Laboratory Animal Anaesthesia, Third Edition
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A Murine Model of Experimental Metastasis to Bone and Bone Marrow1
(CANCER RESEARCH 48. 6876-6881, December 1, 1988] A Murine Model of Experimental Metastasis to Bone and Bone Marrow1 Francisco Arguello,2 Raymond B. Baggs, and Christopher N. Frantz3 Department of Pediatrics and the Cancer Center ¡F.A., C. N. F.], and Department of Pathology and Division of Laboratory Animal Medicine [R. B. B.], University of Rochester School of Medicine and Dentistry, Rochester, New York 14642 ABSTRACT In this model, tumor cells are injected in the mouse tail vein. Most of the cells die, but a few survive, grow, and form tumor Bone is a common site of metastasis in human cancer. A major colonies in the lung. The colonies are counted to quantify the impediment to understanding the pathogenesis of bone metastasis has experimental metastasis. The ability of the lung to kill the vast been the lack of an appropriate animal model. In this paper, we describe an animal model in which B16 melanoma cells injected in the left cardiac majority of injected tumor cells (11, 12) may preclude the use ventricle reproducibly colonize specific sites of the skeletal system of of i.v. injection to study metastasis to extrapulmonary organs. mice. Injection of 10*cells resulted in melanotic tumor colonies in most Bone metastasis models have involved direct injection of tumor organs, including the skeletal system. Injection of IO4 or fewer cells cells into the medullary cavity of bones (13, 14) or into the rat resulted in experimental metastasis almost entirely restricted to the abdominal aorta (15). In this paper, we describe our experience skeletal system and ovary. -
Veterinary Emergency & Anaesthesia Pfizer
AVA ECVA & AVEF Thank all their sponsors for this spring edition PARIS 2007 On VETERINARY EMERGENCY & ANAESTHESIA PFIZER MERIAL FORT DODGE BAYER BOEHRINGER MEDISUR COVETO OPTOMED HALLOWELL SCIL JANSSEN SOGEVAL KRUSSE TECHNIBELT MILA TEM The Organisatiors 7th AVEF European Meeting- 10th March 2007-ROISSY 2 AVA – ECVA Spring Meeting 2007 on Veterinary Emergency & Anesthesia 7 – 10 March 2007, Paris, France AVA PARIS 2007 — Wednesday March 7th RESIDENT DAY RUMINANT ANAESTHESIA Hyatt Regency Hotel, Roissy CDG, France K OTTO, D HOLOPHERNE, G TOUZOT 8.30 REGISTRATIONS 9.00-9.45 Specific anatomo-physiology to consider for ruminant peri-anaesthetic period K OTTO 10.00-10.30 COFFEE BREAK 10.30-11.15 Post-anaesthetic and pain management in ruminants K OTTO 11.30-12.15 Physical restraint and sedation of ruminants D HOLOPHERNE 12.30-1.30 LUNCH 1.30-2.15 Anaesthesia of Lamas & Alpagas G TOUZOT 2.30-3.15 Regional & local anaesthesia for ruminants D HOLOPHERNE 3.30-4.00 COFFEE BREAK 4.00-4.45 Pharmacology and protocols for ruminant anaesthesia G TOUZOT AVA-ECVA PARIS 2007, Veterinary Emergency & Anaesthesia, 7-10th March AVA-ECVA PARIS 2007, Veterinary Emergency & Anaesthesia, 7-10th March AVA – ECVA Spring Meeting 2007 on Veterinary Emergency & Anesthesia 7 – 10 March 2007, Paris, France Specific anatomo-physiology to consider for ruminants peri-anaesthetic period Klaus A. Otto Institut für Versuchstierkunde und Zentrales Tierlaboratorium, Medizinische Hochschule Hannover, D-30623 Hannover, Germany The suborder “ruminantia” includes members of the family “bovidae” such as cattle (bos taurus), sheep (ovis spp) and goats (capra spp). Members of the family “camelidae” (camelus spp, llama spp, vicugna spp) belong to the suborder “tylopodia” and therefore are not true ruminants. -
Cyclopropane Anaesthesia by JOHN BOYD, M.D., D.A
Cyclopropane Anaesthesia By JOHN BOYD, M.D., D.A. TLHIS paper is based on my experience of one thousand cases of cyclopropane anaesthesia personally conducted by me since October, 1938, both in hospital and in private. But before discussing these it might be convenient for me to mention here something about the drug itself. HISTORY. Cyclopropane was first isolated in Germany in 1882 by Freund, who also demonstrated its chemical structure, C3H6. He did not, however, describe its anaesthetic properties. Following its discovery it seems to have been forgotten until 1928, when Henderson and Lucas of Toronto, in investigating contaminants of propylene, another anesthetic with undesirable side-effects, and itself'an isomer of cyclopropane, found that the supposed cause of the cardiac disturbances was in reality a better and less toxic anaesthetic. They demonstrated its anaesthetic properties first on animals, and then, before releasing it to the medical profession for clinical trial, they anaesthetised each other, and determined the quantities necessary for administration to man. In 1933 the first clinical trials of cyclopropane were made by Waters and his associates of the University of Wisconsin. In October of that year Waters presented a preliminary report on its anaesthetic properties in man,1 confirming the findings of Henderson and Lucas. Rowbotham introduced it to England first in 1935, and since then its use has spread rapidly throughout the country. PREPARATION. Cyclopropane is prepared commercially by the reduction of trimethylene bromide in the presence of metallic zinc in ethyl alcohol. It is also made commercially from propane in natural gas by progressive thermal chlorination. -
Analgesia and Sedation in Hospitalized Children
Analgesia and Sedation in Hospitalized Children By Elizabeth J. Beckman, Pharm.D., BCPS, BCCCP, BCPPS Reviewed by Julie Pingel, Pharm.D., BCPPS; and Brent A. Hall, Pharm.D., BCPPS LEARNING OBJECTIVES 1. Evaluate analgesics and sedative agents on the basis of drug mechanism of action, pharmacokinetic principles, adverse drug reactions, and administration considerations. 2. Design an evidence-based analgesic and/or sedative treatment and monitoring plan for the hospitalized child who is postoperative, acutely ill, or in need of prolonged sedation. 3. Design an analgesic and sedation treatment and monitoring plan to minimize hyperalgesia and delirium and optimize neurodevelopmental outcomes in children. INTRODUCTION ABBREVIATIONS IN THIS CHAPTER Pain, anxiety, fear, distress, and agitation are often experienced by GABA γ-Aminobutyric acid children undergoing medical treatment. Contributory factors may ICP Intracranial pressure include separation from parents, unfamiliar surroundings, sleep dis- PAD Pain, agitation, and delirium turbance, and invasive procedures. Children receive analgesia and PCA Patient-controlled analgesia sedatives to promote comfort, create a safe environment for patient PICU Pediatric ICU and caregiver, and increase patient tolerance to medical interven- PRIS Propofol-related infusion tions such as intravenous access placement or synchrony with syndrome mechanical ventilation. However, using these agents is not without Table of other common abbreviations. risk. Many of the agents used for analgesia and sedation are con- sidered high alert by the Institute for Safe Medication Practices because of their potential to cause significant patient harm, given their adverse effects and the development of tolerance, dependence, and withdrawal symptoms. Added layers of complexity include the ontogeny of the pediatric patient, ongoing disease processes, and presence of organ failure, which may alter the pharmacokinetics and pharmacodynamics of these medications. -
Unnamed Document
Mutations M287L and Q266I in the Glycine Receptor ␣1 Subunit Change Sensitivity to Volatile Anesthetics in Oocytes and Neurons, but Not the Minimal Alveolar Concentration in Knockin Mice Cecilia M. Borghese, Ph.D.,* Wei Xiong, Ph.D.,† S. Irene Oh, B.S.,‡ Angel Ho, B.S.,§ S. John Mihic, Ph.D.,ʈ Li Zhang, M.D.,# David M. Lovinger, Ph.D.,** Gregg E. Homanics, Ph.D.,†† Edmond I. Eger 2nd, M.D.,‡‡ R. Adron Harris, Ph.D.§§ ABSTRACT What We Already Know about This Topic • Inhibitory spinal glycine receptor function is enhanced by vol- Background: Volatile anesthetics (VAs) alter the function of atile anesthetics, making this a leading candidate for their key central nervous system proteins but it is not clear which, immobilizing effect if any, of these targets mediates the immobility produced by • Point mutations in the ␣1 subunit of glycine receptors have been identified that increase or decrease receptor potentiation VAs in the face of noxious stimulation. A leading candidate is by volatile anesthetics the glycine receptor, a ligand-gated ion channel important for spinal physiology. VAs variously enhance such function, and blockade of spinal glycine receptors with strychnine af- fects the minimal alveolar concentration (an anesthetic What This Article Tells Us That Is New EC50) in proportion to the degree of enhancement. • Mice harboring specific mutations in their glycine receptors Methods: We produced single amino acid mutations into that increased or decreased potentiation by volatile anesthetic in vitro did not have significantly altered changes in anesthetic the glycine receptor ␣1 subunit that increased (M287L, third potency in vivo transmembrane region) or decreased (Q266I, second trans- • These findings indicate that this glycine receptor does not me- membrane region) sensitivity to isoflurane in recombinant diate anesthetic immobility, and that other targets must be receptors, and introduced such receptors into mice. -
Management of Chronic Problems
MANAGEMENT OF CHRONIC PROBLEMS INTERACTIONS BETWEEN ALCOHOL AND DRUGS A. Leary,* T. MacDonald† SUMMARY concerned. Alcohol may alter the effects of the drug; drug In western society alcohol consumption is common as is may change the effects of alcohol; or both may occur. the use of therapeutic drugs. It is not surprising therefore The interaction between alcohol and drug may be that concomitant use of these should occur frequently. The pharmacokinetic, with altered absorption, metabolism or consequences of this combination vary with the dose of elimination of the drug, alcohol or both.2 Alcohol may drug, the amount of alcohol taken, the mode of affect drug pharmacokinetics by altering gastric emptying administration and the pharmacological effects of the drug or liver metabolism. Drugs may affect alcohol kinetics by concerned. Interactions may be pharmacokinetic or altering gastric emptying or inhibiting gastric alcohol pharmacodynamic, and while coincidental use of alcohol dehydrogenase (ADH).3 This may lead to altered tissue may affect the metabolism or action of a drug, a drug may concentrations of one or both agents, with resultant toxicity. equally affect the metabolism or action of alcohol. Alcohol- The results of concomitant use may also be principally drug interactions may differ with acute and chronic alcohol pharmacodynamic, with combined alcohol and drug effects ingestion, particularly where toxicity is due to a metabolite occurring at the receptor level without important changes rather than the parent drug. There is both inter- and intra- in plasma concentration of either. Some interactions have individual variation in the response to concomitant drug both kinetic and dynamic components and, where this is and alcohol use. -
268 Part 522—Implantation Or Injectable Dosage Form
§ 520.2645 21 CFR Ch. I (4–1–18 Edition) (ii) Indications for use. For the control 522.82 Aminopropazine. of American foulbrood (Paenibacillus 522.84 Beta-aminopropionitrile. larvae). 522.88 Amoxicillin. 522.90 Ampicillin injectable dosage forms. (iii) Limitations. The drug should be 522.90a Ampicillin trihydrate suspension. fed early in the spring or fall and con- 522.90b Ampicillin trihydrate powder for in- sumed by the bees before the main jection. honey flow begins, to avoid contamina- 522.90c Ampicillin sodium. tion of production honey. Complete 522.144 Arsenamide. treatments at least 4 weeks before 522.147 Atipamezole. main honey flow. 522.150 Azaperone. 522.161 Betamethasone. [40 FR 13838, Mar. 27, 1975, as amended at 50 522.163 Betamethasone dipropionate and FR 49841, Dec. 5, 1985; 59 FR 14365, Mar. 28, betamethasone sodium phosphate aque- 1994; 62 FR 39443, July 23, 1997; 68 FR 24879, ous suspension. May 9, 2003; 70 FR 69439, Nov. 16, 2005; 73 FR 522.167 Betamethasone sodium phosphate 76946, Dec. 18, 2008; 75 FR 76259, Dec. 8, 2010; and betamethasone acetate. 76 FR 59024, Sept. 23, 2011; 77 FR 29217, May 522.204 Boldenone. 17, 2012; 79 FR 37620, July 2, 2014; 79 FR 53136, 522.224 Bupivacaine. Sept. 8, 2014; 79 FR 64116, Oct. 28, 2014; 80 FR 522.230 Buprenorphine. 34278, June 16, 2015; 81 FR 48702, July 26, 2016] 522.234 Butamisole. 522.246 Butorphanol. § 520.2645 Tylvalosin. 522.275 N-Butylscopolammonium. 522.300 Carfentanil. (a) Specifications. Granules containing 522.304 Carprofen. 62.5 percent tylvalosin (w/w) as 522.311 Cefovecin. -
Evaluating the Translational Potential of Progesterone Treatment Following
Wong et al. BMC Neuroscience 2014, 15:131 http://www.biomedcentral.com/1471-2202/15/131 RESEARCH ARTICLE Open Access Evaluating the translational potential of progesterone treatment following transient cerebral ischaemia in male mice Raymond Wong1, Claire L Gibson2*, David A Kendall3 and Philip MW Bath1 Abstract Background: Progesterone is neuroprotective in numerous preclinical CNS injury models including cerebral ischaemia. The aim of this study was two-fold; firstly, we aimed to determine whether progesterone delivery via osmotic mini-pump would confer neuroprotective effects and whether such neuroprotection could be produced in co-morbid animals. Results: Animals underwent transient middle cerebral artery occlusion. At the onset of reperfusion, mice were injected intraperitoneally with progesterone (8 mg/kg in dimethylsulfoxide). Adult and aged C57 Bl/6 mice were dosed additionally with subcutaneous infusion (1.0 μl/h of a 50 mg/ml progesterone solution) via implanted osmotic minipumps. Mice were allowed to survive for up to 7 days post-ischaemia and assessed for general well-being (mass loss and survival), neurological score, foot fault and t-maze performance. Progesterone reduced neurological deficit [F(1,2) = 5.38, P = 0.027] and number of contralateral foot-faults [F(1,2) = 7.36, P = 0.0108] in adult, but not aged animals, following ischaemia. In hypertensive animals, progesterone treatment lowered neurological deficit [F(1,6) = 18.31, P = 0.0001], reduced contralateral/ipsilateral alternation ratio % [F(1,2) = 17.05, P = 0.0006] and time taken to complete trials [F(1,2) = 15.92, P = 0.0009] for t-maze. Conclusion: Post-ischemic progesterone administration via mini-pump delivery is effective in conferring functional improvement in a transient MCAO model in adult mice. -
<I>Iguana Iguana</I>
Journal of the American Association for Laboratory Animal Science Vol 58, No 6 Copyright 2019 November 2019 by the American Association for Laboratory Animal Science Pages 810–816 Use of Rodent Sedation Tests to Evaluate Midazolam and Flumazenil in Green Iguanas (Iguana iguana) Thais F Bressan, Thayanee Sobreira, and Adriano B Carregaro* This study aimed to evaluate the applicability of rodent behavioral tests to assess the effects of midazolam and flumazenil in green iguanas. Four tests commonly used to assess sedation in rodents—the open field test, forced swim test, behavioral scale, and traction test—were conducted in 10 juveniles iguanas. The animals received midazolam (2 mg/kg IM) or 0.9% NaCl (0.4 mL/kg IM), and the tests were conducted between 0 and 300 min thereafter. To verify the effects of midazolam and flumazenil, the most informative tests from the evaluation stage and the limb withdrawal latency time (LWLT) were used. All 10 iguanas were tested under 4 conditions, as follows: MS, midazolam (2 mg/kg IM), followed 30 min later by 0.9% NaCl (0.4 mL/kg IM); FS, flumazenil (0.05 mg/kg IM), followed by 0.9% NaCl (0.4 mL/kg IM) 30 min later; MF, midazolam (2 mg/ kg IM), followed by flumazenil (0.05 mg/kg IM) 30 min later; and CON, 0.9% NaCl (0.4 mL/kg IM). The behavioral scale and the forced swim test showed the best detection of the onset, peak effect, and the differences between the sedated and con- trol iguanas, with testing done between 15 and 240 min after drug administration. -
Euthanasia of Experimental Animals
EUTHANASIA OF EXPERIMENTAL ANIMALS • *• • • • • • • *•* EUROPEAN 1COMMISSIO N This document has been prepared for use within the Commission. It does not necessarily represent the Commission's official position. A great deal of additional information on the European Union is available on the Internet. It can be accessed through the Europa server (http://europa.eu.int) Cataloguing data can be found at the end of this publication Luxembourg: Office for Official Publications of the European Communities, 1997 ISBN 92-827-9694-9 © European Communities, 1997 Reproduction is authorized, except for commercial purposes, provided the source is acknowledged Printed in Belgium European Commission EUTHANASIA OF EXPERIMENTAL ANIMALS Document EUTHANASIA OF EXPERIMENTAL ANIMALS Report prepared for the European Commission by Mrs Bryony Close Dr Keith Banister Dr Vera Baumans Dr Eva-Maria Bernoth Dr Niall Bromage Dr John Bunyan Professor Dr Wolff Erhardt Professor Paul Flecknell Dr Neville Gregory Professor Dr Hansjoachim Hackbarth Professor David Morton Mr Clifford Warwick EUTHANASIA OF EXPERIMENTAL ANIMALS CONTENTS Page Preface 1 Acknowledgements 2 1. Introduction 3 1.1 Objectives of euthanasia 3 1.2 Definition of terms 3 1.3 Signs of pain and distress 4 1.4 Recognition and confirmation of death 5 1.5 Personnel and training 5 1.6 Handling and restraint 6 1.7 Equipment 6 1.8 Carcass and waste disposal 6 2. General comments on methods of euthanasia 7 2.1 Acceptable methods of euthanasia 7 2.2 Methods acceptable for unconscious animals 15 2.3 Methods that are not acceptable for euthanasia 16 3. Methods of euthanasia for each species group 21 3.1 Fish 21 3.2 Amphibians 27 3.3 Reptiles 31 3.4 Birds 35 3.5 Rodents 41 3.6 Rabbits 47 3.7 Carnivores - dogs, cats, ferrets 53 3.8 Large mammals - pigs, sheep, goats, cattle, horses 57 3.9 Non-human primates 61 3.10 Other animals not commonly used for experiments 62 4. -
The Effects of Antipsychotic Treatment on Metabolic Function: a Systematic Review and Network Meta-Analysis
The effects of antipsychotic treatment on metabolic function: a systematic review and network meta-analysis Toby Pillinger, Robert McCutcheon, Luke Vano, Katherine Beck, Guy Hindley, Atheeshaan Arumuham, Yuya Mizuno, Sridhar Natesan, Orestis Efthimiou, Andrea Cipriani, Oliver Howes ****PROTOCOL**** Review questions 1. What is the magnitude of metabolic dysregulation (defined as alterations in fasting glucose, total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, and triglyceride levels) and alterations in body weight and body mass index associated with short-term (‘acute’) antipsychotic treatment in individuals with schizophrenia? 2. Does baseline physiology (e.g. body weight) and demographics (e.g. age) of patients predict magnitude of antipsychotic-associated metabolic dysregulation? 3. Are alterations in metabolic parameters over time associated with alterations in degree of psychopathology? 1 Searches We plan to search EMBASE, PsycINFO, and MEDLINE from inception using the following terms: 1 (Acepromazine or Acetophenazine or Amisulpride or Aripiprazole or Asenapine or Benperidol or Blonanserin or Bromperidol or Butaperazine or Carpipramine or Chlorproethazine or Chlorpromazine or Chlorprothixene or Clocapramine or Clopenthixol or Clopentixol or Clothiapine or Clotiapine or Clozapine or Cyamemazine or Cyamepromazine or Dixyrazine or Droperidol or Fluanisone or Flupehenazine or Flupenthixol or Flupentixol or Fluphenazine or Fluspirilen or Fluspirilene or Haloperidol or Iloperidone -
Redalyc.Tissue Depletion of Azaperone and Its Metabolite
Revista de Toxicología ISSN: 0212-7113 [email protected] Asociación Española de Toxicología España Mestorino, N.; Marchetti, M. L.; Daniele, M.; Martínez, M. A.; Martínez-Larrañaga, M. R.; Anadón, A. Tissue depletion of azaperone and its metabolite azaperol after oral administration of azaperone in food-producing pigs Revista de Toxicología, vol. 30, núm. 2, julio-diciembre, 2013, pp. 209-214 Asociación Española de Toxicología Pamplona, España Available in: http://www.redalyc.org/articulo.oa?id=91931189013 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Rev. Toxicol. (2013) 30: 209-214 Tissue depletion of azaperone and its metabolite azaperol after oral administration of azaperone in food-producing pigs Mestorino N1* , Marchetti M L1 , Daniele M1 , Martínez M A2 , Martínez-Larrañaga M R2 , Anadón A2 . 1Laboratorio de Estudios Farmacológicos y Toxicológicos (LEFyT), Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, 1900- La Plata, Buenos Aires, Argentina. 2Departamento de Toxicología y Farmacología, Facultad de Veterinaria, Universidad Complutense de Madrid, 28040-Madrid, España. Recibido 5 de noviembre de 2013 / Aceptado 20 de diciembre de 2013 Abstract: Azaperone is a butyrophenone tranquilizer for swine. establecidos por la Unión Europea (100 mg / kg en el músculo, el Food producing pigs are particularly sensitive to stress during hígado, los riñones y la piel + grasa) en ningún momento del handling and transport to the abattoir. In vivo, azaperone is partially muestreo. Como consecuencia, según los resultados obtenidos en el metabolised to azaperol, a metabolite with pharmacological activity.