistência vascular periférica. Este estudo objetivou avaliar os efeitos cardiopulmonares da dobutamina versus levosimendana após infusão de dexmedetomidina em pôneis com hipotensão induzida pelo isoflurano. Dez pôneis saudáveis (média 13,9 ± DP 2,4 anos) foram anestesiados com detomidina, seguido por quetamina e midazolam e mantidos em um estado hipotensivo induzido por um nível profundo de anestesia com isoflurano (2 CAM). Os animais foram randomizados para receber dexmedetomidina e dobutamina (DD; n=5) ou dexmedetomidina e levosimendana (DL; n=5). Após 45 minutos do estado estável de hipotensão, as variáveis basais foram registradas. Dexmedetomidina foi administrada em 10 minutos (3,5 μg.Kg-1) e as variáveis foram registradas; em seguida, infusão contínua de dexmedetomidina iniciou (1,75 μg.Kg-1.hr-1) e as variáveis foram registradas após 45 minutos. Dobutamina (5 μg.Kg-1.min-1) ou levosimendana (12 μg.Kg-1) foram administradas e as variáveis foram registradas após 10 minutos, seguido por ITC de dobutamina ou de levosimendana (0,2 μg.Kg-1.min-1) com novo registro das variáveis após 45 minutos. Por fim, as infusões foram interrompidas e as variáveis foram registradas após 45 minutos. Isoflurano (2 CAM) reduziu as PAs, o IS e o IC, mas não afetou o IRVS. Em relação ao isoflurano, bolus de dexmedetomidina aumentou as PAs pelo aumento do IRVS e da PVC, mas não afetou o IS e o IC previamente reduzidos pelo isoflurano. Após 45 minutos, dexmedetomidina elevou a PMAP, o VD/VT, o lactato e a creatinina e reduziu as PAs, o IRVS e a FC, mas não afetou o IC. Dexmedetomidina também reduziu o CaO2, a PaO2, a Pv̅O2, a Sv̅O2, o Cv̅O2, a Hb e o ḊO2I em ambos grupos em relação ao tempo basal. Dobutamina e levosimendana aumentaram significativamente o IS e o IC, mas dobutamina aumentou as PAs, o IRVS, o IRVP, a PMAP, a PVC, o CaO2, o Cv̅O2, a Hb, o ḊO2I e reduziu a creatinina e a O2ER, enquanto levosimendana não afetou as PAs, reduziu a PVC e o IRVS e aumentou o VD/VT e o Q̇s/Q̇t. Infusão de dexmedetomidina causa prejuízos cardiopulmonares importantes a despeito de aumentar as PAs após dose em bolus IV durante hipotensão induzida pelo isoflurano em pôneis. Dobutamina é melhor alternativa que levosimendana para restaurar as funções cardiovasculares e manter oxigenação durante infusão de dexmedetomidina associada a dose alta de isoflurano em pôneis.
Isoflurane decreases cardiac output and produces peripheral vasodilation resulting in systemic hypotension. Hypotension may contribute to morbidity and mortality in equines. Drop in blood pressure can be treated with inotropic and or vasopressors. Levosimendan is a calcium sensitizer that produces increase in contractility and decrease in systemic vascular resistance. Dexmedetomidine is an α2 adrenergic-receptor agonist that increases systemic vascular resistance. This study aimed to evaluate the cardiopulmonary effects of dobutamine versus levosimendan after infusion of dexmedetomidine on isoflurane-induced hypotension in ponies. Ten healthy ponies (mean 13,9 ± SD 2,4 years) were anesthetized with detomidine followed by ketamine and midazolam and maintained at a steady hypotensive state induced by a deep level of isoflurane anesthesia (2 MAC). Animals were randomized to receive dexmedetomidine and dobutamine (DD; n=5) or dexmedetomidine and levosimendan (DL; n=5). After 45 min of steady state, baseline variables were recorded. Dexmedetomidine was administered over 10 minutes (3,5 μg.Kg-1), and variables were recorded; thereafter, dexmedetomidine CRI started (1,75 μg.Kg-1.hr-1), and variables were recorded after 45 minutes. Dobutamine (5 μg.Kg-1.min-1) or levosimendan (12 μg.Kg-1) were administered over 10 minutes and variables were recorded, followed by dobutamine or levosimendan CRI (0,2 μg.Kg-1.min-1) for 45 minutes, then variables were recorded a sixth time. Lastly, infusions were interrupted and the variables were again recorded after 45 minutes. Isoflurane (2 MAC) decreased arterial blood pressures (ABPs), SI and CI, but not affected SVR. In relation to isoflurane, bolus of dexmedetomidine increased ABPs due to augmentation on RVS and PCV, but not affected SI and CI already reduced by isoflurane. After 45 minutes, dexmedetomidine raised MPAP, VD/VT, lactate and creatinine and reduced ABPs, SVR, and HR, but not affected CI. Dexmedetomidine also reduced CaO2, PaO2, Pv̅O2, Sv̅O2, Cv̅O2, Hb and ḊO2I in both groups compared to baseline. Dobutamine and levosimendan increased SI and CI, but dobutamine increased ABPs, SVRI, PVRI, MPAP, CVP, CaO2, Cv̅O2, Hb, ḊO2I and decreased creatinine and O2ER, while levosimendan not affected ABPs, decreased CVP and SVRI and increased VD/VT and Q̇s/Q̇t. Dexmedetomidine CRI during isoflurane-induced hypotension in ponies causes statistically significant cardiopulmonary effects regardless of increasing the ABPs after bolus administration. Dobutamine is better alternative than levosimendan for restoring cardiovascular function and maintaining oxygenation during CRI dexmedetomidine associated with high-dose isoflurane in ponies. Because the proposed vasoconstriction model produced late opposite physiological effect, further studies with levosimendan in ponies and horses remain to be performed, especially in clinical patients. Likewise, further studies are justified to evaluate the effect of levosimendan on regional tissue perfusion.
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Prem, Susanne [Verfasser], and Robert H. G. [Akademischer Betreuer] Schwinger. "Levosimendan bei Patienten mit akuter Herzinsuffizienz / Susanne Prem. Betreuer: Robert H.G. Schwinger." Regensburg : Universitätsbibliothek Regensburg, 2016. http://d-nb.info/1082128104/34.

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Berg, Blomkvist Sofia, and Linda Eriksson. "Psykosocialt stöd vid kronisk hjärtsvikt och planerade repetitiva behandlingar med levosimendan : -en kvalitativ intervjustudie-." Thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-255832.

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Taipe, Quispe Neri Nohemi. "Levosimendan y mortalidad en pacientes con síndrome de bajo gasto cardiaco post cirugía cardiaca." Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2013. https://hdl.handle.net/20.500.12672/12927.

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Objetivo: Determinar que el uso de Levosimendan disminuye la mortalidad hospitalaria en el síndrome de bajo gasto post cirugía cardiaca en pacientes adultos admitidos en el servicio de UCI del HNERM en el periodo 2009-2011. Material y Métodos: La presente investigación es de tipo Descriptivo, Analítico .La población está conformada por 63 pacientes adultos con síndrome de bajo gasto post cirugía cardiaca y que recibieron Levosimendan a una dosis continua de 0.1 mcg/kg/min en una solución glucosada al 5%. Resultados: La investigación concluye que hay una mejora estadísticamente significativa en la fracción de eyección, la media de la Fracción de eyección por ecografía preoperatoria por Simpson aumenta de 28.4% a 38.9% significativamente P<0.05 ,el 50% del total paciente mujeres con síndrome de bajo gasto cardiaco y con uso de Levosimendan tienen edad de 71 a 80 años. Asimismo se aprecia que del total de varones con síndrome de bajo gasto cardiaco y con uso de Levosimendan el 38.2% tiene edad de 61 a 70 años los pacientes en el preoperatorios el 63.5% presentan clase funcional III y el 36.5% presentan clase funcional IV , que del total de pacientes en el postoperatorios el 50.8% presentan clase funcional I y el 44.4% presentan clase funcional II. Se encontró que la media de la estancias hospitalaria es de 2.3 días . Los pacientes síndrome de Bajo Gasto Cardiaco Post Cirugía Cardiaca con el uso de levosimendan el 90.5% permanecen vivos y el 9.5% fallecieron en el posoperatorio temprano. Se encontró un índice cardiaco de 3.8. Conclusiones: Se observó que los pacientes posoperados de cirugía cardiaca que cursaron con sindrome de bajo gasto cardiaco y que recibieron levosimendan, infusión continua de 0.1 mcg/kg/min. presentaron una disminución en la mortalidad postoperatoria, asimismo hay una mejora estadísticamente significativa en la fracción de eyección.
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Kohnke, Anja [Verfasser]. "Experimentelle Untersuchungen zur proarrhythmischen Wirkung des Kalzium-Sensitizers Levosimendan sowie möglicher protektiver Therapieoptionen / Anja Kohnke." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2017. http://d-nb.info/1136279342/34.

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Kivikko, Matti. "Hemodynamic effects and pharmacokinetics of levosimendan and its metabolites in patients with severe heart failure." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/kivikko/.

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Kleinebrahm, Maria [Verfasser]. "Einfluss der Gabe von Levosimendan auf die Nierenfunktion bei herzchirurgischen Eingriffen unter Einsatz der extrakorporalen Zirkulation / Maria Kleinebrahm." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2014. http://d-nb.info/1063815916/34.

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de, Winter J. M., B. Joureau, V. Sequeira, N. F. Clarke, der Velden J. van, G. J. Stienen, H. Granzier, A. H. Beggs, and C. A. Ottenheijm. "Effect of levosimendan on the contractility of muscle fibers from nemaline myopathy patients with mutations in the nebulin gene." BioMed Central, 2015. http://hdl.handle.net/10150/610333.

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BACKGROUND: Nemaline myopathy (NM), the most common non-dystrophic congenital myopathy, is characterized by generalized skeletal muscle weakness, often from birth. To date, no therapy exists that enhances the contractile strength of muscles of NM patients. Mutations in NEB, encoding the giant protein nebulin, are the most common cause of NM. The pathophysiology of muscle weakness in NM patients with NEB mutations (NEB-NM) includes a lower calcium-sensitivity of force generation. We propose that the lower calcium-sensitivity of force generation in NEB-NM offers a therapeutic target. Levosimendan is a calcium sensitizer that is approved for use in humans and has been developed to target cardiac muscle fibers. It exerts its effect through binding to slow skeletal/cardiac troponin C. As slow skeletal/cardiac troponin C is also the dominant troponin C isoform in slow-twitch skeletal muscle fibers, we hypothesized that levosimendan improves slow-twitch muscle fiber strength at submaximal levels of activation in patients with NEB-NM. METHODS: To test whether levosimendan affects force production, permeabilized slow-twitch muscle fibers isolated from biopsies of NEB-NM patients and controls were exposed to levosimendan and the force response was measured. RESULTS: No effect of levosimendan on muscle fiber force in NEB-NM and control skeletal muscle fibers was found, both at a submaximal calcium level using incremental levosimendan concentrations, and at incremental calcium concentrations in the presence of levosimendan. In contrast, levosimendan did significantly increase the calcium-sensitivity of force in human single cardiomyocytes. Protein analysis confirmed that the slow skeletal/cardiac troponin C isoform was present in the skeletal muscle fibers tested. CONCLUSIONS: These findings indicate that levosimendan does not improve the contractility in human skeletal muscle fibers, and do not provide rationale for using levosimendan as a therapeutic to restore muscle weakness in NEB-NM patients. We stress the importance of searching for compounds that improve the calcium-sensitivity of force generation of slow-twitch muscle fibers. Such compounds provide an appealing approach to restore muscle force in patients with NEB-NM, and also in patients with other neuromuscular disorders.
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Alomari, Abdul-Hakeem Hussein Electrical Engineering &amp Telecommunications Faculty of Engineering UNSW. "Spectral analysis of arterial blood prssure and stroke volume variability: the role of Calcium channel blockers and sensitizers." Publisher:University of New South Wales. Electrical Engineering & Telecommunications, 2008. http://handle.unsw.edu.au/1959.4/43923.

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In this thesis, we included results from two studies. The first one considered the effects of the blood volume changes, during blood donation, on the heart rate variability (HRV) measured, non-invasively, form electrocardiographic (ECG) and photoplethysmographic (PPG) signals. Our results showed that, during blood donation, there were no significant changes in the pulsatile area of PPG signal, while heart rate increased. No significant changes were noticed in HRV extracted from both signals. Error analysis between the HRV extracted from ECG and peak interval variability (PIV) suggested that the error during blood donation was increased which means that the use of PIV extracted from PPG signal, used as a replacement diagnostic tool in clinical applications, needs further investigations and should be carefully studied in non-stationary cardiovascular situations such as blood donation. The imbalance between the two branches of the autonomic nervous system, sympathetic and parasympathetic, vagal, may result in a harmful activation of myocardial tissues which cause arrhythmias and sudden cardiac death. Although the study of the sympathovagal balance have been attracting many researchers, further studies are needed to elucidate the effects of many kinds of drugs on the autonomic modulation of the cardiac muscle, specifically, the cells of sinoatrial (SA) node. The aim of the second part of this thesis was to assess the effects of calcium channel blocker (Verapamil), calcium channel sensitizer (Levosimendan), calcium chloride (CaCl2), the combinations of verapamil/ CaCl2, levosimendan/ CaCl2, and noradrenaline infusion on beat-to-beat cardiovascular variability represented, in this research, by systolic blood pressure variability (SBPV), and stroke volume variability (SVV) signals. We used Fat Fourier Transform (FFT) to evaluate the power spectral density of the fluctuations in both signals to evaluate the effects of short-term treatments with those drugs on the sympathovagal balance in normal rats. Then, we compared the spectra obtained from SBPV and SVV to decide which of these fluctuations along with corresponding spectrum was more able to provide a clear feedback about the autonomic nervous system. Our data suggests that there were a significant correlations between low- (LF), mid- (MF), and high-frequency (HF) spectra obtained from SBPV and SVV except between the HF spectra estimated from after the infusion of levosimendan where a poor correlation (r = 0.530, p = 0.281) was noticed. This that both HF components obtained provide different information regarding the autonomic nervous system modulation of the SA node cells, while the results obtained from the rest of experiments showed that both signals provide same information about the modulation of sympathetic and parasympathetic tone due to all stages of different drugs infusion studied in this thesis. Besides that, we found that both spectra may be used to track the fluctuations in the cardiac output as a result of the drugs infusion.
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Axelsson, Birger. "Cardiac effects of non-adrenergic inotropic drugs : clinical and experimental studies." Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-68967.

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Background: Myocardial failure and dysfunction is not uncommon during critical illness and following cardiac surgery. For optimal treatment, a better understanding of the effects of inotropic drugs is needed. In this thesis, two non-adrenergic mediated inotropes, milrinone and levosimendan were studied in different models of myocardial dysfunction. The study aims were to assess the following: the effects of milrinone on blood flow in coronary artery bypass grafts during CABG surgery; the effects of milrinone on left ventricular diastolic function during post-ischaemic myocardial dysfunction; whether milrinone or levosimendan are protective or injurious during acute myocardial ischaemia, and if levosimendan potentiates myocardial function when added to milrinone in an experimental model of post-ischaemic (stunned) myocardium. Material and Methods: In Study I, 44 patients undergoing coronary artery bypass surgery(CABG) were included as subjects. Milrinone or saline was administrated in a single dose during cardio-pulmonary bypass (CPB) and coronary graft flow measurements were recorded after 10 and 30 min following CPB. In Study II; 24 patients undergoing CABG had estimations of peak ventricular filling rates made before and after CPB with administration of milrinone or saline as a single dose during CPB, performed by assessment of the rate of change in diastolic cross-sectional left ventricular area. In Study III, energy-metabolic effects of milrinone and levosimendan were measured in an anaesthetized porcine model during 45 minutes of regional myocardial ischemia. Microdialysis sampling of metabolites of local ischemic metabolism allowed assessment of glycolytic activity and the degree of myocardial calcium overload. In Study IV, in a porcine model of postischaemic myocardial stunning, ventricular pressure-volume relationships were analyzed when milrinone or a combination of milrinone and levosimendan were given together. Results: In Study I, there was a clear increase in non-sequential saphenous vein graft blood flow with milrinone at 10 minutes (64.5 ± 37.4 compared to placebo 43.6 ± 25.7 ml/min (mean ± SD).). A decreasing but still measureable flow increase was seen for milrinone at 30 minutes. In Study II, an increase in early left ventricular filling rate (ventricular cross-sectional area rate of change,dA/dt) was seen in the milrinone treated group. Pre-bypass milrinone group dA/dt 22.0 ± 9.5 changed to post-bypass values dA/dt 27.8 ± 11.5 cm2/sec). Placebo group pre-bypass dA/dt was 21.0 ± 8.7 and post-bypass 17.1 ± 7.1 cm2/sec. A milrinone effect was demonstrated in an adjusted regression model (p = 0.001). In Study III, neither milrinone nor levosimendan led to a change in energy-metabolic activity during ischemia as reflected by interstitial glucose, pyruvate, lactate orglycerol. Neither drug exacerbated the relative myocardial calcium overload during ischemia. In Study IV, milrinone improved active relaxation (tau) in post-ischemic stunned myocardium, but did not markedly improve systolic function by preload recruitable stroke work. Levosimendan added to milrinone showed minimal effect on active relaxation but a positive effect on systolic function in combination with milrinone. Conclusions: We conclude that milrinone treatment leads to an increase in blood flow in newly implanted coronary saphenous vein grafts, and improves ventricular relaxation post-cardiopulmonary bypass. Neither milrinone nor levosimendan, in this porcine model, negatively influence myocardial energy metabolism or calcium overload during acute ischaemia. Addition of levosimendan to milrinone treatment during post-ischaemic ventricular dysfunction may provide additive inotropic effects on systolic function but probably not for active relaxation.
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Books on the topic "Levosimendan"

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Fayssoil, Abdallah, and Djillali Annane. Inotropic agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0036.

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Inotropes are drugs commonly used in the intensive care unit. This class of agents includes a broad variety of molecules that improve cardiac index by increasing intracellular concentrations of cyclic AMP, or sensitivity to intracellular calcium, or by inhibiting the sodium/potassium pump. The main inotropic agents available are digoxin, catecholamines, and non-catecholergic drugs, e.g. phosphodiesterase inhibitors and levosimendan. In practice, dobutamine, a beta1 and beta2 agonist, is the inotrope of choice in patients with acute heart failure, or in patients with severe sepsis and evidence for left ventricle dysfunction. Levosimendan may be an alternative choice in patients with severe heart failure, particularly for those previously treated with beta-blockers. The main serious adverse events related to any inotrope are life-threatening arrhythmias.
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Book chapters on the topic "Levosimendan"

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Greco, Massimiliano, Gianluca Paternoster, and Daniela Mamo. "Levosimendan." In Reducing Mortality in the Perioperative Period, 47–54. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46696-5_7.

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Greco, Massimiliano, Gianluca Paternoster, and Daniela Mamo. "Levosimendan to Reduce Perioperative Mortality." In Reducing Mortality in the Perioperative Period, 49–55. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-02186-7_7.

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Lomivorotov, Vladimir, Martina Baiardo Redaelli, and Vladimir Boboshko. "Levosimendan in Cardiogenic Shock and Low Cardiac Output Syndrome." In Reducing Mortality in Critically Ill Patients, 107–14. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71917-3_12.

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Rehberg, S., P. Enkhbaatar, and D. L. Traber. "Role of the Calcium Sensitizer, Levosimendan, in Perioperative Intensive Care Medicine." In Intensive Care Medicine, 498–510. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-92278-2_47.

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Rehberg, S., P. Enkhbaatar, and D. L. Traber. "Role of the Calcium Sensitizer, Levosimendan, in Perioperative Intensive Care Medicine." In Yearbook of Intensive Care and Emergency Medicine, 498–510. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-92276-6_47.

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Mebazaa, Alexandre, John R. Teerlink, and Piero Pollesello. "Calcium Sensitizer Levosimendan and Its Use in Acute Heart Failure and Related Conditions." In Acute Heart Failure, 595–607. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84628-782-4_55.

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Morelli, A., M. Passariello, and M. Singer. "Inotropic Support in the Treatment of Septic Myocardial Dysfunction: Pathophysiological Implications Supporting the Use of Levosimendan." In Annual Update in Intensive Care and Emergency Medicine 2014, 407–19. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-03746-2_31.

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Jain, Vidyut, and Avani Jain. "Levosimendan." In CSI: Cardiology Update 2016, 757. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/13035_100.

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Antoniades, Charalambos, Michael Demosthenous, Dimitris Tousoulis, Costantinos Bakogiannis, Nikolaos Koumallos, and Christodoulos Ste. "Levosimendan in Heart Failure." In Frontiers in Cardiovascular Drug Discovery, 259–69. BENTHAM SCIENCE PUBLISHERS, 2012. http://dx.doi.org/10.2174/978160805160111001010259.

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Ainsworth, Sean. "L." In Neonatal Formulary, edited by Sean Ainsworth, 425–72. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198840787.003.0024.

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Abstract:
This chapter presents information on neonatal drugs that begin with L, including use, pharmacology, adverse effects, fetal and infant implications of maternal treatment, treatment, and supply of Labetalol hydrochloride, Lactoferrin, Lamivudine, Lamotrigine, Lansoprazole, Levetiracetam, Levosimendan, Levothyroxine sodium, Lidocaine = Lignocaine (former BAN), Linezolid, Lipid emulsions for parenteral nutrition, Loperamide, Lopinavir with ritonavir, Lorazepam, and Low-molecular-weight heparins and other anticoagulants
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Conference papers on the topic "Levosimendan"

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Sudy, Roberta, Adam L. Balogh, Gergely H. Fodor, Barna Babik, Ferenc Petak, and Orsolya Ivankovitsne Kiss. "Levosimendan reduces cholinergic bronchoconstriction: The role of KATPchannels." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2235.

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Welk, E., M. Heep, P. Grieshaber, B. Niemann, K. D. Schlüter, and A. Boening. "Levosimendan during Cardiac Surgery Deteriorates Cardiac Function in Rats." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678927.

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Kalampokas, N., S. Erbel-Kurdtsize, M. Arkikan, P. Rellecke, U. Boeken, A. Albert, A. Lichtenberg, H. Aubin, and P. Akhyari. "Effects of Preoperative Levosimendan on Perioperative Outcome after LVAD Implantation." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705351.

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Schellekens, Wilhelmus J., Hieronymus W. van Hees, Marianne Linkels, J. G. van der Hoeven, P. N. R. Dekhuijzen, G. J. Scheffer, and Leo M. Heunks. "Effects Of Levosimendan On Ventilator-Induced Diaphragm Injury In Septic Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4256.

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Böttger, C., A. Mehdiani, H. Aubin, R. Westenfeld, S. Erbel, F. Sipahi, H. Dalyanoglu, P. Akhyari, A. Lichtenberg, and U. Boeken. "Primary Graft Dysfunction after Heart Transplantation: Optimal Timing of Levosimendan Application." In 49th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1705446.

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van Hees, HW, M. Linkels, PN Dekhuijzen, and LM Heunks. "Levosimendan Enhances Force Generation of Diaphragm Muscle from Patients with COPD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6129.

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Rieg, Annette D., Rolf Rossaint, Stefan Uhlig, and Christian Martin. "Levosimendan Relaxes Pulmonary Arteries And Veins In Precision-Cut Lung Slices." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2627.

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Böning, A., B. Niemann, M. Heep, C. Hemmerich, E. Welk, and K. D. Schlüter. "Levosimendan during Cardiac Surgery Improves Cardiac Function in Ischemic Rat Hearts." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725668.

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Deschka, H., B. Schäfers, A. Gottschalk, M. Scherer, S. Martens, and H. Welp. "Effects of Levosimendan Therapy in Patients Undergoing Extracorporeal Membrane Oxygenation after Cardiac Surgery." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679012.

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Luo, Q., Q. Jin, Z. Liu, Y. Zhang, Z. Zhao, and C. Xiong. "Clinical Observation of Levosimendan in Patients with Severe Pulmonary Hypertension and Right Heart Failure." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2498.

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Reports on the topic "Levosimendan"

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Luo, Jing-Chao, Wen-He Zheng, Chang Meng, Hui-Bin Huang, Hua Zhou, Zhe Luo, and Yuan Xu. Levosimendan to facilitate weaning from cardiorespiratory support in critically ill patients: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0024.

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The heart failure drug levosimendan doesn’t improve outcomes in adults with severe infections. National Institute for Health Research, December 2016. http://dx.doi.org/10.3310/signal-000347.

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