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Journal articles on the topic 'Guanethidine'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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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 (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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2

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 (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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4

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 (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.

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5

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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6

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

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7

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

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8

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

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9

Walters, Karen M., Magalie Boucher, Germaine G. Boucher, et al. "No Evidence of Neurogenesis in Adult Rat Sympathetic Ganglia Following Guanethidine-Induced Neuronal Loss." Toxicologic Pathology 48, no. 1 (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 n

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10

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 (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

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11

Navegantes, Luiz Carlos C., Neusa M. Z. Resano, Renato H. Migliorini, and Isis C. Kettelhut. "Effect of guanethidine-induced adrenergic blockade on the different proteolytic systems in rat skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 277, no. 5 (1999): E883—E889. http://dx.doi.org/10.1152/ajpendo.1999.277.5.e883.

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Overall proteolysis and the activity of skeletal muscle proteolytic systems were investigated in rats submitted to guanethidine-induced adrenergic blockade for 4 days. In soleus, overall proteolysis increased by 15–20% during the first 2 days of guanethidine treatment but decreased to levels below control values after 4 days. Extensor digitorum longus (EDL) did not show the initial increase in total proteolysis, which was already reduced after 2 days of guanethidine treatment. The initial rise in the rate of protein degradation in soleus was accompanied by an increased activity of the Ca2+-dep

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12

Maronde, Robert F., Benjamin Barbour, L. Julian Haywood, and John Denney. "CLINICAL EVALUATION OF GUANETHIDINE IN HYPERTENSION." Annals of the New York Academy of Sciences 88, no. 4 (2006): 990–1002. http://dx.doi.org/10.1111/j.1749-6632.1960.tb20090.x.

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13

Juul, Per, and Ole Sand. "Determination of Guanethidine in Sympathetic Ganglia." Acta Pharmacologica et Toxicologica 32, no. 6 (2009): 487–99. http://dx.doi.org/10.1111/j.1600-0773.1973.tb01495.x.

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14

Castrén, J. A., and S. Pohjola. "EFFECT OF GUANETHIDINE ON GLAUCOMATOUS EYES." Acta Ophthalmologica 40, no. 3 (2009): 308–12. http://dx.doi.org/10.1111/j.1755-3768.1962.tb02372.x.

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15

ABRAHAMSEN, A. M., S. HUMERFELT, and H. SIGSTAD. "Effects of Guanethidine on Renal Function." Acta Medica Scandinavica 176, no. 1 (2009): 59–63. http://dx.doi.org/10.1111/j.0954-6820.1964.tb00645.x.

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16

Holeček, Milan, Marcela Bielavská, and Luděk Šprongl. "Protein metabolism in guanethidine-treated rats." International Journal of Experimental Pathology 85, no. 5 (2004): 257–64. http://dx.doi.org/10.1111/j.0959-9673.2004.00400.x.

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17

Wright, P. "Adverse reactions to guanethidine eye drops." British Journal of Ophthalmology 71, no. 4 (1987): 323. http://dx.doi.org/10.1136/bjo.71.4.323.

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18

Ferwerda, J. G., P. J. E. Blommaart, G. N. J. Tytgat, and G. E. Boeckxstaens. "Nicotinic receptor blocking effect of guanethidine." European Journal of Gastroenterology & Hepatology 10, no. 12 (1998): A42. http://dx.doi.org/10.1097/00042737-199812000-00147.

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19

Nelson, Daniel K., Jennifer E. Service, Daniel R. Studelska, Stephen Brimijoin, and Vay Liang W. Go. "Gastrointestinal neuropeptide concentrations following guanethidine sympathectomy." Journal of the Autonomic Nervous System 22, no. 3 (1988): 203–10. http://dx.doi.org/10.1016/0165-1838(88)90108-7.

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20

Eulry, F., D. Lechevalier, B. Pats, et al. "Regional intravenous guanethidine blocks in algodystrophy." Clinical Rheumatology 10, no. 4 (1991): 377–83. http://dx.doi.org/10.1007/bf02206656.

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21

Dimaline, R., N. Carter, and S. Barnes. "Evidence for reflex adrenergic inhibition of acid secretion in the conscious rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 5 (1986): G615—G618. http://dx.doi.org/10.1152/ajpgi.1986.251.5.g615.

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In conscious gastric fistula rats, gastric distension with saline to a pressure of 7 cm caused a threefold reduction of basal gastric acid secretion. Distension with 6.25% peptone solution to the same pressure doubled basal acid secretion. The saline distension-induced inhibition was abolished by guanethidine and markedly reduced by propranolol; phentolamine was ineffective. The response to peptone was unaffected by guanethidine. The results suggest that in the rat, gastric distension at physiological pressures inhibits acid secretion by a beta-adrenergic reflex. The inhibition can be masked b

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22

Walker, C. D. "Chemical sympathectomy and maternal separation affect neonatal stress responses and adrenal sensitivity to ACTH." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 5 (1995): R1281—R1288. http://dx.doi.org/10.1152/ajpregu.1995.268.5.r1281.

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The participation of sympathetic adrenal innervation in the control of the neonatal adrenocortical system and in changes in adrenal sensitivity after maternal separation for 24 h was tested in 10- and 23-day-old pups. Chemical sympathectomy by guanethidine (20 mg/kg body wt) decreased basal and stimulated corticosterone compound B (B) secretion without affecting adrenocorticotropic hormone (ACTH) release, abolished the enhanced adrenal sensitivity to ACTH induced by maternal separation in 10-day-old pups, but did not modify adrenal sensitivity following ether stress in 23-day-old pups. Guaneth

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23

Hopper, Richard A., and Kenneth Anderson. "Relief of Sympathetically Maintained Pain Associated with a Venous Malformation of the Hand Using Intravenous Regional Guanethidine." Canadian Journal of Plastic Surgery 1, no. 4 (1993): 188–90. http://dx.doi.org/10.1177/229255039300100406.

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RA Hopper, K Anderson. Relief of sympathetically maintained pain associated with a venous malformation of the hand using intravenous regional guanethidine. Can J Plast Surg 1994;1(4):188-190. A 28-year-old woman with a venous malformation of the hand, unresponsive to previous surgical therapy, experienced significant relief from her incapacitating symptoms after a series of four intravenous regional guanethidine blocks. The effects of the blocks lasted an average of six weeks each. Continuation of the treatments was delayed following an unexpected hypersensitivity reaction to the last block. T

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24

&NA;. "Intra-articular guanethidine improves resistant shoulder pain." Inpharma Weekly &NA;, no. 1041 (1996): 12. http://dx.doi.org/10.2165/00128413-199610410-00024.

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25

McGrath, P. "Accidental Intra-Arterial Flucloxacillin: Management Using Guanethidine." Anaesthesia and Intensive Care 20, no. 4 (1992): 517–18. http://dx.doi.org/10.1177/0310057x9202000425.

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26

Juul, Anders, Per Juul, and Henning Bjørn Christensen. "Guanethidine-Induced Sympathectomy in the Nude Rat." Pharmacology & Toxicology 64, no. 1 (1989): 20–22. http://dx.doi.org/10.1111/j.1600-0773.1989.tb00593.x.

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27

Abrahamsen, A. M., S. Humerfelt, and H. Sigstad. "Combined Guanethidine and Hydrochlorothiazide Therapy in Hypertension." Acta Medica Scandinavica 173, no. 2 (2009): 155–64. http://dx.doi.org/10.1111/j.0954-6820.1963.tb16517.x.

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28

Haddad, Heskel M. "Lid Retraction Therapy With a Guanethidine Solution." Archives of Ophthalmology 107, no. 2 (1989): 169. http://dx.doi.org/10.1001/archopht.1989.01070010175011.

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29

McManus, M. E., D. S. Davies, A. R. Boobis, P. H. Grantham, and P. J. Wirth. "Guanethidine N-oxidation in human liver microsomes." Journal of Pharmacy and Pharmacology 39, no. 12 (1987): 1052–55. http://dx.doi.org/10.1111/j.2042-7158.1987.tb03163.x.

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30

HANNINGTON-KIFF, J. G., and S. M. DUNNE. "Topical Guanethidine Relieves Dental Hypersensitivity and Pain." Survey of Anesthesiology 38, no. 2 (1994): 101. http://dx.doi.org/10.1097/00132586-199404000-00040.

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31

Fazan, R., J. A. Castania, G. Ballejo, M. C. O. Salgado, and H. C. Salgado. "Influence of sympathetic blockade on the acute hypertensive response to aortic constriction." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 6 (1997): H2648—H2651. http://dx.doi.org/10.1152/ajpheart.1997.273.6.h2648.

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The objective of the present study was to determine the contribution of the sympathetic nervous system to the hypertensive response to acute (45-min) aortic coarctation in conscious intact or sinoaortic-denervated (SAD) rats. Rats were treated chronically (5 wk) with guanethidine (50 mg ⋅ kg−1 ⋅ day−1ip) to induce sympathetic nerve degeneration or acutely with the α1-adrenergic receptor antagonist prazosin (1 mg/kg iv). Aortic constriction elicited a prompt and sustained rise in mean carotid pressure that was significantly greater in SAD than in intact rats. The increase in pressure was associ

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32

Kidd, G. J., J. W. Heath, B. D. Trapp, and P. R. Dunkley. "Myelin sheath survival after guanethidine-induced axonal degeneration." Journal of Cell Biology 116, no. 2 (1992): 395–403. http://dx.doi.org/10.1083/jcb.116.2.395.

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Membrane-membrane interactions between axons and Schwann cells are required for initial myelin formation in the peripheral nervous system. However, recent studies of double myelination in sympathetic nerve have indicated that myelin sheaths continue to exist after complete loss of axonal contact (Kidd, G. J., and J. W. Heath. 1988. J. Neurocytol. 17:245-261). This suggests that myelin maintenance may be regulated either by diffusible axonal factors or by nonaxonal mechanisms. To test these hypotheses, axons involved in double myelination in the rat superior cervical ganglion were destroyed by

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33

Wang, Donna H., and Wei Wu. "Neuronal Control of Salt Sensitivity: Role of Sensory and Sympathetic Nerves." Hypertension 36, suppl_1 (2000): 681. http://dx.doi.org/10.1161/hyp.36.suppl_1.681-a.

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18 Neonatal degeneration of capsaicin-sensitive sensory nerves renders a rat responsive to a salt load with an increase in blood pressure and a decrease in natriuretic response (Wang, et al, Hypertension 1998;32:649-653). To test the hypothesis that the sympathetic nervous system contributes to the development of salt sensitive hypertension induced by sensory denervation, newborn Wistar rats were given 50mg/kg capsaicin and/or 80mg/kg guanethidine s.c.. Control rats were treated with vehicle. After the weaning period, male rats were grouped as the following and given high sodium diet (4%) for

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34

Kaplan, R., M. Claudio, E. Kepes, and X. F. Gu. "Intravenous guanethidine in patients with reflex sympathetic dystrophy." Acta Anaesthesiologica Scandinavica 40, no. 10 (1996): 1216–22. http://dx.doi.org/10.1111/j.1399-6576.1996.tb05553.x.

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35

Galskov, Å., E. Clausen, T. Hilden, and A. R. Krogsgaard. "Guanethidine in the Ambulatory Treatment of Arterial Hypertension." Acta Medica Scandinavica 170, no. 1 (2009): 31–42. http://dx.doi.org/10.1111/j.0954-6820.1961.tb00209.x.

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36

Rønnov-Jessen, Vagn. "Blood-volume During Treatment of Hypertension with Guanethidine." Acta Medica Scandinavica 174, no. 3 (2009): 307–10. http://dx.doi.org/10.1111/j.0954-6820.1963.tb07927.x.

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37

Gonnering, Russell S. "Lid Retraction Therapy With a Guanethidine Solution-Reply." Archives of Ophthalmology 107, no. 2 (1989): 169. http://dx.doi.org/10.1001/archopht.1989.01070010175012.

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38

Davies, John A. H., Trevor Beswick, and Graeme Dickson. "Ketanserin and Guanethidine in the Treatment of Causalgia." Anesthesia & Analgesia 66, no. 6 (1987): 575???576. http://dx.doi.org/10.1213/00000539-198706000-00016.

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39

Manchikanti, Laxmaiah. "Intravenous Guanethidine and Resperine in Reflex Sympathetic Dystrophy." Clinical Journal of Pain 6, no. 2 (1990): 158. http://dx.doi.org/10.1097/00002508-199006000-00016.

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40

Manchikanti, Laxmaiah. "Intravenous Guanethidine and Resperine in Reflex Sympathetic Dystrophy." Clinical Journal of Pain 6, no. 2 (1990): 158–59. http://dx.doi.org/10.1097/00002508-199006000-00017.

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41

Rocco, Angelo G., Steven R. Ford, and Robert Johnston. "Intravenous Guanethidine and Resperine in Reflex Sympathetic Dystrophy." Clinical Journal of Pain 6, no. 2 (1990): 159. http://dx.doi.org/10.1097/00002508-199006000-00018.

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42

Frenneaux, Michael, Juan Carlos Kaski, Maurice Brown, and Attilio Maseri. "Refractory variant angina relieved by guanethidine and clonidine." American Journal of Cardiology 62, no. 10 (1988): 832–33. http://dx.doi.org/10.1016/0002-9149(88)91238-6.

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43

FIELD, J., C. MONK, and R. M. ATKINS. "Objective Improvements in Algodystrophy Following Regional Intravenous Guanethidine." Journal of Hand Surgery 18, no. 3 (1993): 339–42. http://dx.doi.org/10.1016/0266-7681(93)90058-n.

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17 patients with established algodystrophy following trauma were treated with serial intravenous regional guanethidine blockade. Subjective improvement occurred in all cases. This improvement could be confirmed quantitatively using objective assessment criteria. The subjective and objective improvements demonstrated in each of the features of algodystrophy correlate closely ( p < 0.001). There appears to be no difference in the effectiveness of one block compared to another in the same patient.

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44

Zochodne, Douglas W., and Lam T. Ho. "The Influence of Indomethacin and Guanethidine on Experimental Streptozotocin Diabetic Neuropathy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, no. 4 (1992): 433–41. http://dx.doi.org/10.1017/s0317167100041615.

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ABSTRACT:In diabetic animals, reduced endoneurial perfusion and oxygen content have been linked to neuropathic abnormalities and might be amenable to pharmacological manipulation. In streptozotocin-induced diabetic rats, we studied the influence of guanethidine adrenergic sympathectomy, indomethacin treatment and a combined strategy on: serial in vivo motor and sensory conduction, resistance to ischemic conduction failure, in vitro myelinated and unmyelinated conduction, endoneurial perfusion and endoneurial oxygen tension. Unlike previous work diabetic animals had normal endoneurial perfusion

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45

Filali-Zegzouti, Younes, Jean-Louis Rouanet, Toufiq Fechtali, and Damien Roussel. "Mitochondrial oxidative energy metabolism in guanethidine-induced sympathectomized ducklings." General physiology and biophysics 33, no. 01 (2014): 91–97. http://dx.doi.org/10.4149/gpb_2013072.

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46

SHARPE, E., R. MILASZKIEWICZ, and F. CARLI. "A case of prolonged hypotension following intravenous guanethidine block." Anaesthesia 42, no. 10 (1987): 1081–84. http://dx.doi.org/10.1111/j.1365-2044.1987.tb05173.x.

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47

Jensen-Holm, J. "Cholinesterase and Protein Changes in Sympathetic Ganglia after Guanethidine *)." Acta Pharmacologica et Toxicologica 25, S4 (2009): 74. http://dx.doi.org/10.1111/j.1600-0773.1967.tb03060.x.

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48

Juul, Per. "Accumulation of Guanethidine by Sympathetic Ganglia of Reserpinized Rats." Acta Pharmacologica et Toxicologica 33, no. 1 (2009): 79–80. http://dx.doi.org/10.1111/j.1600-0773.1973.tb01510.x.

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49

Nielsen, Gunnar Damgård. "Guanethidine-induced Acute Hypersensitivity to Noradrenaline in Anaesthetized Rats." Acta Pharmacologica et Toxicologica 40, no. 2 (2009): 273–79. http://dx.doi.org/10.1111/j.1600-0773.1977.tb02078.x.

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50

Fristedt, Bengt, and Jan Philipson. "Some Clinical Experiences with Guanethidine: A New Hypotensive Agent." Acta Medica Scandinavica 169, no. 2 (2009): 155–67. http://dx.doi.org/10.1111/j.0954-6820.1961.tb07819.x.

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