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Relevant bibliographies by topics / Verapamil

Academic literature on the topic 'Verapamil'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 February 2023

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Journal articles on the topic "Verapamil"

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Vukovic-Ercegovic, Gordana, Natasa Perkovic-Vukcevic, Snezana Djordjevic, Zoran Segrt, Olivera Potrebic, Snezana Jankovic, Jasmina Jovic-Stosic, and Nadica Marinkovic. "Successful usage of intravenous lipid emulsion in treatment of acute verapamil poisoning: A case report." Vojnosanitetski pregled 74, no. 3 (2017): 278–81. http://dx.doi.org/10.2298/vsp150901010v.

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Introduction. During the last few years, intravenous lipid emulsions have been effectively used in treatment of acute poisonings with lipophilic substances, including verapamil. Case report. A 37-year-old women presented 1 hour after ingestion of 2.8 g verapamil with hypotension and complete heart block. Because of the applied standard therapy failure and further patients impairment, Intralipid? 20% was used. Sinus rhythm was restored, arterial blood pressure increased and verapamile concentrations, both total and free decreased. Conclusion. Intravenous lipid emulsion can be important in treatment of severe acute intoxication and cardiotoxicity caused by verapamil.

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Cartee, G. D., C. Briggs-Tung, and J. O. Holloszy. "Diverse effects of calcium channel blockers on skeletal muscle glucose transport." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 1 (July 1, 1992): R70—R75. http://dx.doi.org/10.1152/ajpregu.1992.263.1.r70.

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Verapamil, a calcium channel blocker, inhibited the insulin-stimulated glucose transport rate in isolated rat epitrochlearis muscle in a dose-dependent manner (1-200 microM) without affecting basal glucose transport rate. Verapamil's inhibition was rapid in onset and disappearance; changes in glucose transport rate were detectable when verapamil was added to or removed from the incubation medium 15 min prior to measurement of glucose transport. Verapamil also inhibited the stimulation of muscle glucose transport caused by hypoxia, indicating that the effect was not limited to insulin action. Although the optical isomers of verapamil vary considerably in their potency as Ca2+ channel blockers, they were equally effective inhibitors of insulin-stimulated glucose transport rate. Nifedipine (10-200 microM), a more potent blocker of skeletal muscle Ca2+ channels than verapamil, was less effective as an inhibitor of insulin-stimulated glucose transport. Furthermore, nifedipine (10 microM) did not inhibit hypoxia-stimulated glucose transport. Diltiazem (200 microM), another Ca2+ channel blocker, did not reduce insulin-stimulated glucose transport.

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Boyer, Allison Jo, Rachael Erin Ketcham, Clint Allen Hostetler, Jeffrey Paul Orlowski, and Ronald A. Squires. "Performance of Renal Allografts Perfused With Verapamil-Treated Perfusion Solution." Progress in Transplantation 31, no. 4 (October 29, 2021): 373–80. http://dx.doi.org/10.1177/15269248211045999.

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Verapamil has been used in perfusion solution to improve kidney performance, but evidence was anecdotal, and no research has been reported on recipient outcomes. Our organization began a program to evaluate Verapamil’s effect on pump performance, transplant rate, and recipient outcomes. One kidney in a pair was treated with Verapamil and one with standard perfusion. Donor inclusion criteria were age 18 or older and both kidneys were placed on the pump. The laterality of the treated kidney was changed every month to reduce bias. From January 1, 2020 to June 30, 2020, 88 kidneys were evaluated. Of those, 21 donors had both kidneys transplanted to different recipients, so for those 42 kidneys, recipient outcomes were evaluated. Small improvements in pump performance were observed in the Verapamil-treated kidneys and more were transplanted. No clinical differences were found in recipients between the Verapamil-treated and standard perfused kidneys. A larger cohort is needed to determine whether differences are significant.

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&NA;. "Verapamil see Lithium/verapamil." Reactions Weekly &NA;, no. 290 (March 1990): 8. http://dx.doi.org/10.2165/00128415-199002900-00042.

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Gowarty, Jasmine L., and Jon D. Herrington. "Verapamil as a culprit of palbociclib toxicity." Journal of Oncology Pharmacy Practice 25, no. 3 (March 9, 2018): 743–46. http://dx.doi.org/10.1177/1078155218761798.

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A promising drug, palbociclib, received accelerated approval as a first line treatment when used with the aromatase inhibitor, letrozole, for postmenopausal women with hormone receptor positive advanced or metastatic breast cancer. We report a case of a patient who presented with febrile neutropenia, grade 3 stomatitis with lip swelling, periorbital edema, and transaminitis while on palbociclib and verapamil. Labs normalized upon discontinuation of verapamil and our patient was able to continue treatment with palbociclib and letrozole. Verapamil’s inhibition of both permeability-glycoprotein (P-gp) and CYP3A4 is suspected to have led to the adverse side effects seen in our patient.

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&NA;. "Verapamil see Diltiazem/nifedipine/verapamil." Reactions Weekly &NA;, no. 310 (July 1990): 12. http://dx.doi.org/10.2165/00128415-199003100-00068.

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&NA;. "Verapamil." Reactions Weekly &NA;, no. 1382 (December 2011): 34. http://dx.doi.org/10.2165/00128415-201113820-00125.

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&NA;. "Verapamil." Reactions Weekly &NA;, no. 1183 (January 2008): 30. http://dx.doi.org/10.2165/00128415-200811830-00096.

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&NA;. "Verapamil." Reactions Weekly &NA;, no. 1153 (May 2007): 26. http://dx.doi.org/10.2165/00128415-200711530-00086.

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&NA;. "Verapamil." Reactions Weekly &NA;, no. 1158 (June 2007): 27. http://dx.doi.org/10.2165/00128415-200711580-00077.

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Dissertations / Theses on the topic "Verapamil"

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Anacleto, Ana Isabel. "Interpatient variability with the disposition of verapamil." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ44115.pdf.

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Peng, Yao. "Time-dependent kinetics of verapamil in rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0017/NQ46903.pdf.

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Leonardi, Luca. "Cardiovascular effects of verapamil in essential hypertension /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Khamanga, Sandile Maswazi Malungelo. "Formulation and assessment of verapamil sustained release tablets." Thesis, Rhodes University, 2005. http://hdl.handle.net/10962/d1018236.

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The oral route of drug administration is most extensively used due to the obvious ease of administration. Verapamil hydrochloride is a WHO listed phenylalkylarnine, L-type calcium channel antagonist that is mainly indicated for cardiovascular disorders such as angina pectoris, supraventricular tachycardia and hypertension. Due to its relatively short half-life of approximately 4.0 hours, the formulation of a sustained-release dosage form is useful to improve patient compliance and to achieve predictable and optimized therapeutic plasma concentrations. Direct compression and wet granulation were initially used as methods for tablet manufacture. The direct compression method of manufacture produced tablets that exhibited formulation and manufacturing difficulties. Mini-tablets containing veraparnil hydrochloride were then prepared by wet granulation using Surelease® E-7-19010.and Eudragit® NE 30D as the granulating agents after which the granules were incorporated with an hydrophilic matrix material, Carbopol® 974P NF. Granule and powder blends were evaluated using the angle of repose, loose and tapped bulk density, Can's compressibility index, Hausner's ratio and drug content. Granules with good flow properties and satisfactory compressibility were used for further studies. Tablets were subjected to thickness, diameter and weight variation tests, crushing strength, tensile strength, friability and content uniformity studies. Tablets that showed acceptable pharmaco-technical properties were selected for further analysis. Drug content uniformity and dissolution release rates were determined using a validated isocratic HPLC method. Initially, USP apparatus 1 and 3 dissolution apparatus were used to determine in-vitro drug release rates from the formulations over a 22-hour period. USP apparatus 3 was finally selected as it offers the advantages of mimicking, in part, the changes in the physicochemical environment experienced by products in the gastro-intestinal tract. Differences in release rates between the test formulations and a commercially available product, Isoptin® SR were observed at different pH's using USP apparatus 1. The release of veraparnil hydrochloride from matrix tablets was pH dependent and was markedly reduced at higher pH values. This may be due, in part, to the poor solubility of veraparnil hydrochloride at these pH values and also the possible interaction of verapamil hydrochloride with anionic polymers used in these formulations. Swelling and erosion behaviour of the tablets were evaluated and differences in behaviour were observed which may be attributed to the physico-chemical characteristics of the polymers used in this study. In-vitro dissolution profiles were characterized by the difference (j1) and similarity factor (j2) and also by a new similarity factor, Sct. In addition, the mechanism of drug release from these dosage forms was mainly evaluated using the Korsmeyer-Peppas model and the kinetics of drug release assessed using other models, including Zero order, First order, Higuchi, HixsonCrowell, Weibull and the Baker-Lonsdale model. Dissolution kinetics were best described by application of the Weibull model, and the Korsmeyer-Peppas model. The release exponent, n, confirmed that drug release from these dosage forms was due to the mixed effects of diffusion and swelling and therefore, anomalous release kinetics are predominant. In conclusion, two test batches were found to be comparable to the reference product Isoptin® SR with respect to their in-vitro release profiles.

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Mooij, Jacob Manuel Victor. "Studies on the pharmacokinetics and antihypertensive action of verapamil." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1986. http://arno.unimaas.nl/show.cgi?fid=6204.

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Walles, Markus. "Neue Analysenmethoden für Metabolismusstudien am Beispiel des Calciumantagonisten Verapamil." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=967332400.

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Al-Khalili, Luna. "Modification of acetominophen hepatotoxicity by the administration of verapamil." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq31176.pdf.

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KHAIRALLAH, JOSEPH. "Hepatites induites par le verapamil : a propos de deux observations et revue de la litterature." Toulouse 3, 1989. http://www.theses.fr/1989TOU31111.

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GEFFROY, SYLVIE. "Tachycardie ventriculaire idiopathique sensible au verapamil intraveineux : a propos de six observations." Nantes, 1994. http://www.theses.fr/1994NANT022M.

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Stow, Martin William. "Molecular analysis of verapamil hypersensitive multidrug resistant hamster cell lines." Thesis, University of York, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258425.

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Books on the topic "Verapamil"

1

Bender, F., and K. Greeff, eds. Kombinationstherapie der Herzrhytmusstörungen mit Chinidin und Verapamil. Heidelberg: Steinkopff, 1985. http://dx.doi.org/10.1007/978-3-642-85346-3.

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Weinstock, Barry S. Influence of verapamil on total and regional intravascular volume in the dog. [New Haven: s.n.], 1987.

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International Symposium, Calcium Antagonists in Cardiovascular Care (1991 : Basle, Switzerland), ed. Verapamil-- a cardioprotective strategy: Highlights from a satellite symposium to the International Symposium, Calcium Antagonists in Cardiovascular Care, Basle, Switzerland, Feb. 13, 1991. New York, NY: Raven Health Care Communications, 1991.

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4

Parker, Philip M., and James N. Parker. Verapamil: A medical dictionary, bibliography, and annoted research guide to Internet references. San Diego, CA: ICON Health Publications, 2004.

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5

Niels, Gadsbøll, Hansen Jørgen Fischer, Jespersen Christian M, and Sigurd Bjarn, eds. Danish verapamil infarction trials: Festschrift in honour of Jorgen Fischer Hansen's 60th birthday. [Copenhagen: Dept. of Cardiovascular Medicine, University of Copenhagen, Bispebjerg Hospital, 1997.

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Dubois, Natalie C. Inhibition of small cell lung cancer cell line (H-69) with the calcium channel blocker, Verapamil. Sudbury, Ont: Laurentian University, 1995.

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Albrecht, Fleckenstein, and Laragh John H. 1924-, eds. Hypertension--the next decade: Verapamil in focus : proceedings of an international symposium, Berlin ICC, 10-11 October 1985. Edinburgh: Churchill Livingstone, 1987.

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Muredda, Mario. The effects of calcium channel antagonist verapamil on the growth and energy metabolism of human MCF7 breast cancer cells. Sudbury, Ont: Laurentian University, 1998.

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9

J, Norris R., Wale Laurence, and Revlon Health Care Group, eds. Sustained release verapamil workshop. London: Medical News Tribune Group, 1985.

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10

Kombinationstherapie Der Herzrhytmusst Rungen Mit Chinidin Und Verapamil. Steinkopff-Verlag Darmstadt, 2012.

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Book chapters on the topic "Verapamil"

1

Beyer, Karl-Heinz. "Verapamil." In Biotransformation der Arzneimittel, 554–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74386-3_325.

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Schneeweiss, Adam, and Gotthard Schettler. "Verapamil." In Developments in Cardiovascular Medicine, 114–35. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-2063-0_14.

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Mehlhorn, Heinz. "Verapamil." In Encyclopedia of Parasitology, 3014. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4378.

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Mehlhorn, Heinz. "Verapamil." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4378-1.

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Peter, Helga. "Verapamil." In Springer Reference Medizin, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-642-54672-3_662-1.

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Mulhall, John P., and Lawrence C. Jenkins. "Intralesional Verapamil." In Atlas of Office Based Andrology Procedures, 87–95. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42178-0_12.

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Raschack, M., J. Gries, W. Heimann, M. Kirchengast, C. D. Müller, L. Szabo, H. J. Teschendorf, and L. Unger. "Pharmakologisches Profil neuer Verapamil-Derivate." In Therapie und Prävention mit Kalziumantagonisten, 115–34. Heidelberg: Steinkopff, 1988. http://dx.doi.org/10.1007/978-3-642-85362-3_11.

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Bachour, G. "Therapie der Kammerextrasystolie mit Chinidin-Verapamil." In Kombinationstherapie der Herzrhytmusstörungen mit Chinidin und Verapamil, 127–38. Heidelberg: Steinkopff, 1985. http://dx.doi.org/10.1007/978-3-642-85346-3_10.

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Schlepper, M. "Antiarrhythmisches Wirkungsprofil von Verapamil und Chinidin." In Kombinationstherapie der Herzrhytmusstörungen mit Chinidin und Verapamil, 27–45. Heidelberg: Steinkopff, 1985. http://dx.doi.org/10.1007/978-3-642-85346-3_3.

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Kadane, Joseph B. "Introduction to the Verapamil/Nitroprusside Study." In Bayesian Methods and Ethics in a Clinical Trial Design, 127–30. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118150603.ch5.

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Conference papers on the topic "Verapamil"

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Sheehy, Ryan M., Zoe C. Bachman, and Raymond J. Hohl. "Abstract 811: Schweinfurthin activity enhanced by verapamil." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-811.

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Mistry, Tuhin, Jaya Sharma, Shobha Purohit, and Gunjan Arora. "Attenuation of extubation responses: Comparison of prior treatment with verapamil and dexmedetomidine." In 15th Annual Conference of the Indian Society of Neuroanaesthesiology and Critical Care. Thieme Medical and Scientific Publishers Private Ltd., 2015. http://dx.doi.org/10.1055/s-0038-1667534.

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Hajighasemi, Fatemeh, and Abbas Mirshafiey. "Effect of verapamil on vascular endothelial growth factor production in immunocompetent cells." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4011.

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Methaneethorn, Janthima, Munlikar Chamnansua, Natnaree Kaewdang, and Manupat Lohitnavy. "A pharmacokinetic drug-drug interaction model of simvastatin and verapamil in humans." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944924.

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Bevan, Jane, and S. Heptinstall. "BOW CAN WE INHIBIT 5HT-INDUCED PLATELET AGGREGATION AND WHY SHOULD WE BOTHER?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643853.

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Platelets are induced to aggregate when 5-hydraxytryptamine (5HT) is added to citrated whole blood and the extent of aggregation can be measured using a Whole Blood Platelet Counter. We have used this method to study a) 5HT-induced platelet aggregation in normal human blood and the effects of 14 5HT receptor antagonists and 2 Ca++-channel blockers, and b) aggregation in blood from patients with peripheral vascular disease (PVD). Previous studies of platelet aggregation in platelet-rich plasma have indicated an increased platelet sensitivity to 5HT in PVD, and a multicentre study of ketanserin (a S2 antagonist) is in progress.5HT induces a transient reversible aggregation in human whole blood which can be prevented by 5HT receptor antagonists. The inhibitory effects of 7 relatively potent antagonists (IC50 7 -41nM, e.g. ketanserin and pizotifen) could not be surmounted by increasing the concentration of 5HT, but the inhibitory effects of 7 less potent antagonists (IC50 0.28 - 53uM, e.g. mepyramine and amitriptyline) could be surmounted by 5-HT. One Ca++-channel blocker (verapamil) inhibited platelet aggregation but another (amlodipine) had very little effect. Verapamil inhibited 5HT-induced aggregation at much lower concentrations (IC50 1.6μM) than those required for aggregation induced by PAF, adrenaline or ADP (IC50 values 32, 33 and >100uM respectively) and the inhibition was insurmountable.5HT-induced platelet aggregation in blood from patients with PVD does not differ qualitatively or quantitatively from aggregation in blood from healthy, age- and sex-matched controls: patients (n = 13), aggregation 30 seconds after adding 5uM 5HT = 55.1% ± 13.3(s.d.); controls (n = 13) aggregation = 48.3% ± 18.9(s.d.). Neither was the platelet aggregation induced by ADP, U46619 or PAF different in patients and controls.We conclude that different 5HT receptor antagonists inhibit 5HT-induced platelet aggregation with different potencies and, apparantly, different mechanisms of action, and that verapamil has a selective effect on 5HT-induced aggregation at relatively low concentrations. Results obtained in PVD do not encourage the use of a 5HT antagonist in this condition.

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Dias, Thales Augusto Oliveira, and Silvia Graciela Ruginsk Leitão. "Participation of calcium channels in the action of angiotensin II in astrocytes." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.299.

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Background: The renin-angiotensin-aldosterone system is the main regulator of blood pressure and blood volume, with most effects being mediated by angiotensin II (Ang-II) - responsible, in the central nervous system, for actions such as thirst and sodium appetite. Astrocytes are believed to mediate such a response, as they express receptors for Ang-II and respond directly to dehydration with impacting morphological changes in the synaptic microenvironment. Many of its functions involve L-type calcium channels (LTCCs). Objectives: Evaluate the participation of LTCCs in the effects induced by AngII in cultured hypothalamic astrocytes. Methods: The effect of incubation with verapamil on the morphological responses induced by Ang-II was evaluated in hypothalamic astrocyte culture, by analyzing the expression of the cytoskeletal protein GFAP and the cell viability by the MTT assay, by immunofluorescence. Results: Incubation with Ang-II reduced the cell area considerably due to GFAP expression in relation to the control group (DMEM p<0.001), indicating that the results observed on GFAP expression did not result from cell death. Conclusion: Incubation with Ang-II alters the astrocyte morphology, reducing its area, effect at least in part, blocked by the action of Verapamil, indicating the participation of LTCCs in the mediation of this process.

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Chen, Zulin, Haiyan Ge, Yan Lai, Jian-Min Tang, and Zhi-Tang Shan. "Experimental study on synergistic mechanism of verapamil for photodynmaic therapy on colonic adenocarcinoma cells." In Third International Conference on Photonics and Imaging in Biology and Medicine, edited by Qingming Luo, Valery V. Tuchin, Min Gu, and Lihong V. Wang. SPIE, 2003. http://dx.doi.org/10.1117/12.546539.

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Gardiner, Philip, Alexandra Jauhiainen, Robert Palmér, Jukka Mäenpää, Kristina Stenvall, and Bengt Larsson. "Effect of CYP3A4 inhibitors verapamil and itraconazole on the pharmacokinetics of AZD7986, an oral DPP1 inhibitor." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3977.

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Ho, A. T. N., T. N. Pham, and C. R. Barrios. "Catastrophic Non-Cardiogenic Pulmonary Edema Secondary to Massive Verapamil Overdose and Treatment with Extracorporeal Membrane Oxygenation." 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.a1665.

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Romeo, D., M. Salem, J. Burkhardt, and B. Jankowitz. "E-067 Verapamil and its association with hives in radial artery catheterization for neuroendovascular diagnostic angiograms." In SNIS 19th Annual Meeting Abstracts. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2022. http://dx.doi.org/10.1136/neurintsurg-2022-snis.178.

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