DOCSLIB.ORG

5-Hydroxytryptamine Andhuman Small Intestinal Motility

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
5-Hydroxytryptamine Andhuman Small Intestinal Motility 496 Gut 1994; 35:496-500 5-Hydroxytryptamine and human small intestinal motility: effect ofinhibiting 5-hydroxytryptamine reuptake D A Gorard, G W Libby, M J G Farthing Abstract nature is poorly understood.'0 In animals, Parenteral 5-hydroxytryptamine stimulates migrating motor complex cycling can be small intestinal motility, but the effect of con- modified by administration of 5-HT, its pre- tinuous stimulation with 5-hydroxytryptamine cursor 5-hydroxytryptophan, and its antago- on the human migrating motor complex is nists." '4 The effect of 5-HT on the migrating unknown. Using a selective 5-hydroxytrypta- motor complex in humans has not been studied. mine reuptake inhibitor, paroxetine, this study Tachyphylaxis to 5-HT given intravenously,45 investigated the effect of indirect 5-hydroxy- and associated cardiovascular and pulmonary tryptamine agonism on fasting small responses limit prolonged infusion of 5-HT in intestinal motility and transit. Eight healthy humans. The effect, however, of 5-HT agonism subjects were studied while receiving paroxe- on human small intestinal motor function might tine 30 mg daily for five days and while receiv- be alternatively investigated using a selective ing no treatment, in random order. Ambulant 5-HT reuptake inhibitor. Paroxetine selectively small intestinal motility was recorded from five inhibits the neuronal reuptake of 5-HT, increas- sensors positioned from the duodenojejunal ing the availability of synaptic 5-HT. Its ability flexure to the ileum for 16-18 hours. Paroxe- to inhibit 5-HT reuptake exceeds its ability to tine reduced the migrating motor complex inhibit noradrenaline reuptake by a factor of periodicity mean (SEM) from 81 (6) min to 67 320," making it four to five hundred times (4) min (p<005), and increased the propaga- as selective as the standard tricycic anti- tion velocity of phase III from 3-1 to 4-7 cm/ depressants imipramine and amitriptyline. min in the proximal jejunum (p<0-01), and Unlike traditional tricyclic drugs, paroxetine has from 1-6 to 3-4 cm/min distally (p<0-001). negligible affinity for muscarinic cholinergic Orocaecal transit time measured by lactulose receptors and does not bind at other neurotrans- hydrogen breath test was reduced by paroxe- mitter receptor sites. Although paroxetine is tine from 70 (9) min to 48 (7) min (p<005). used for its action in the central nervous system, These data suggest that 5-hydroxytryptamine enteric 5-HT neurones resemble central 5-HT participates in the control of migrating motor neurones in their response to 5-HT reuptake complexes in humans, and that selective 5- inhibitors.'6 The aim of this study was to use the hydroxytryptamine reuptake inhibitors have a 5-HT reuptake inhibitor paroxetine as an prokinetic action in the human small intestine. indirect 5-HT agonist, to examine the longer (Gut 1994; 35: 496-500) term effects of 5-HT on human small intestinal motility and transit. The gastrointestinal tract is the main source of 5- hydroxytryptamine (5-HT) in humans. In the Methods small intestine, 5-HT is found predominantly Eight healthy volunteers (five men, median age within the enterochromaffin cells of the mucosa, 25 years, range 23-33) without history of gastro- but significant amounts of 5-HT are also found intestinal symptoms or surgery were studied. within the myenteric plexus. In addition to its Each had small intestinal motility and transit role in the intestinal secretion of water and studies while receiving no treatment and while electrolytes, and its influence on mesenteric taking paroxetine in a randomised order. For the blood flow, 5-HT has prominent effects on paroxetine studies, a single daily dose of 30 mg intestinal motility. There is compelling evidence oral paroxetine was taken for five days. The that 5-HT is a neurotransmitter within the transit and motility studies were performed on enteric nervous system.'2 Enteric serotonergic the fourth and fifth days respectively. Drug free neurones are interneurones, innervating (control) studies and those where paroxetine was All Department of ganglion cells of the submucosal and myenteric given were separated by at least three weeks. Gastroenterology, St plexuses. subjects gave written informed consent and the Bartholomew's Hospital, 5-HT given intravenously over short periods study was approved by the research ethics com- London of the and Health District. D A Gorard of time has been shown to alter human small mittee City Hackney G W Libby intestinal motility-7 although such studies pre- M J G Farthing dated the recognition of the migrating motor Correspondence to: complex in humans.8 The migrating motor com- SMALL INTESTINAL MOTILITY Dr D A Gorard, Department of Gastroenterology, plex is a distally migrating pattern of motility Small intestinal motility was recorded using St Bartholomew's Hospital, seen during the fasting state in mammals.9 The a fine (2-7 mm diameter) flexible catheter West Smithfield, London EC1A 7BE. migrating motor complex is programmed by the incorporating five miniature electronic strain Accepted for publication circuitry of the enteric nervous system, but the gauge transducers (Gaeltec Ltd, Isle of Skye, 9 August 1993 oscillatory mechanism controlling its cyclical UK). The transducers were sited at 3 cm, 48 cm, 5-Hydroxytryptamine andhuman smallintestinal motility: effectofinhibitingS-hydroxytryptamine reuptake 497 68 cm, 83 cm, and 98 cm from the distal tip ofthe contractile activity. Migrating motor complex catheter. Fasting subjects were nasally intubated cycle length or periodicity was defined as the with the catheter at 0900. The tip of the catheter time interval between the onset of successive was guided through the pylorus using fluoro- phase III fronts occurring at site jI in the scopy, and a small balloon attached to the tip was proximal jejunum. This site was used for calcula- inflated with air to facilitate the propagative tion of periodicity, as phase III fronts occur activity of the intestine in pulling the catheter maximally in the proximal jejunum."7 Propaga- distally. Distal migration of the catheter con- tion velocity of phase III between adjacent tinued until the most proximal transducer was sensors was calculated by dividing the distance sited at the duodenojejunal flexure (site DJ) and between sensors by the time taken to pass from the other four transducers were 15 cm (site JI), one sensor to the next. The duration of each 30 cm (site J2), 50 cm (site J3), and 95 cm (site I) activity front at each sensor was measured from distal to the duodenojejunal flexure. The balloon the onset of regular contractions to quiescence. was then deflated, any redundant catheter was The maximum contractile rate during phase III withdrawn from the stomach, and the catheter at each site was determined. The extent to which secured to the face with tape. Recording of small each phase III migrated aborally, and the per- intestinal motility then began, with pressure centage of phase III fronts originating at sites sampling occurring at 8 Hertz. Data were stored beyond site JI were noted. digitally in a portable lightweight recorder A motility index for non-phase III - that is, (7-MPR recorder, Gaeltec Ltd, Isle of Skye, combined phase I and II - activity in the proximal UK) carried in a holster over the subject's jejunum (site JI), was calculated using computer shoulder. assisted analysis. Motility index was calculated Motility was recorded for 16-18 hours during as: which subjects were ambulant but discouraged from taking vigorous exercise because intense mean amplitude ofcontraction (mm Hg)xmean duration (min)x no ofcontractions physical activity masks the intestinal intra- time (min) luminal pressure recording with external pres- This analysis excluded contractile waves <15 sure artefact. Subjects spent the rest of the day mm Hg above the current baseline, which might and night at home and returned the next morn- represent respiratory excursion. Simultaneous ing. They were not allowed to eat, but were brief contractions seen at all sensors as a result permitted small amounts of clear fluids, which of artefacts such as coughing were similarly were recorded. When each recording was com- excluded from analysis. pleted, data were transferred from the 512 Kbyte Characteristics of migrating motor complexes memory of the recorder to a computer for recorded during the day were compared with graphic display and analysis. those occurring at night (2300-0500). ANALYSIS OF MOTILITY OROCAECAL TRANSIT TIME Figure 1: Motility recording Motility data were analysed without knowledge On a separate occasion, orocaecal transit time from thefive small intestinal of whether control or paroxetine recordings was determined after an overnight fast and a 20 sites. Phase III activityfront Contractile patterns were ml mouthwash with 0-2% wt/vol chlorhexidine ofthe migrating motor were being studied. complex propagates distally, analysed visually (Fig 1). The activity front or gluconate. End expiratory breath samples were preceded by irregularphase phase III of the migrating motor complex was analysed before and at 10 minute intervals after II activity andfollowed by recognised as at least three minutes of uninter- ingestion of20 ml (13 4 g) lactulose for hydrogen quiescence ofphase I. Site DJ represents pressure at the rupted phasic contractions at the maximum rate concentration (Hydrogen monitor, GMI duodenojejunalflexure, sites for that intestinal site, followed by motor quies- Medical Ltd, Renfrew, UK). Orocaecal transit J1 J2' J3, and I represent cence (phase I). Phase II consisted of irregular time was defined as the period of time between pressure at 15 cm, 30 cm, 50 and 95 cm aborally. lactulose ingestion and a sustained (>10 ppm cm, above baseline) rise in breath hydrogen. STATISTICAL ANALYSIS Site DJ Data are expressed as mean (SEM). Statistical significance was assessed using analysis of Site J, variance, and Student's t tests for paired and unpaired data. SiteJ2 Results Eighty one complete migrating motor complexes SiteJ3 were recorded while subjects were drug free (control), and 102 complete migrating motor complexes were recorded while subjects received paroxetine.
Load more

Recommended publications
  • The In¯Uence of Medication on Erectile Function
    International Journal of Impotence Research (1997) 9, 17±26 ß 1997 Stockton Press All rights reserved 0955-9930/97 $12.00 The in¯uence of medication on erectile function W Meinhardt1, RF Kropman2, P Vermeij3, AAB Lycklama aÁ Nijeholt4 and J Zwartendijk4 1Department of Urology, Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands; 2Department of Urology, Leyenburg Hospital, Leyweg 275, 2545 CH The Hague, The Netherlands; 3Pharmacy; and 4Department of Urology, Leiden University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands Keywords: impotence; side-effect; antipsychotic; antihypertensive; physiology; erectile function Introduction stopped their antihypertensive treatment over a ®ve year period, because of side-effects on sexual function.5 In the drug registration procedures sexual Several physiological mechanisms are involved in function is not a major issue. This means that erectile function. A negative in¯uence of prescrip- knowledge of the problem is mainly dependent on tion-drugs on these mechanisms will not always case reports and the lists from side effect registries.6±8 come to the attention of the clinician, whereas a Another way of looking at the problem is drug causing priapism will rarely escape the atten- combining available data on mechanisms of action tion. of drugs with the knowledge of the physiological When erectile function is in¯uenced in a negative mechanisms involved in erectile function. The way compensation may occur. For example, age- advantage of this approach is that remedies may related penile sensory disorders may be compen- evolve from it. sated for by extra stimulation.1 Diminished in¯ux of In this paper we will discuss the subject in the blood will lead to a slower onset of the erection, but following order: may be accepted.
    [Show full text]
  • In Vivo Olanzapine Occupancy of Muscarinic Acetylcholine Receptors in Patients with Schizophrenia Thomas J
    In Vivo Olanzapine Occupancy of Muscarinic Acetylcholine Receptors in Patients with Schizophrenia Thomas J. Raedler, M.D., Michael B. Knable, D.O., Douglas W. Jones, Ph.D., Todd Lafargue, M.D., Richard A. Urbina, B.A., Michael F. Egan, M.D., David Pickar, M.D. , and Daniel R. Weinberger, M.D. Olanzapine is an atypical antipsychotic with potent than low-dose in the same regions. Muscarinic occupancy ϭ antimuscarinic properties in vitro (Ki 2–25 nM). We by olanzapine ranged from 13% to 57% at 5 mg/dy and studied in vivo muscarinic receptor occupancy by 26% to 79% at 20 mg/dy with an anatomical pattern olanzapine at both low dose (5 mg/dy) and high dose (20 indicating M2 subtype selectivity. The [I-123]IQNB data mg/dy) in several regions of cortex, striatum, thalamus and indicate that olanzapine is a potent and subtype-selective pons by analyzing [I-123]IQNB SPECT images of seven muscarinic antagonist in vivo, perhaps explaining its low schizophrenia patients. Both low-dose and high-dose extrapyramidal side effect profile and low incidence of olanzapine studies revealed significantly lower anticholinergic side effects. [Neuropsychopharmacology [I-123]IQNB binding than that of drug-free schizophrenia 23:56–68, 2000] Published by Elsevier Science Inc. on patients (N ϭ 12) in all regions except striatum. behalf of the American College of Neuropsychopharmacology [I-123]IQNB binding was significantly lower at high-dose KEY WORDS: Muscarinic receptor; Olanzapine; IQNB; cologically (Watling et al. 1995) and correspond to SPECT; Schizophrenia; Antipsychotic genes (respectively, m1–m5) that have been cloned (Bonner et al.
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 7,893,053 B2 Seed Et Al
    US0078.93053B2 (12) United States Patent (10) Patent No.: US 7,893,053 B2 Seed et al. (45) Date of Patent: Feb. 22, 2011 (54) TREATING PSYCHOLOGICAL CONDITIONS WO WO 2006/127418 11, 2006 USING MUSCARINIC RECEPTORM ANTAGONSTS (75) Inventors: Brian Seed, Boston, MA (US); Jordan OTHER PUBLICATIONS Mechanic, Sunnyvale, CA (US) Chau et al. (Nucleus accumbens muscarinic receptors in the control of behavioral depression : Antidepressant-like effects of local M1 (73) Assignee: Theracos, Inc., Sunnyvale, CA (US) antagonist in the porSolt Swim test Neuroscience vol. 104, No. 3, pp. 791-798, 2001).* (*) Notice: Subject to any disclaimer, the term of this Lind et al. (Muscarinic acetylcholine receptor antagonists inhibit patent is extended or adjusted under 35 chick Scleral chondrocytes Investigative Ophthalmology & Visual U.S.C. 154(b) by 726 days. Science, vol.39, 2217-2231.* Chau D., et al., “Nucleus Accumbens Muscarinic Receptors in the (21) Appl. No.: 11/763,145 Control of Behavioral Depression: Antidepressant-like Effects of Local M1 Antagonists in the Porsolt Swin Test.” Neuroscience, vol. (22) Filed: Jun. 14, 2007 104, No. 3, Jun. 14, 2001, pp. 791-798. Bechtel, W.D., et al., “Biochemical pharmacology of pirenzepine. (65) Prior Publication Data Similarities with tricyclic antidepressants in antimuscarinic effects only.” Arzneimittelforschung, vol. 36(5), pp. 793-796 (May 1986). US 2007/O293480 A1 Dec. 20, 2007 Chau, D.T. et al., “Nucleus accumbens muscarinic receptors in the control of behavioral depression: antidepressant-like effects of local Related U.S. Application Data Mantagonist in the Porsolt Swim test.” Neuroscience, vol. 104(3), (60) Provisional application No.
    [Show full text]
  • Gastrointestinal Motility
    Gastrointestinal Motility H. J. Ehrlein and M.Schemann 1. Motility of the stomach Anatomic regions of the stomach are the fundus, corpus (body), antrum and pylorus. The functional regions of the stomach do not correspond to the anatomic regions. Functionally, the stomach can be divided into the gastric reservoir and the gastric pump (Fig. 1). The gastric reservoir consists of the fundus and corpus. The gastric pump is represented by the area at which peristaltic waves occur: it includes the distal part of the corpus and the antrum. Due to different properties of the smooth muscle cells the gastric reservoir is characterised by tonic activity and the gastric pump by phasic activity. AB Gastric reservoir Fundus tonic contractions Pylorus Corpus Antrum Gastric pump phasic contractions Figure 1 . The stomach can be divided into three anatomic (A) and two functional regions (B) 1.1 Function of the gastric reservoir At the beginning of the 20 th century it was already observed that with increasing volume of the stomach the internal pressure of the stomach increases only slightly. In dogs, for instance, the increase in pressure is only 1.2 cm of water/100 ml volume. The small increase in gastric pressure indicates that the stomach does not behave like an elastic balloon but that it relaxes as it fills. Three kinds of gastric relaxation can be differentiated: a receptive, an adaptive and a feedback-relaxation of the gastric reservoir. The receptive relaxation consists of a brief relaxation during chewing and swallowing. The stimulation of mechano-receptors in the mouth and pharynx induces vago-vagal reflexes which cause a relaxation of the gastric reservoir (Fig.
    [Show full text]
  • There Is More to Healing Ulcers Than Suppressing Acid
    Gut, 1986, 27, 475-480 Gut: first published as 10.1136/gut.27.5.475 on 1 May 1986. Downloaded from Leading article There is more to healing ulcers than suppressing acid The finding that a given acid output might be associated with a normal stomach, or with an ulcer, has stimulated only modest interest in factors such as pepsin and the mucosal barrier, as recently discussed in these columns by Mr Venables.' This is because it is difficult to make objective measurements, (especially in man) of the mucosal barrier2 and even of pepsin.3 The mucosal barrier is a theoretical concept dealing with the ability of the mucosa to resist digestion by acid and pepsin. There are many factors involved in preserving an intact epithelium: mucus and its adherence to the epithelium, bicarbonate secretion deep to the mucus, epithelial cellular integrity, hydrophobicity, mucosal blood flow and interstitial bicarbonate. These factors have been extensively reviewed by several authors,2 5-7 and so will not be discussed further. Pepsin is also important but comprises several proteolytic enzymes which have slightly different characteristics such as varying pH for optimal activity,8 with a predominance of pepsin I secretion in duodenal ulceration. Pepsin secretion is substantially increased in duodenal ulcer patients.9 In patients whose ulcers do not heal with cimetidine there is not only poor http://gut.bmj.com/ suppression of acid secretion, but an even smaller reduction in pepsin output. 10 On the other hand attempts to correlate pepsin with ulcer activity and individual response to cimetidine have been disappointing"l and inhibition of peptic activity by amylopectin sulphate has not proved advantageous in healing duodenal ulcers.'2 Against this uncertain background Baron et al, have investigated the on October 1, 2021 by guest.
    [Show full text]
  • The Use of Stems in the Selection of International Nonproprietary Names (INN) for Pharmaceutical Substances
    WHO/PSM/QSM/2006.3 The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances 2006 Programme on International Nonproprietary Names (INN) Quality Assurance and Safety: Medicines Medicines Policy and Standards The use of stems in the selection of International Nonproprietary Names (INN) for pharmaceutical substances FORMER DOCUMENT NUMBER: WHO/PHARM S/NOM 15 © World Health Organization 2006 All rights reserved. Publications of the World Health Organization can be obtained from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected]). Requests for permission to reproduce or translate WHO publications – whether for sale or for noncommercial distribution – should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; e-mail: [email protected]). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.
    [Show full text]
  • Jp Xvii the Japanese Pharmacopoeia
    JP XVII THE JAPANESE PHARMACOPOEIA SEVENTEENTH EDITION Official from April 1, 2016 English Version THE MINISTRY OF HEALTH, LABOUR AND WELFARE Notice: This English Version of the Japanese Pharmacopoeia is published for the convenience of users unfamiliar with the Japanese language. When and if any discrepancy arises between the Japanese original and its English translation, the former is authentic. The Ministry of Health, Labour and Welfare Ministerial Notification No. 64 Pursuant to Paragraph 1, Article 41 of the Law on Securing Quality, Efficacy and Safety of Products including Pharmaceuticals and Medical Devices (Law No. 145, 1960), the Japanese Pharmacopoeia (Ministerial Notification No. 65, 2011), which has been established as follows*, shall be applied on April 1, 2016. However, in the case of drugs which are listed in the Pharmacopoeia (hereinafter referred to as ``previ- ous Pharmacopoeia'') [limited to those listed in the Japanese Pharmacopoeia whose standards are changed in accordance with this notification (hereinafter referred to as ``new Pharmacopoeia'')] and have been approved as of April 1, 2016 as prescribed under Paragraph 1, Article 14 of the same law [including drugs the Minister of Health, Labour and Welfare specifies (the Ministry of Health and Welfare Ministerial Notification No. 104, 1994) as of March 31, 2016 as those exempted from marketing approval pursuant to Paragraph 1, Article 14 of the Same Law (hereinafter referred to as ``drugs exempted from approval'')], the Name and Standards established in the previous Pharmacopoeia (limited to part of the Name and Standards for the drugs concerned) may be accepted to conform to the Name and Standards established in the new Pharmacopoeia before and on September 30, 2017.
    [Show full text]
  • Octreotide in Gastrointestinal Motility Disorders Gut: First Published As 10.1136/Gut.35.3 Suppl.S11 on 1 January 1994
    Gut 1994; supplement 3: S11 -S 14 Sll Octreotide in gastrointestinal motility disorders Gut: first published as 10.1136/gut.35.3_Suppl.S11 on 1 January 1994. Downloaded from C Owyang Abstract Intestinal effects of octreotide in The effects of octreotide on six normal scleroderma subjects and five patients with sclero- About 50% of patients with scleroderma have derma were investigated. Changes in small bowel dysfunction.5 In such patients, intestinal motility and in plasma motilin manometry shows patterns (known as the were examined after a single injection of migrating motor complex) in the small bowel octreotide. Octreotide stimulated intense during fasting6 and this may be clinically intestinal motor activity in normal sub- manifested as intestinal pseudo-obstruction jects. Motility patterns in the scleroderma and bacterial overgrowth. These problems are patients were chaotic and non-pro- difficult to treat because standard stimulatory pagative, but, after octreotide was given, prokinetic agents are not effective in sclero- became well coordinated, aborally derma.6 We therefore recently undertook a directed, and nearly as intense as in study to determine the effects of octreotide in normal volunteers. Clinical responses and six normal subjects and in five patients with changes in breath hydrogen were also scleroderma who had abdominal pain, nausea, evaluated in the five scleroderma patients bloating, and a change in intestinal contrac- who had further treatment with octreotide tility.7 We examined the changes in intestinal at a dose of 50 pugtday subcutaneously for motility and in plasma motilin, a gastrointesti- three weeks. A reduction in symptoms of nal hormone that stimulates intestinal motor abdominal pain, nausea, vomiting, and activity, after single injections of octreotide bloating was seen.
    [Show full text]
  • A Method to Determine the Ability of Drugs to Diffuse Through the Blood-Brain Barrier ANNA SEELIG*T, RUDOLF GOTTSCHLICHI, and RALF M
    Proc. Natl. Acad. Sci. USA Vol. 91, pp. 68-72, January 1994 Pharmacology A method to determine the ability of drugs to diffuse through the blood-brain barrier ANNA SEELIG*t, RUDOLF GOTTSCHLICHI, AND RALF M. DEVANTf *Biocenter of the University of Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland; and tMedicinal Chemistry Research Laboratories, CNS Department, E. Merck, Frankfurter Strasse 250, 6100 Darmstadt, Germany Communicated by Harden M. McConnell, September 13, 1993 ABSTRACT A method has been devised for predicting the groups, (ii) the number of charged groups and their extent of ability of drugs to cross the blood-brain barrier. The criteria ionization, and (iii) the molecular size. Interestingly, the depend on the amphiphilic properties of a drug as reflected in same three parameters also determine the surface activity Its surface activity. The assessment was made with various and their combined action can be evaluated in a single drugs that either penetrate or do not penetrate the blood-brain experiment by measuring the Gibbs adsorption isotherm. barrier. The surface activity of these drugs was quantified by Here the chromatographically determined lipophilicity their Gibbs adsorption isotherms in terms ofthree parameters: constants are compared with measurements of the surface (i) the onset of surface activity, (ii) the critical micelle concen- activity for a large number of structurally different com- tration, and (iii) the surface area requirement ofthe drug at the pounds known to cross or not to cross the BBB. The air/water interface. A calibration diagram is proposed in predictive value of the surface activity measurements as a which the critical miceUe concentration is plotted against the function of concentration is distinctly higher than that of the concentration required for the onset of surface activity.
    [Show full text]
  • Aandp2ch25lecture.Pdf
    Chapter 25 Lecture Outline See separate PowerPoint slides for all figures and tables pre- inserted into PowerPoint without notes. Copyright © McGraw-Hill Education. Permission required for reproduction or display. 1 Introduction • Most nutrients we eat cannot be used in existing form – Must be broken down into smaller components before body can make use of them • Digestive system—acts as a disassembly line – To break down nutrients into forms that can be used by the body – To absorb them so they can be distributed to the tissues • Gastroenterology—the study of the digestive tract and the diagnosis and treatment of its disorders 25-2 General Anatomy and Digestive Processes • Expected Learning Outcomes – List the functions and major physiological processes of the digestive system. – Distinguish between mechanical and chemical digestion. – Describe the basic chemical process underlying all chemical digestion, and name the major substrates and products of this process. 25-3 General Anatomy and Digestive Processes (Continued) – List the regions of the digestive tract and the accessory organs of the digestive system. – Identify the layers of the digestive tract and describe its relationship to the peritoneum. – Describe the general neural and chemical controls over digestive function. 25-4 Digestive Function • Digestive system—organ system that processes food, extracts nutrients, and eliminates residue • Five stages of digestion – Ingestion: selective intake of food – Digestion: mechanical and chemical breakdown of food into a form usable by
    [Show full text]
  • (12) Patent Application Publication (10) Pub. No.: US 2006/0078604 A1 Kanios Et Al
    US 20060078604A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2006/0078604 A1 Kanios et al. (43) Pub. Date: Apr. 13, 2006 (54) TRANSDERMAL DRUG DELIVERY DEVICE Related U.S. Application Data INCLUDING AN OCCLUSIVE BACKING (60) Provisional application No. 60/616,861, filed on Oct. 8, 2004. (75) Inventors: David Kanios, Miami, FL (US); Juan A. Mantelle, Miami, FL (US); Viet Publication Classification Nguyen, Miami, FL (US) (51) Int. Cl. Correspondence Address: A 6LX 9/70 (2006.01) DCKSTEIN SHAPRO MORN & OSHINSKY (52) U.S. Cl. .............................................................. 424/449 LLP (57) ABSTRACT 2101 L Street, NW Washington, DC 20037 (US) A transdermal drug delivery system for the topical applica tion of one or more active agents contained in one or more (73) Assignee: Noven Pharmaceuticals, Inc. polymeric and/or adhesive carrier layers, proximate to a non-drug containing polymeric backing layer which can (21) Appl. No.: 11/245,180 control the delivery rate and profile of the transdermal drug delivery system by adjusting the moisture vapor transmis (22) Filed: Oct. 7, 2005 sion rate of the polymeric backing layer. Patent Application Publication Apr. 13, 2006 Sheet 1 of 2 US 2006/0078604 A1 Fis ZZZZZZZZZZZZZZZZZZZ :::::::::::::::::::::::::::::::: Patent Application Publication Apr. 13, 2006 Sheet 2 of 2 US 2006/0078604 A1 3. s s 3. a 3 : 8 g US 2006/0078604 A1 Apr. 13, 2006 TRANSIDERMAL DRUG DELVERY DEVICE 0008. In the “classic' reservoir-type device, the active INCLUDING AN OCCLUSIVE BACKING agent is typically dissolved or dispersed in a carrier to yield a non-finite carrier form, Such as, for example, a fluid or gel.
    [Show full text]
  • Appendix 1 BNF Codes of Drugs Lists Used to Define Exposure Groups
    Appendix 1 BNF Codes of drugs lists used to define exposure groups. Anticholinergic antipsychotics d411. Chlorpromazine d412. Chlorpromazine d413. Chlorpromazine d414. Chlorpromazine d415. Chlorpromazine d41a. Chlorpromazine d41b. Chlorpromazine d41c. Chlorpromazine d41d. Chlorpromazine d4b1. Perphenazine d4e1. PROMAZINE d4ex. PROMAZINE d4g.. Thioridazine d4g1. Thioridazine d4g2. Thioridazine d4g3. Thioridazine d4g5. Thioridazine d4g7. Thioridazine d4gp. Thioridazine d4gt. Thioridazine d4gu. Thioridazine d4gv. Thioridazine d4gw. Thioridazine d4gz. Thioridazine d4h.. Trifluoperazine d4h1. Trifluoperazine d4h2. Trifluoperazine d4h3. Trifluoperazine d4h4. Trifluoperazine d4hs. Trifluoperazine d4ht. Trifluoperazine d4hu. Trifluoperazine d4hx. Trifluoperazine d4l2. CLOZAPINE d4r1. OLANZAPINE d4r3. OLANZAPINE d4r7. OLANZAPINE d4s1. QUETIAPINE d4s2. QUETIAPINE d4s3. QUETIAPINE d4s5. QUETIAPINE d4ss. QUETIAPINE d4sx. QUETIAPINE Tricyclic antidepressants d7... d71.. Amitriptyline d711. Amitriptyline d712. Amitriptyline d713. Amitriptyline d719. Amitriptyline d71a. Amitriptyline d71b. Amitriptyline d71c. Amitriptyline d71d. Amitriptyline d71e. Amitriptyline d71f. Amitriptyline d71u. Amitriptyline d71v. Amitriptyline d71w. Amitriptyline d71y. Amitriptyline d71z. Amitriptyline d73.. Clomipramine d731. Clomipramine d732. Clomipramine d733. Clomipramine d736. Clomipramine d73s. Clomipramine d73t. Clomipramine d73u. Clomipramine d73v. Clomipramine d73w. Clomipramine d73z. Clomipramine d75.. DOSULEPIN d751. DOSULEPIN d752. DOSULEPIN d755. DOSULEPIN d756.
    [Show full text]