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Relevant bibliographies by topics / Guanethidine

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Academic literature on the topic 'Guanethidine'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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Journal articles on the topic "Guanethidine"

1

GSCHWIND, C., R. FRICKER, G. LACHER, and M. JUNG. "Does Peri-Operative Guanethidine Prevent Reflex Sympathetic Dystrophy?" Journal of Hand Surgery 20, no. 6 (December 1995): 773–75. http://dx.doi.org/10.1016/s0266-7681(95)80045-x.

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The use of intravenous guanethidine blocks is an accepted treatment for established reflex sympathetic dystrophy (RSD). Some units administer intravenous guanethidine peri-operatively with the intention of protecting their patients from post-operative dystrophy. There have been no studies confirming this protective effect of peri-operative guanethidine. Between 1992 and 1994 we performed a prospective randomized double blind study in 71 patients undergoing fasciectomy for Duputyren’s disease. Peri-operative guanethidine did not prevent post-operative RSD in our series.

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Valenti, Piero, Angela Rampa, Maria Carrara, Stefano Zampiron, Pietro Giusti, and Lorenzo Cima. "Cyclovinylogues of Guanethidine." Archiv der Pharmazie 321, no. 2 (1988): 57–59. http://dx.doi.org/10.1002/ardp.19883210202.

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3

POVLSEN, B., and A. SIRSJÖ. "Sympathetic Block Significantly Improves Reperfusion in Skeletal Muscle Following Prolonged Use of Tourniquet." Journal of Hand Surgery 24, no. 6 (December 1999): 738–40. http://dx.doi.org/10.1054/jhsb.1999.0252.

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The effects of guanethidine sympathetic nerve blocks on reperfusion of skeletal muscle was studied in rats. After 3 hours of ischaemia reperfusion was significantly better in animals that had received guanethidine.

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Dwyer, Kelley W., Paolo P. Provenzano, Peter Muir, Wilmot B. Valhmu, and Ray Vanderby. "Blockade of the sympathetic nervous system degrades ligament in a rat MCL model." Journal of Applied Physiology 96, no. 2 (February 2004): 711–18. http://dx.doi.org/10.1152/japplphysiol.00307.2003.

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We hypothesize that blockade of the sympathetic nervous system degrades ligament. We tested this hypothesis in a rat medial collateral ligament (MCL) model. Fifteen animals were treated for 10 days with the sympathetic chemotoxin guanethidine using osmotic pumps, whereas 15 control rats received pumps containing saline. A reduction in plasma concentrations of norepinephrine in the guanethidine rats indicated a significant decrease in sympathetic nerve activity. Vasoactive intestinal peptide and neuropeptide Y were decreased in MCLs from guanethidine animals, as quantified by radioimmunoassays. Tissue vascularity was substantially increased in guanethidine MCLs, whereas mechanical properties were significantly decreased. Proteases, such as matrix metalloproteinases (MMP) and cysteine proteases, play a major role in ligament degradation. The proteases MMP-13, cathepsin K, and tartrate-resistant acid phosphatase (TRAP) have collagenolytic activity and have been shown in rat ligament tissues. To determine whether the degradation seen in this study was due to protease activity, we determined the expression of these enzymes in control and treated MCLs. Real-time quantitative PCR revealed that guanethidine treatment increased expression of MMP-13 and cathepsin K mRNAs, although overall expression levels of MMP-13 and TRAP were relatively low. Histology also identified increases in TRAP and cathepsin K, but not MMP-13, in guanethidine-treated tissues. Results support our hypothesis that blockade of the sympathetic nervous system substantially degrades ligament.

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TANAKA, Rumiko, Masayuki HARAMURA, Akito TANAKA, and Noriaki HIRAYAMA. "Structure of Guanethidine Monosulfate." Analytical Sciences: X-ray Structure Analysis Online 21 (2005): x111—x112. http://dx.doi.org/10.2116/analscix.21.x111.

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Richardson, D. W., and E. M. Wyso. "HUMAN PHARMACOLOGY OF GUANETHIDINE." Annals of the New York Academy of Sciences 88, no. 4 (December 15, 2006): 944–55. http://dx.doi.org/10.1111/j.1749-6632.1960.tb20086.x.

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Kalmanovitch, D. V. A., and P. B. Hardwick. "Hypotension after guanethidine block." Anaesthesia 43, no. 3 (February 22, 2007): 256. http://dx.doi.org/10.1111/j.1365-2044.1988.tb05580.x.

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Castrén, J. A., and S. Pohjola. "GUANETHIDINE AND AQUEOUS HUMOR DYNAMICS." Acta Ophthalmologica 40, no. 4 (May 27, 2009): 358–61. http://dx.doi.org/10.1111/j.1755-3768.1962.tb02381.x.

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Walters, Karen M., Magalie Boucher, Germaine G. Boucher, Alan C. Opsahl, Peter R. Mouton, Chang-Ning Liu, Casey R. Ritenour, Thomas T. Kawabe, Hayley N. Pryski, and Christopher J. Somps. "No Evidence of Neurogenesis in Adult Rat Sympathetic Ganglia Following Guanethidine-Induced Neuronal Loss." Toxicologic Pathology 48, no. 1 (April 15, 2019): 228–37. http://dx.doi.org/10.1177/0192623319843052.

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The potential for neurogenesis in the cranial (superior) cervical ganglia (SCG) of the sympathetic nervous system was evaluated. Eleven consecutive daily doses of guanethidine (100 mg/kg/d) were administered intraperitoneally to rats in order to destroy postganglionic sympathetic neurons in SCG. Following the last dose, animals were allowed to recover 1, 3, or 6 months. Right and left SCG from guanethidine-treated and age-matched, vehicle-treated control rats were harvested for histopathologic, morphometric, and stereologic evaluations. Both morphometric and stereologic evaluations confirmed neuron loss following guanethidine treatment. Morphometric analysis revealed a 50% to 60% lower number of tyrosine hydroxylase (TH)-positive neurons per unit area of SCG at both 3 and 6 months of recovery, compared to ganglia of age-matched controls, with no evidence of restoration of neuron density between 3 and 6 months. Reductions in TH-positive neurons following guanethidine treatment were corroborated by unbiased stereology of total hematoxylin and eosin-stained neuron numbers in SCG. Stereologic analyses revealed that total neuron counts were lower by 37% at 3 months of recovery when compared to age-matched vehicle controls, again with no obvious restoration between 3 and 6 months. Thus, no evidence was found that postganglionic neurons of the sympathetic nervous system in the adult rat have a neurogenic capacity.

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Kinoshita, Y., and W. W. Monafo. "Guanethidine chemical sympathectomy: spinal cord and sciatic nerve blood flow." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1155—H1159. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1155.

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The spinal cord vasculature is innervated by noradrenergic nerve fibers, the role of which in the regulation of regional spinal cord blood flow (RSCBF) is presently unclear. We used the distribution of [14C]butanol to simultaneously measure RSCBF at seven cord levels and the regional blood flow in sciatic nerve (NBF), truncal skin, and biceps femoris muscle. The subjects were control rats and rats that had been given parenteral guanethidine sulfate for 5 wk to induce selective postganglionic "chemical sympathectomy." Flows were measured under basal conditions (group I) and immediately after an arterial hemorrhage (group II). The results indicate that RSCBF was unchanged from control after guanethidine administration in both groups; however, NBF was elevated after guanethidine by 47% in group I and by 41% in group II. We conclude that in the spinal cord as in the brain, sympathetic inflow does not appear to have an important role in the regulation of regional blood flow. Sympathetic inflow appears to partly regulate NBF, however, probably by varying vascular tone.

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Dissertations / Theses on the topic "Guanethidine"

1

PERNETT, BOLANO IVET DEL CARMEN. "Traitement des angiodermites necrotiques par les blocs a la guanethidine : evaluation a partir de 13 cas." Nantes, 1994. http://www.theses.fr/1994NANT043M.

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HARDY, BENOIT. "Algodystrophie reflexes : etude ouverte de 20 cas traites par blocs intraveineux associant guanethidine et buflomedil." Rennes 1, 1993. http://www.theses.fr/1993REN1M003.

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Livingstone, James Alexander. "Investigation of the treatment of post traumatic algodystrophy by intravenous guanethidine blockade." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341498.

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Cherruau, Marc. "Effets d'une sympathectomie chimique a la guanethidine sur une sequence de resorption osseuse synchronisee chez le rat." Paris 5, 2000. http://www.theses.fr/2000PA05M008.

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Bezie, Yvonnick. "Role des attachements cellule-matrice dans les proprietes mecaniques des gros troncs arteriels : etudes in vivo chez le rat spontanement hypertendu, le rat baro-denerve, et le rat sympathectomise par la guanethidine ; role de la fibronectine et de son recepteur l'integrine alpha5-betal." Paris 6, 1998. http://www.theses.fr/1998PA066032.

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Le remodelage arteriel induit par des modifications des contraintes mecaniques est associe le plus souvent a des modifications des proprietes elastiques des gros troncs arteriels (gta). Ces proprietes sont determinees par les cellules musculaires lisses vasculaires (cmlv), le rapport des densites d'elastine et de collagene, et les attachements de ces composants au sein de la paroi. Ce travail a pour but d'etudier le role des interactions cellule-matrice, au travers de la fibronectine (fn) et de l'integrine 51, dans les proprietes mecaniques de la paroi de l'aorte abdominale chez le rat. Trois modeles experimentaux ont ete choisis pour leurs caracteristiques hemodynamiques : augmentation de la contrainte parietale circonferentielle (#) chez le rat spontanement hypertendu (shr), diminution de # en presence de modifications opposees de tonus sympathique : le rat baro-denerve (sad ; augmentation du tonus) et le rat sympathectomise par la guanethidine (gn ; diminution du tonus). La distensibilite arterielle a ete etudiee par les courbes pression-diametre in vivo dans l'intervalle systolo-diastolique de pression a l'aide d'un angiometre de haute resolution. Les proprietes mecaniques du materiau ont ete etudiees par les courbes module elastique de young (einc)-contrainte circonferentielle. Les arnm de la fn ont ete quantifies par northern-blot, le rapport elastine-collagene par histomorphometrie, la fn et son recepteur par immunohistochimie, et les attachements cmlv-lames elastiques par microscopie electronique. La distensibilite aortique a la pam est significativement diminuee dans les 3 modeles, de meme qu'est augmentee la rigidite du materiau constituant la paroi (einc). La fn et son recepteur sont augmentees dans la media aortique du shr et du sad, ce qui suggere une augmentation des attachements cellule-matrice. En effet, les connections elastine-cmlv sont plus nombreuses chez le shr que chez son controle wistar. L'augmentation de la densite du collagene aortique chez le sad, associee a une augmentation de la fn, suggere une augmentation des connections collagene-cmlv. Chez le gn, l'absence d'augmentation de la fn totale et de son recepteur suggerent que le nombre des attachements cellule-matrice n'est pas modifie. Lorsque les proprietes elastiques du materiau constituant la paroi arterielle sont comparees a meme contrainte circonferentielle (#), elles apparaissent differentes d'un modele a l'autre. Einc## est augmente chez le sad et le gn, ce qui demontre l'augmentation de la rigidite intrinseques de la paroi, tandis qu'il n'est pas modifie chez le shr, ce qui temoigne de la conservation des proprietes mecaniques du materiau dans ce dernier modele. Nous suggerons que, chez le sad, l'augmentation des attachements du collagene a la cmlv, par la fn, intervient dans l'augmentation de la rigidite. Chez le gn, la diminution de la densite en elastine explique en partie l'augmentation de la rigidite intrinseque. L'accumulation de la fn eiiia pourrait cependant contribuer a augmenter la rigidite passive du materiau en augmentant les connections entre les proteines de la mec. Chez le shr, l'augmentation de la fn et des connections elastine-cellule pourrait redistribuer les forces mecaniques vers les composants les plus distensibles et expliquer ainsi la plus grande distensibilite arterielle isobarique, a meme proprietes elastiques intrinseques du materiau. Par ailleurs, un plus grand nombre d'attachements cellule-matrice chez le shr pourrait augmenter la resistance du materiau constituant la paroi pour les hauts niveaux de contraintes. En conclusion, la prise en compte des attachements cellule-matrice par la quantification des proteines d'adhesion de la media arterielle permet une nouvelle approche de la relation entre la structure du materiau constituant la paroi et ses proprietes elastiques, en faisant intervenir l'organisation spatiale de ses differents composants.

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Donners, Ricardo [Verfasser]. "Renale Sympathikolyse durch CT-gesteuerte periarterielle Applikation von Vincristin und Guanethidin im Schwein zur Evaluation innovativer Therapieoptionen bei therapierefraktärer arterieller Hypertonie / Ricardo Donners." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1082537691/34.

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Books on the topic "Guanethidine"

1

Hoyng, Ph F. J. Pharmacological Denervation and Glaucoma: A Clinical Trial Report with Guanethidine and Adrenaline in One Eye Drop. Springer, 2011.

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Pharmacological Denervation and Glaucoma: A Clinical Trial Report with Guanethidine and Adrenaline in One Eye Drop. Springer, 2012.

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Book chapters on the topic "Guanethidine"

1

Louis, W. J., and L. G. Howes. "Guanethidine and Related Compounds." In Pharmacology of Antihypertensive Therapeutics, 287–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74209-5_8.

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2

Waldvogel, Herman Hans. "Guanethidin." In Analgetika Antinozizeptiva Adjuvanzien, 644–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56710-0_85.

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3

Gruetter, Carl A. "Guanethidine." In xPharm: The Comprehensive Pharmacology Reference, 1–6. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.61859-8.

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4

"Guanethidine." In Meyler's Side Effects of Drugs, 633. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.00826-x.

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5

"GUANETHIDINE." In Litt's Drug Eruptions & Reactions Manual, 282–84. CRC Press, 2010. http://dx.doi.org/10.3109/9781841847665-109.

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6

"Guanethidine." In Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions, 1562. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/01070-6.

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7

Taich, Alexander, and Adam S. Hassan. "Management of Eyelid Retraction." In Surgery of the Eyelid, Lacrimal System, and Orbit. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780195340211.003.0015.

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Eyelid retraction has numerous causes. Most notably eyelid retraction is caused by thyroid eye disease (TED), trauma, and postsurgical changes. The upper eyelid margin is typically measured at 3.5 to 4.5 mm above the center of the cornea. The lower eyelid margin is typically situated at the inferior border of the limbus. Eyelid retraction is a condition in which the upper eyelid margin is displaced superiorly or the lower eyelid margin is displaced inferiorly. Eyelid retraction may result in exposure keratopathy and disturbing ocular symptoms, including blurred vision, photophobia, foreign body sensation, burning, and reactive tearing. Eyelid retraction in TED is thought to be due to a combination of inflammation, fibrosis, and adrenergic stimulation of the eyelid retractors. Proptosis can also contribute to eyelid retraction. In the upper eyelid, factors responsible for eyelid retraction include (1) inflammation and fibrosis of the levator and Müller’s muscles, (2) adrenergic stimulation of Müller’s muscle, and (3) inflammation and fibrosis of the inferior rectus muscle, causing hypodeviation of the globe and compensatory overaction of the superior rectus–levator complex. In the lower eyelid, factors responsible for eyelid retraction include (1) inflammation and fibrosis of the inferior rectus muscle with consequent traction on its anterior extension, the capsulopalpebral fascia, which is the main lower lid retractor, and (2) adrenergic stimulation of the smooth muscle fibers within the lower lid retractor complex. A combination of eyelid retraction and proptosis in TED may result in ocular exposure with symptoms of ocular irritation, an undesirable cosmetic appearance, corneal erosion and infection, or (rarely) globe luxation. Mild exposure problems can be managed with topical lubricants. Guanethidine, a topical sympatholytic agent, is of limited usefulness in the management of eyelid retraction due to its variable efficacy and frequent ocular side effects, including irritation, hyperemia, photophobia, pain, edema, burning sensation, and punctate keratitis. It may be more tolerable if used in lower concentrations. Exposure problems in the inflammatory phase of the condition present a special challenge as surgical correction of eyelid retraction is best performed in the pos-tinflammatory, stable phase. Several reports have described using Botulinum toxin injections, 2.5 to 15 U, either subconjunctivally or percutaneously, just above the superior border of the tarsus.

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8

"8.11 Intravenöse regionale Sympathikusblockade mit Guanethidin (Ismelin)." In Lokalanästhesie, Regionalanästhesie, Regionale Schmerztherapie, edited by Hans Christoph Niesel and Hugo Van Aken. Stuttgart: Georg Thieme Verlag, 2003. http://dx.doi.org/10.1055/b-0034-46318.

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"10.11 Intravenöse regionale Sympathikusblockade mit Guanethidin (Ismelin)." In Lokalanästhesie, Regionalanästhesie, Regionale Schmerztherapie, edited by Hugo Van Aken, Hinnerk Wulf, and Hans Christoph Niesel. Stuttgart: Georg Thieme Verlag, 2010. http://dx.doi.org/10.1055/b-0034-47952.

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