Academic literature on the topic 'Opioid agonists'
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Journal articles on the topic "Opioid agonists"
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María Martín Orejas and Víctor Martín Mora. "AT-121, ¿el opioide perfecto?" Revista Electrónica AnestesiaR 12, no. 7 (August 3, 2020): 4. http://dx.doi.org/10.30445/rear.v12i7.862.
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Los opioides son los analgésicos más potentes y efectivos de que disponemos en la actualidad. Su cara oscura la encarna el creciente aumento de pacientes adictos a su consumo en todo el mundo, principalmente en Estados Unidos. Desde el descubrimiento de los primeros opioides sintéticos, la industria farmacéutica se halla en busca de un analgésico que no genere tolerancia ni dependencia, ni efectos adversos respiratorios. La mayoría de los opiáceos son agonistas del receptor mu, cuya activación aumenta la disponibilidad sináptica de dopamina, neurotransmisor vehicular en circuitos de recompensa. Sin embargo, un cuarto receptor opioide ha sido descrito recientemente: el receptor de nociceptina/orfanina. Su activación inhibe la liberación de dopamina, evitando el refuerzo positivo que ocurre tras el consumo del fármaco. AT-121 es un agonista bifuncional MOP/NOP que ha sido probado en primates no humanos con resultados prometedores en cuanto a potencia analgésica, menores efectos secundarios sistémicos y menor tasa de adicción y abuso. Tales características hacen de esta molécula un arma esperanzadora en el tratamiento del dolor crónico o de la propia adicción a fármacos opioides. En los últimos años se han explorado distintos agonistas bifuncionales en roedores y primates no humanos con interesantes resultados; quedamos pues a la espera de futuras investigaciones en humanos. ABSTRACT Is AT121 the perfect opioid? Opioids are the most powerful and effective analgesics available today. Their dark side is reflected in the growing number of patients addicted to their use around the world, mainly in the United States. Since the discovery of the first synthetic opioids, the pharmaceutical industry has been searching for an analgesic that does not generate tolerance or dependence, nor adverse respiratory effects. Most opioids are mu receptor agonists, whose activation increases the synaptic availability of dopamine, a neurotransmitter that is a carrier in reward circuits. However, a fourth opioid receptor has recently been described: the nociceptin/orphanine receptor. Its activation inhibits the release of dopamine, preventing the positive reinforcement that occurs after drug consumption. AT-121 is a bifunctional MOP/NOP agonist that has been tested in non-human primates with promising results in terms of analgesic potency, fewer systemic side effects, and lower rate of addiction and abuse. Such characteristics make this molecule a hopeful weapon in the treatment of chronic pain or addiction to opioid drugs. In recent years, different bifunctional agonists have been explored in rodents and non-human primates with interesting results; we are therefore awaiting future research in humans.
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Colson, James. "Office-Based Opioid Dependence Treatment." July 2012 3S;15, no. 3S;7 (July 14, 2012): ES231—ES236. http://dx.doi.org/10.36076/ppj.2012/15/es231.
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Background: Opioid misuse and abuse occurring in association with the treatment of chronic non-cancer pain are not new phenomena, but their increasing prevalence in recent years is unprecedented. Advancements in pharmaceutical technologies have provided opioid-related drugs, which lack the pure mu agonist activity characteristic of the typical opioid congeners. This absent or altered mu receptor activity imparts an opioid receptor antagonistic or partial agonistic pharmacologic action, which serves to modulate the development of opioid-induced tolerance and physical dependence and facilitate detoxification and withdrawal from opioids. Opioid antagonists and partial agonists are being used in abuse deterrent strategy regimens to prevent opioid tolerance and the development of dependence, as well as in the management of opioid detoxification and treatment of withdrawal. The specific opioid antagonists and partial agonists used in these various therapeutic modalities will be the focus of this review. Objectives: Evaluate the comparative therapeutic utility of opioid antagonists and partial agonists in preventing the development of opioid tolerance and treating opioid dependence, detoxification, and withdrawal. A primary focus is the use of opioid antagonists and partial agonists within an office-based practice. Methods: A narrative review of the current literature involving the therapeutic use of opioid antagonists and partial agonists in the management of opioid tolerance, dependence, detoxification, and withdrawal. A computerized literature search in the PubMed, EMBASE, BioMed, and Cochrane Library review databases from 2008 through 2010 was performed. This search included systematic and narrative reviews, prospective and retrospective studies, as well as cross-references from bibliographies of notable primary and review articles and abstracts from scientific meetings. US Food and Drug Administration records and pharmaceutical manufacturers’ product literature were also used in the search. Conclusion: Opioid dependency, whether it results from the misuse or abuse of prescription or street drugs, continues to be a significant public health issue. Passage of DATA 2000 and US Food and Drug Administration approval of buprenorphine and buprenorphine/ naloxone has revolutionized opioid dependence therapy. The traditional addiction medicine therapy regimen of methadone maintenance, with its inherent legal limitations and restrictions, has been challenged by an office-based dependence practice with buprenorphine serving as a prominent therapeutic tool. Key words: opioid antagonist, opioid partial agonist, tolerance, dependence, detoxification, withdrawal, hyperalgesia, buprenorphine, suboxone, naloxone, naltrexone, methylnaltrexone, nalmefene, tramadol, butorphanol, nalbupine, pentazocine.
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Haddad, G. G., H. J. Jeng, and T. L. Lai. "Effect of endorphins on heart rate and blood pressure in adult dogs." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 5 (May 1, 1986): H796—H805. http://dx.doi.org/10.1152/ajpheart.1986.250.5.h796.
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To investigate the role of opioids in regulating cardiovascular function, we administered delta-opioid receptor agonists D-Ala-D-Leu enkephalin (DADLE) and D-Ala-Met enkephalinamide (DAME), and mu-opioid receptor agonist, a morphiceptin analogue (MA), intracisternally in 13 unanesthetized, chronically instrumented adult dogs in 2 doses (25 and 125 micrograms/kg). After an initial transient drop, the R-R interval increased (peak approximately 25–60 min) postadministration of opioids. The time course and the magnitude of the change in R-R interval depended on the agonist: delta-agonists induced a more prolonged and marked change in R-R interval than mu-agonists at both doses. Mean arterial blood pressure (MAP) increased initially but dropped toward or even below base line 30 min after opioids administration. Atropine, given intravenously or intra-arterially at peak action of agonist in relatively low doses (0.02 mg/kg), induced an AV block followed by a marked decrease in R-R interval. There was also an increase in MAP after atropine. Naloxone, given intracisternally, reversed both delta- and mu-opioid effects but did not induce changes in the R-R interval without prior administration of opioids. We conclude that in unanesthetized adult dogs 1) both mu- and delta-receptor opioid agonists prolong the R-R interval, and this depends on the type of receptor stimulated; 2) opioids induce slowing in heart rate, possibly by increasing parasympathetic activity to the heart; 3) enkephalin and morphiceptin analogues induce a biphasic response in MAP; and 4) endorphins do not modulate cardiovascular function tonically; we speculate that they can alter the R-R interval and MAP in the presence of stimuli.
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Trescot, Andrea M. "Opioid Pharmacology." Pain Physician 2s;11, no. 3;2s (March 14, 2008): S133—S153. http://dx.doi.org/10.36076/ppj.2008/11/s133.
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Background: Mu agonists have been an important component of pain treatment for thousands of years. The usual pharmacokinetic parameters (half-life, clearance, volume of distribution) of opioids have been known for some time. However, the metabolism has, until recently, been poorly understood, and there has been recent interest in the role of metabolites in modifying the pharmacodynamic response in patients, in both analgesia and adverse effects. A number of opioids are available for clinical use, including morphine, hydromorphone, levorphanol, oxycodone, and fentanyl. Advantages and disadvantages of various opioids in the management of chronic pain are discussed. Objective: This review looks at the structure, chemistry, and metabolism of opioids in an effort to better understand the side effects, drug interactions, and the individual responses of patients receiving opioids for the treatment of intractable pain. Conclusion: Mu receptor agonists and agonist-antagonists have been used throughout recent medical history for the control of pain and for the treatment of opiate induced side effects and even opiate withdrawal syndromes. Key words: Opioid metabolism, opioid interactions, morphine, codeine, hydrocodone, oxycodone, hydromorphone, methadone, intractable pain, endorphins, enkephalins, dynorphins, narcotics, pharmacology, propoxyphene, fentanyl, oxymorphone, tramadol
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Zappi, Lucia, Francesco Nicosia, Danilo Rocchi, Pingfang Song, and Kai Rehder. "Opioid Agonists Modulate Release of Neurotransmitters in Bovine Trachealis Muscle." Anesthesiology 83, no. 3 (September 1, 1995): 543–51. http://dx.doi.org/10.1097/00000542-199509000-00013.
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Background Stimulation of opioid receptors in the airways can modulate cholinergic neurotransmission and thereby reduce bronchoconstriction. This protecting effect of opioids against bronchoconstriction may be of clinical interest. Inhalation of opioids as a method of analgesia is likely to result in an opioid concentration at airway receptors sufficient to protect against bronchoconstriction; the concentration may be insufficient when opioids are administered by conventional techniques. In addition, new selective opioids may be developed that could more selectively protect the airways against bronchoconstriction. Methods The effect of three selective opioid agonists on the contractile response to electric field stimulation (EFS) was studied in isolated muscle strips from four regions of the bovine trachea (upper, or laryngeal; upper middle; lower middle; lower, or carinal). Results The selective kappa agonist trans-3,4-dichloro-N-methyl-N-(2-1-pyrrolidinyl) cyclohexyl benzene acetamide (U-50488 H) and the selective mu-opioid agonist D-Ala2-N-MePhe4-Gly-ol5-enkephalin (DAMGO) reduced significantly (P < 0.001 and P < 0.001, respectively) the contractile response to EFS. The attenuation of the contractile response by U-50488 H was concentration-dependent (P < 0.0001) and tended to be larger at low stimulating frequencies (P = 0.055). The attenuation of the contractile response by DAMGO was frequency-dependent (P < 0.01). The selective delta-opioid agonist D-penicillamine2-D-penicillamine5-enkephalin had no significant effect on the contractile response to EFS (P = 0.71). There were no significant differences among the four regions of the trachea in their responses to the selective opioid agonists U-50488 H (P = 0.50) and DAMGO (P = 0.44). Neither U-50488 H nor DAMGO altered the contractile response to acetylcholine P > 0.11, P > 0.21, respectively), suggesting that the opioid agonists have a prejunctional effect. The attenuation of the contractile response to EFS by U-50488 H was partially but significantly antagonized by 10(-5) M naloxone (P < 0.01) and by 10(-5) and 10(-6) M of the selective kappa-opioid antagonist 2,2'-[1,1'-biphenyl] 4,4'-diyl- bis [2-hydroxy-4,4-dimethyl-morpholinium] (P < 0.05). Naloxone (10(-5) M) abolished the inhibitory effect of DAMGO, suggesting that opioid receptors are involved in the attenuation of the contractile response to EFS afforded by DAMGO and U-50488 H. Conclusions We conclude that prejunctional kappa- and mu-opioid receptors attenuate the contractile response of isolated bovine trachealis muscle to EFS by inhibiting cholinergic neurotransmission. This effect is uniform throughout the trachealis muscle. delta-Opioid receptors are apparently not present in the bovine trachealis muscle. Caution must be used in extrapolating these results to the intact human. In this study little or no inhibitory effect of the opioids was observed at concentrations expected at airway receptor sites when administered by conventional techniques. However, the effect may be large enough to protect against bronchoconstriction when nebulized opioids are administered by inhalation.
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El-Sharkawy, T. Y., M. F. Al-Shireida, and C. W. T. Pilcher. "Vascular effects of some opioid receptor agonists." Canadian Journal of Physiology and Pharmacology 69, no. 6 (June 1, 1991): 846–51. http://dx.doi.org/10.1139/y91-128.
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Opioid peptides have been implicated in shock-associated hypotension. Our aim was to find out whether opioid agonists have direct vasodilator actions on vascular smooth muscle. The study was conducted on rat abdominal aortic rings. In rings precontracted with either norepinephrine, prostaglandin F2α, or high potassium Krebs (HPK), the effects of the opioid agonists tested (morphine, U50488H, ethylketocyclazocine (EKC), and bremazocine) depended on the precontracting agent used. HPK-precontracted rings were relaxed by all agonists tested. In norepinephrine-precontracted rings, all caused contraction at low concentrations and relaxation at high concentrations except bremazocine, which caused only relaxation. In prostaglandin F2α-precontracted rings, U50488H produced contraction at low concentrations and relaxation at high concentrations while EKC caused only relaxation and morphine or bremazocine caused only contraction. All relaxant responses were endothelium-independent and were antagonized by verapamil but not by a number of antagonists including naloxone, MR2266, propranolol, diphenhydramine, cimetidine, and indomethacin. They may reflect calcium channel blockade. Morphine-induced vasoconstriction was antagonized by high concentrations of naloxone or mepyramine and may be due to release of histamine by a naloxone-sensitive mechanism. We conclude that (a) the opioid agonists tested exert direct actions on vascular smooth muscle; (b) the nature of the response depended not only on the agonist used and its concentration but also on the agent used to precontract the tissue; and (c) it is unlikely that direct actions of endogenous opioids contribute to the shock-associated hypotension because high doses were needed to elicit them.Key words: vascular smooth muscle, opioids, neurohormonal peptides, circulatory shock.
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Sandner-Kiesling, Andreas, and James C. Eisenach. "Estrogen Reduces Efficacy of μ- but Not κ-Opioid Agonist Inhibition in Response to Uterine Cervical Distension." Anesthesiology 96, no. 2 (February 1, 2002): 375–80. http://dx.doi.org/10.1097/00000542-200202000-00024.
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Background Although the uterine cervix is a common source of acute and chronic visceral pain in women, there is practically no neurobiological investigation of nociception from this visceral organ. With use of a novel model of uterine cervical distension nociception in rats, the estrogen dependency of opioid agonist-induced inhibition was investigated. Methods Sprague Dawley rats were anesthetized with halothane and bilateral ovariectomy was performed, after which placebo or estrogen treatment was administered for 1 week. Animals were reanesthetized and fine metal rods were inserted into the uterine cervix for manual distension. Reflex contraction of the rectus abdominis in response to distension was recorded before and after cumulative dosing with the mu-opioid agonist morphine and the kappa-opioid agonist (-)U50488. Results Uterine cervical distension increased reflex abdominal muscle contraction with a threshold of 75 g, regardless of estrogen treatment. Morphine and (-)U50488 reduced the reflex response to cervical distension in a dose-dependent manner. Estrogen reduced the inhibitory effect of morphine but not that of (-)U50488. Conclusions It has been suggested that mu-opioid agonists are less potent in females than males, whereas kappa-opioid agonists are more potent in females than males. These data suggest that estrogen may influence the action of opioids, at least against visceral pain, which may explain this sex difference. In addition, these data suggest that kappa-opioid agonists may be effective in the treatment of pain originating from the uterine cervix, regardless of estrogen status.
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Webster, Lynn, and William K. Schmidt. "Dilemma of Addiction and Respiratory Depression in the Treatment of Pain: A Prototypical Endomorphin as a New Approach." Pain Medicine 21, no. 5 (June 5, 2019): 992–1004. http://dx.doi.org/10.1093/pm/pnz122.
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Abstract Objective Although mu-opioid receptor agonists have been the mainstay of analgesic regimens for moderate to severe pain, they are associated with serious side effects, risks, and limitations. We evaluate the most serious risks associated with conventional opioids and compare these with the pharmacology of CYT-1010, a prototypical endomorphin and mu-opioid receptor agonist. Results Addiction and respiratory depression are serious risks of traditional mu-opioid analgesics. Mitigation strategies have been inadequate at addressing the opioid crisis and may interfere with the effective treatment of pain. Improved understanding of mu-opioid receptor biology and the discovery in 1997 of an additional and unique family of endogenous opioid peptides (endomorphins) have provided a pathway for dissociating analgesia from opioid-related adverse events and developing new classes of mu-opioid receptor agonists that use biased signaling and/or target novel sites to produce analgesia with reduced side effect liability. Endomorphin-1 and -2 are endogenous opioid peptides highly selective for mu-opioid receptors that exhibit potent analgesia with reduced side effects. CYT-1010 is a cyclized, D-lysine-containing analog of endomorphin-1 with a novel mechanism of action targeting traditional mu- and exon 11/truncated mu-opioid receptor 6TM variants. CYT-1010 preclinical data have demonstrated reduced abuse potential and analgesic potency exceeding that of morphine. In an initial phase 1 clinical study, CYT-1010 demonstrated significant analgesia vs baseline and no respiratory depression at the dose levels tested. Conclusions CYT-1010 and other novel mu-opioid receptor agonists in clinical development are promising alternatives to conventional opioids that may offer the possibility of safer treatment of moderate to severe pain.
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Herz, Albert. "Opioid reward mechanisms: a key role in drug abuse?" Canadian Journal of Physiology and Pharmacology 76, no. 3 (March 1, 1998): 252–58. http://dx.doi.org/10.1139/y98-017.
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There is increasing evidence to implicate the mesolimbic dopamine system in the rewarding effects of drugs of abuse such as opioids, psychostimulants, and alcohol, and in addition endogenous opioids may play a key role in the underlying adaptive mechanisms. Opioid agonists with affinity for µ and delta opioid receptors are rewarding, whereas opioid agonists with affinity for kappa receptors are aversive. These opposing motivational effects are paralleled by an increase and decrease, respectively, of dopamine release in the nucleus accumbens. Opposite effects are induced in response to selective antagonists for these different receptor types, pointing to tonically active endogenous opioid reward mechanisms. Withdrawal from chronic morphine results in sensitization for opioid reward; an effect that is counteracted by kappa opioid agonists. The rewarding effects of psychostimulants such as cocaine and amphetamine, mediated by the mesolimbic dopamine pathway, are modulated by opioid mechanisms in both directions: sensitization by morphine pretreatment, inhibition by kappa receptor agonists. A modulatory role of endogenous opioids is also suggested from biochemical data, showing increased dynorphin and kappa receptor expression after chronic cocaine treatment. Alcohol reward involves the mesolimbic reward system also, and opioids modulate this behaviour. Naltrexone as well as selective µ and delta opioid receptor antagonists decrease alcohol consumption in operant conditioning models. Biochemical approaches point to a functional deficit of endogenous opioids in genetic models exhibiting high prevalence for alcohol intake. The therapeutic implications of these data are discussed.Key words: reward mechanisms, endogenouos opioid systems, psychostimulants, alcohol.
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Ikoma, Miho, Tatsuro Kohno, and Hiroshi Baba. "Differential Presynaptic Effects of Opioid Agonists on Aδ- and C-afferent Glutamatergic Transmission to the Spinal Dorsal Horn." Anesthesiology 107, no. 5 (November 1, 2007): 807–12. http://dx.doi.org/10.1097/01.anes.0000286985.80301.5e.
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Background Although intrathecal administration of opioids produces antinociceptive effects in the spinal cord, it has not been established whether intrathecal opioid application more effectively terminates C fiber-mediated pain than A fiber-mediated pain. Here, the authors focus on the differences in opioid actions on Adelta- and C-afferent responses. Methods Using the whole cell patch clamp technique, the authors investigated the presynaptic inhibitory actions of micro-, delta-, and kappa-opioid receptor agonists on primary afferent-evoked excitatory postsynaptic currents (EPSCs) in substantia gelatinosa neurons of adult rat spinal cord slices. Results The micro agonist DAMGO (0.1, 1 microM) reduced the amplitude of glutamatergic monosynaptic Adelta- or C fiber-evoked EPSCs. C fiber-evoked EPSCs were inhibited to a greater extent than Adelta fiber-evoked EPSCs. The delta agonist DPDPE (1, 10 microM) produced modest inhibition of Adelta- or C fiber-evoked EPSCs. In contrast, the kappa agonist U69593 (1 microM) did not affect the amplitude of either Adelta or C fiber-evoked EPSCs. Conclusions These results indicate that opioids suppress excitatory synaptic transmission mainly through activation of micro receptors on primary afferent C fibers. Given that the substantia gelatinosa is the main termination of Adelta and C fibers transmitting nociceptive information, the current findings may partially explain the different potency of opioid agonists.
Dissertations / Theses on the topic "Opioid agonists"
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Fischer, Bradford D. Dykstra Linda A. "Interactions between opioid agonists and glutamate receptor antagonists." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1694.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Psychology Behavioral Neuroscience." Discipline: Psychology; Department/School: Psychology.
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Basti, Vida. "Ligand biased signaling of opioid agonists forphosphorylation and regulation of μ -opioid receptors." Thesis, Uppsala universitet, Farmakologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-192584.
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Abstract Ligand biased signaling of opioid agonists for phosphorylation andregulation of μ -opioid receptors Student: Vida Basti. Supervisor: Prof Macdonald Christie. Departmement of Neuropharmacology, The University of Sydney. Examiner: Prof Ingrid Nylander. Departement of Phamacology, University of Uppsala. Opioid drugs are of great use in the medical practise. The drugs are commonly prescribed formany types of illnesses, mostly in cases of pain management. Although opioids come withmany benefits they are causing a lot of problems as well. The side effects are many andamongst these is tolerance development which may lead to abuse and addiction. Because ofthe fast tolerance development in patients, higher doses up to 10 times the therapeutic doseare being prescribed. This is a major issue in today’s society and must be addressed.Scientists are trying to figure out the mechanism behind tolerance by comparing differenttypes opioid drugs. Some opioids causes tolerance in a much faster rate than others but it isstill uncertain why and what is causing this. Two of the most commonly prescribed opioidsare oxycodone and morphine and so in this rapport these opioids are compared with respectto their capability to cause internalization in neurons. In the experiments a positive control,DAMGO, is being used as well as a negative control. The method being used is an indirectmethod of immunohistochemistry on AtT20 transfected cell culture. The results show thatOxycodone seems to cause no internalization at all in comparison to the control.
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Blackburn, Thomas P. "Renal, vascular and endocrine effects of Kappa opioid agonists." Thesis, University of Manchester, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237570.
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Moore, Tisha T. "The effects of Kappa Opioid Agonists on Ocular Hydrodynamics." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2000. http://digitalcommons.auctr.edu/dissertations/3602.
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Opioid receptors have been demonstrated to modulate various functions in the eye. This research was designed to determine and compare the effects of kappa agonists on ocular hydrodynamics. Experiments were done to determine the effects of ICI 204,448 (ICI), which is not capable of penetrating the blood-brain barrier, and U-62066 (spiradoline) on: 1) intraocular pressure (IOP) and pupil diameter (PD), 2) pre- (neuronal) and postjunctional sites of action, and 3) atrial natriuretic peptide (ANP) levels in aqueous humor. Dark-adapted New Zealand White (NZW) male, rabbits were used in all experiments. IOP (mmHg) was measured by a pneumatonometer and PDs (mm) were measured by an optistick before each IOP reading. Baseline readings were taken at 1/2 and 0 hours prior to drug adminstration. Post-drug measurements were made at 1/2, 1, 2, 3, 4, and 5 hours after topical drug application. The release of norepinephrine was measured from perfused ICBs and expressed as the percent change of the control. Cyclic AMP concentrations in the ICBs and ANP levels in aqueous were quantified by radioimmunoassay techniques. The kappa antagonist, norbinaltorphimine (nor-BNI), was applied 30 minutes prior to agonist application in all experiments. ICI and spiradoline decreased IOP in a dose-dependent manner in normal rabbits, but only spiradoline showed significant changes in PD. Both kappa agonist inhibited the release of NE from perfused ICBs. Isoproterenol-stimulated cAMP levels in ICBs were lowered by both kappa receptor agonists. ANP levels in the aqueous humor increased in response to the kappa opioid agonists. These data suggest that spiradoline and ICI lower IOP by activating kappa opioid receptors in the eye. The effect of spiradoline on PD indicates that this kappa agonist activates receptors in the eye and/or the brain. The inhibition of NE release and cAMP accumulation in the ICB, suggests pre- and postjunctional sites of action for kappa agonists. The increase of ANP levels in aqeous suggests a role for ANP in lowering IOP. If these drugs can be shown to lower IOP safely and effectively in humans, then they may be utilized in the treatment of glaucoma.
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Rimoy, Gerald Herman. "Studies on the clinical pharmacology of kappa opioid receptor agonists." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305134.
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Altarifi, Ahmad. "EFFECTS OF MU OPIOID RECEPTOR AGONISTS ON INTRACRANIAL SELF-STIMULATION IN THE ABSENCE AND PRESENCE OF “PAIN” IN RATS." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/518.
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Pain is a significant health problem. Mu opioid receptor agonists are used clinically as analgesics, but their use is constrained by high abuse liability. Intracranial self-stimulation (ICSS) is a preclinical behavioral procedure that has been used to assess abuse potential of opioids, and drug-induced facilitation of ICSS is interpreted as an abuse-related effect. ICSS can also be used as a behavioral baseline to detect affective dimensions of pain. Specifically, pain-related depression of ICSS can model pain-related depression of behavior and mood, and drug-induced blockade of pain-related ICSS depression can serve as a measure of affective analgesia. This dissertation used mu agonists that vary in efficacy at the mu receptor (methadone> fentanyl> morphine> hydrocodone> buprenorphine> nalbuphine) and compared their effects on ICSS in the absence (phase one) or presence (phase 2) of pain. Adult male Sprague-Dawley rats were equipped with intracranial electrodes targeting the medial forebrain bundle and trained to lever press for brain stimulation. Different frequencies of stimulation maintained a frequency-dependent increase in ICSS rates, and permitted detection of both rate-increasing and rate-decreasing treatment effects. During phase 1, medium- and high-efficacy mu agonists produced initial rate-decreasing effects, followed by abuse-related rate-increasing effects at later time points. Repeated morphine administration produced tolerance to its own rate-decreasing effects, cross-tolerance to rate-decreasing effects of other mu agonists, and enhanced expression of rate-increasing effects. Low efficacy mu agonists only produced rate-increasing effects, which were enhanced after repeated morphine. These results suggest that previous opioid exposure increases expression of abuse-related facilitation of ICSS by mu agonists regardless of efficacy. During phase 2, intraperitoneal administration of lactic acid (1.8%) served as a noxious stimulus to depress ICSS. All mu agonists blocked acid-induced depression of ICSS at doses similar to those that facilitated ICSS in the absence of pain. A higher intensity noxious stimulus (5.6 % acid) produced further depression of ICSS and reduced the antinociceptive potency of both methadone and nalbuphine. Morphine antinociception was resistant to tolerance in the assay of acid-depressed ICSS. Overall, these results provide a basis for comparing determinants of abuse-related opioid effects in the absence of pain with their affective analgesic effects in the presence of pain.
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Asghar, Muhammad Junaid. "Studies on the biased signalling of some novel delta opioid receptor agonists." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/40485/.
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The delta opioid receptor (DOR) is a G protein-coupled receptor (GPCR) which is important in the regulation of neuronal function, predominantly via coupling to heterotrimeric Gi/0 proteins. The receptor has been shown to be a potential target for the treatment of chronic pain and affective disorders. Although a large number of opioid agonists exist, their properties vary widely, at least partly due to their differential coupling to post-receptor signalling systems, a phenomenon referred to as ligand-biased signalling or functional selectivity. The aim of the current project was to examine the signalling properties of a set of established and novel DOR agonists in an attempt to identify compounds that have biased signalling profiles. It was hypothesized that DOR agonists with partial efficacy regarding β-arrestin recruitment would be less liable to induce receptor internalization and desensitization of G protein-mediated signalling than full agonists. Chinese hamster ovary (CHO) cells, stably transfected with GFP-tagged human (h)DOR and CHO-K1 and U2OS cells over-expressing hDOR were exposed to a number of novel selective DOR agonists compared with the commercially available agonists, SNC80, ADL5859 and DADLE. The compounds’ potencies and efficacies were measured in four different assay systems; 1. Inhibition of forskolin-stimulated cyclic AMP accumulation, 2. Extracellular signal-regulated kinase (ERK1/2) phosphorylation using an immunocytochemical In-cell Western (I-CW) assay, 3. β-arrestin 2 recruitment and 4. hDOR internalization. The latter two assays employed DiscoverX Enzyme Fragment Complementation technology. An attempt to develop a secreted placental alkaline phosphatase (SPAP) reporter gene assay to measure DOR-mediated cyclic AMP inhibition was not successful. All of the ligands were nearly full agonists in relation to cyclic AMP inhibition although some were less efficacious than the standard SNC80 regarding ERK1/2 activation. Their absolute potencies and rank orders of potency in inhibiting cyclic AMP and activating ERK1/2 were quite different, although both signalling systems were apparently Gi/o- protein mediated. In contrast, the agonists exhibited a full range of efficacies and potencies in both β-arrestin 2 recruitment and hDOR internalization assays and there was a significant correlation between the maximum efficacies of the compounds in the two assays. A potential relationship between β-arrestin 2 recruitment/ hDOR internalization and desensitization of agonist-induced cyclic AMP accumulation was explored. Responses to the highly arrestin-recruiting agonists SNC80 and DADLE desensitized fully after extended exposure, whereas the novel partial agonists PN6047 and OPD00003 resisted desensitization. Bias factors were calculated for the agonist set and both PN6047 and OPD00003 were found to be significantly biased towards G protein-mediated cyclic AMP inhibition. In conclusion, this study reports, for the first time, a detailed characterization of signalling bias for a set of selective DOR agonists in cells over-expressing human DORs. The findings suggest that it is potentially possible to predict wanted and unwanted properties of agonists by determining post-receptor signalling profiles in vitro which will facilitate the discovery and development of novel therapeutics based on the DOR.
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Vanderah, Todd William. "The direct and modulatory antinociceptive actions of endogenous and exogenous opioid delta agonists." Diss., The University of Arizona, 1995. http://hdl.handle.net/10150/187190.
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Opioids are responsible for a number of effects but are employed primarily as analgesics. The discovery of endogenous opioids and multiple receptors have led to a better understanding of how analgesics function, and how both opioid receptors and endogenous ligands are regulated. The hypothesis of this dissertation states that levels of endogenous enkephalins are modulated by stress, inflammation and the endogenous peptide cholecystokinin (CCK) to alter the antinociceptive efficacy of μ and, possibly, δ opioids. Endogenous enkephalin release results in either direct antinociception or synergistically enhances the antinociceptive effects of the μ agonist morphine via δ receptors. This thesis will first detail how the administration of exogenous δ compounds can enhance the antinociceptive effects of a μ agonist. Exposure of mice to a cold-water swim-stress (CWSS) paradigm resulted in direct antinociception that was attenuated by opioid antagonists. Exposure to CWSS for a limited amount of time did not produce significant antinociception, but produced a marked enhancement of morphine antinociception. This enhancement was blocked by the administration of δ antagonists and (Leu⁵) enkephalin antisera. An antisense oligodeoxynucleotide was designed from the δ opioid receptor and administered to animals. Animals treated with the δ antisense and exposed to the CWSS paradigm showed a significant decrease in antinociception. Inflammation produced in the hind-paw of the mouse significantly enhanced the antinociceptive effects of morphine that was inhibited by δ antagonists and (Leu⁵) enkephalin antisera. The administration of a selective CCK(B) antagonist, L365,260 or CCK(B) antisense, enhances the antinociceptive potency of morphine. This enhancement is attenuated by δ antagonists, (Leu⁵) enkephalin antisera, as well as exhibits a two-way cross tolerance with δ agonists. L365,260 and an "enkephalinase" inhibitor, when coadministered, produced significant antinociception that was blocked by a δ antagonist and (Leu⁵) enkephalin antisera. Using polymerase chain reaction in search of a δ opioid receptor subtype, an orphan receptor was cloned and characterized as a member of the G protein-coupled receptor family. These data suggest that stress results in the release of (Leu⁵) enkephalin that enhances the antinociceptive effects of a μ-selective agonist morphine. Release of endogenous enkephalins may be regulated by the interactions of cholecystokinin at the CCK(B)receptor. Such information may lead to appropriate use of opiates in conjunction with CCK antagonists for the management of appropriate pain states.
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Huang, Wei [Verfasser]. "Direct functional effects of opioid agonists on the isolated perfused rat heart / Wei Huang." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1037725727/34.
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Omoniyi, Abimbola T. "The cardiovascular actions of mu and kappa opioid agonists in vivo and in vitro." Thesis, University of Surrey, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267362.
Full textBooks on the topic "Opioid agonists"
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Freye, Enno. Opioid Agonists, Antagonists and Mixed Narcotic Analgesics. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71854-0.
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Freye, Enno. Opioid agonists, antagonists and mixed narcotics analgesics: Theoretical background and considerations for practical use. Berlin: Springer, 1987.
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Opioid Agonists, Antagonists and Mixed Narcotic Analgesics. Springer Verlag, 1987.
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Krondahl, Eva. Transport & Metabolism of Opioid Tetrapeptide Agonists With a Focus on Oral & Respiratory Delivery. Uppsala Universitet, 2001.
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Otis, James A. D. Non-Opioid Pharmacotherapies for Chronic Pain (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190265366.003.0015.
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The objective of chapter 15 is to describe analgesic approaches to chronic pain, excluding opioids. As such, it emphasizes, first, the available pharmacotherapies; and then procedures. The pharmacotherapies divide into analgesics, such as non-steroidal anti-inflammatory drugs (NSAIDs); adjuvant analgesics, such as tricyclic antidepressants and anticonvulsants; oral anesthetic agents (cardiotropics); adrenergic agonists; topical agents such as capsaicin and local anesthetic solutions and ointments; and muscle relaxants such as cyclobenzaprine, tizanidine, and baclofen. Interventions include many best administered by anesthesiologists such as infusions of anesthetic agents; trigger point injections; local and regional blockade, spinal injections including corticosteroids; and electrical spinal cord stimulation. A text box is provided with additional resources.
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Opioid Agonists, Antagonists and Mixed Narcotic Analgesics: Theoretical Background and Considerations for Practical Use. Springer, 2012.
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Opioid Agonists, Antagonists and Mixed Narcotic Analgesics: Theoretical Background and Considerations for Practical Use. Springer, 1987.
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Gevirtz, Clifford M., Elizabeth Frost, and Alan D. Kaye. Ultrarapid Opiate Detoxification. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190495756.003.0035.
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Extended opioid use results in physical dependence and neural adaptation. Opioid dependence treatment can be carried out with opioid receptor agonists, partial agonists, and antagonists. Conventional treatments have low success rates. Methadone and buprenorphine treatments involve substituting long-duration agonists for the opiate of abuse, essentially substituting one opiate for another. Rapid opiate detoxification is a 3-day process involving large amounts of an opiate antagonist. Both treatments have associated problems. Ultrarapid opiate detoxification (UROD) anesthetizes a patient and precipitates withdrawal while unconscious. It shortens withdrawal, avoiding much of the subjective withdrawal discomfort. Clonidine is critical to reduce catecholamine levels and mitigate central nervous system hyperarousal in acute withdrawal. A UROD advantage is that the withdrawal period is markedly shortened to 8 hours or less versus up to several months for conventional treatments. The patient is anesthetized during the acute withdrawal period and does not experience the unpleasant consequences of acute detoxification.
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Patel, Mayur B., and Pratik P. Pandharipande. Analgesics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0043.
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Analgesia is a critical component of intensive care unit (ICU) care. Accordingly, understanding the mechanism, physiological consequences, and assessment of pain is important when caring for the ICU patient. Non-pharmacological approaches should be attempted before supplementing analgesia with pharmacological agents. Pharmacologically-based therapies are divided into regional and systemic therapies. Regional analgesic therapies target specific areas of the body while limiting the systemic effects of intravenous analgesics, but at the risk of invasiveness, local anaesthetic toxicity, and infection of in-dwelling catheters. Systemic analgesic therapy is comprised of two main categories—non-opioids and opioids. Typically, non-opioid analgesics are used as adjunctive therapies and consist of agents such as non-steroidal anti-inflammatory drugs, gabapentinoids, ketamine, or α2 agonists. Opioid analgesia in the ICU is commonly infusion-based using fentanyl, hydromorphone, morphine, or recently, remifentanil.
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Sabbe, Marc. Toxicologic, Pharmacodynamic and Kinetic Studies Following Spinal Administration of U Opioid, B Gaba and A2 Adrenergic Agonists. Coronet Books Inc, 1997.
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Morgan, Michael M., MacDonald J. Christie, Thomas Steckler, Ben J. Harrison, Christos Pantelis, Christof Baltes, Thomas Mueggler, et al. "Mu-Opioid Agonists." In Encyclopedia of Psychopharmacology, 809. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1141.
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Mucha, Ronald F., Michael M. Morgan, MacDonald J. Christie, Paolo Nencini, Michele Stanislaw Milella, Theodora Duka, Michele S. Milella, et al. "Kappa-Opioid Agonists." In Encyclopedia of Psychopharmacology, 673. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1142.
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Casy, Alan F., and Robert T. Parfitt. "Antagonists, Dualists, and Kappa Agonists." In Opioid Analgesics, 405–44. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4899-0585-7_12.
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Kumar, Shathish, and Soumya Itagi. "Opioid Agonists and Antagonists." In Introduction to Basics of Pharmacology and Toxicology, 213–35. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6009-9_12.
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Misery, Laurent. "Opioid Receptor Antagonists or Agonists." In Pruritus, 297–99. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-322-8_46.
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Bidlack, Jean M., and Brian I. Knapp. "Mixed Mu/Kappa Opioid Agonists." In ACS Symposium Series, 257–72. Washington, DC: American Chemical Society, 2013. http://dx.doi.org/10.1021/bk-2013-1131.ch014.
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Misery, Laurent. "Opioid Receptor Antagonists or Agonists." In Pruritus, 389–92. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33142-3_50.
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Freye, Enno. "New Concepts in Opioid Activity." In Opioid Agonists, Antagonists and Mixed Narcotic Analgesics, 64–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71854-0_5.
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Freye, Enno. "The Use of Opioids During Anaesthesia and Their Importance in Clinical Application." In Opioid Agonists, Antagonists and Mixed Narcotic Analgesics, 1–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71854-0_1.
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Freye, Enno. "The Mode of Action of Opioids." In Opioid Agonists, Antagonists and Mixed Narcotic Analgesics, 15–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71854-0_2.
Full textConference papers on the topic "Opioid agonists"
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Pineda, Joseba, Patricia Pablos, and Aitziber Mendiguren. "Effect of neuronal nitric oxide synthase inhibitors and antioxidants on the development of tolerance by different opioid agonists in the rat locus coeruleus." In MOL2NET, International Conference on Multidisciplinary Sciences. Basel, Switzerland: MDPI, 2015. http://dx.doi.org/10.3390/mol2net-1-b022.
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Bravo Sánchez, Marta, Mario De Matteis, and Emilio Ignacio Sánchez Díaz. "Mania con síntomas psicóticos inducida por abuso de tramadol. A propósito de un caso clínico." In 22° Congreso de la Sociedad Española de Patología Dual (SEPD) 2020. SEPD, 2020. http://dx.doi.org/10.17579/sepd2020p068.
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Introducción/Objetivo: El tramadol es un agonista puro, no selectivo sobre los receptores opioides µ,δ y κ, con mayor afinidad por los receptores µ. Actá también inhibiendo la recaptación de noradrenalina, así como la intensificación de liberación de serotonina. Se ha descrito clínica hipomaniaca en pacientes con trastorno bipolar. El objetivo es poner de manifiesto la relación de consumo de tramadol y sintomatología maniforme y psicótica a pesar de la no existencia de alteración del estado de ánimo previa al consumo. Material y métodos:A propósito de un caso clínico. Varon de 65 años, con antecedentes personales de trastorno por uso de alcohol y tabaco. Adenocarcinoma de pulmón hace 10 años, con lobectomía total y posterior tratamiento con quimioterapia. Síndrome de Leriche que le genera importante dolor en miembros inferiores por lo que su MAP le prescribe tramadol/paracetamol 37,5/325 mg. El paciente toma hasta 6-7 comprimidos al día, comenzando a los 10 días con disminución de la necesidad del sueño, irritabilidad, verborrea, necesidad imperiosa de escribir e interpretaciones delirantes de perjuicio. Es traído al servicio de urgencias donde ingresa con el diagnostico: alteraciones conductuales y sintomatología maniforme a estudio. Ingresa en Medicina Interna y es seguido por el equipo de psiquiatría de enlace. Tras la realización de pruebas complementarias (AS: etanol<10 en urgencias. TSH y vitaminas en rango), TAC/RMN sin alteraciones (descartando metástasis cerebrales). MMSE: 22/25. MOCA 24/30. Tras la retirada del tramadol y la toma de cloracepato dipotasico hasta 30mg+ risperidona hasta 3 mg, la sintomatología maniforme con síntomas psicóticos fue difuminándose hasta desaparecer en diez días. Actual seguimiento en consulta externa, tras la retirada del tramadol asintomático. Conclusiones Además de la relación receptorial del tramadol con el sistema serotoninérgico, este caso sugiere la importante del sistema opioide endógeno en la modulación de otros neurotrasmisores clásicamente relacionados con el sistema afectivo.
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Giri, Aswini Kumar, Qiong Xie, Christopher R. Apostol, David Rankin, Peg Davis, Eva Varga, Frank Porreca, Josephine Lai, and Victor J. Hruby. "Design, Synthesis and Biological Evaluation of Multivalent Ligands with μ/δ Opioid Agonist (μ-preferring) /NK-1 Antagonist Activities." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.048.
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Drieu la Rochelle, Armand, Karel Guillemyn, Maria Dumitrascuta, Simon Gonzalez, Charlotte Martin, Valérie Utard, Raphaëlle Quillet, et al. "A Bifunctional Biased Mu Opioid Agonist - Neuropeptide Ff Receptor Antagonist as Analgesic with Improved Acute and Chronic Side Effects." In 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.276.
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Turnaturi, Rita, Carmela Parenti, Girolamo Calò, Santina Chiechio, Agostino Marrazzo, and Lorella Pasquinucci. "From LP2 to 2S-LP2: discovery of a biased dual-target mu/delta opioid receptor agonist for pain management." In 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-07383.
Full textReports on the topic "Opioid agonists"
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Dosaka-Akita, Kumi, Frank C. Tortella, John W. Holaday, and Joseph B. Long. The Kappa Opioid Agonist U-50, 488H Antagonizes Respiratory Effects of Mu Opioid Receptor Agonists in Conscious Rats. Fort Belvoir, VA: Defense Technical Information Center, January 1993. http://dx.doi.org/10.21236/ada263043.
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Schwieger, Alexandra, Kaelee Shrewsbury, and Paul Shaver. Dexmedetomidine vs Fentanyl in Attenuating the Sympathetic Surge During Endotracheal Intubation: A Scoping Review. University of Tennessee Health Science Center, July 2021. http://dx.doi.org/10.21007/con.dnp.2021.0007.
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Purpose/Background Direct laryngoscopy and endotracheal intubation after induction of anesthesia can cause a reflex sympathetic surge of catecholamines caused by airway stimulation. This may cause hypertension, tachycardia, and arrhythmias. This reflex can be detrimental in patients with poor cardiac reserve and can be poorly tolerated and lead to adverse events such as myocardial ischemia. Fentanyl, a potent opioid, with a rapid onset and short duration of action is given during induction to block the sympathetic response. With a rise in the opioid crisis and finding ways to change the practice in medicine to use less opioids, dexmedetomidine, an alpha 2 adrenergic agonist, can decrease the release of norepinephrine, has analgesic properties, and can lower the heart rate. Methods In this scoping review, studies published between 2009 and 2021 that compared fentanyl and dexmedetomidine during general anesthesia induction and endotracheal intubation of surgical patients over the age of 18 were included. Full text, peer-reviewed studies in English were included with no limit on country of study. The outcomes included post-operative reviews of decrease in pain medication usage and hemodynamic stability. Studies that were included focused on hemodynamic variables such as systolic blood pressure, diastolic blood pressure, mean arterial pressure, heart rate, and use of opioids post-surgery. Result Of 2,114 results from our search, 10 articles were selected based on multiple eligibility criteria of age greater than 18, patients undergoing endotracheal intubation after induction of general anesthesia, and required either a dose of dexmedetomidine or fentanyl to be given prior to intubation. Dexmedetomidine was shown to effectively attenuate the sympathetic surge during intubation over fentanyl. Dexmedetomidine showed a greater reduction in heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure than fentanyl, causing better hemodynamic stability in patients undergoing elective surgery.Implications for Nursing Practice Findings during this scoping review indicate that dexmedetomidine is a safe and effective alternative to fentanyl during induction of general anesthesia and endotracheal intubation in attenuating the hemodynamic response. It is also a safe choice for opioid-free anesthesia.
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Halker Singh, Rashmi B., Juliana H. VanderPluym, Allison S. Morrow, Meritxell Urtecho, Tarek Nayfeh, Victor D. Torres Roldan, Magdoleen H. Farah, et al. Acute Treatments for Episodic Migraine. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer239.
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Objectives. To evaluate the effectiveness and comparative effectiveness of pharmacologic and nonpharmacologic therapies for the acute treatment of episodic migraine in adults. Data sources. MEDLINE®, Embase®, Cochrane Central Registrar of Controlled Trials, Cochrane Database of Systematic Reviews, PsycINFO®, Scopus, and various grey literature sources from database inception to July 24, 2020. Comparative effectiveness evidence about triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) was extracted from existing systematic reviews. Review methods. We included randomized controlled trials (RCTs) and comparative observational studies that enrolled adults who received an intervention to acutely treat episodic migraine. Pairs of independent reviewers selected and appraised studies. Results. Data on triptans were derived from 186 RCTs summarized in nine systematic reviews (101,276 patients; most studied was sumatriptan, followed by zolmitriptan, eletriptan, naratriptan, almotriptan, rizatriptan, and frovatriptan). Compared with placebo, triptans resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (high strength of the body of evidence [SOE]). Data on NSAIDs were derived from five systematic reviews (13,214 patients; most studied was ibuprofen, followed by diclofenac and ketorolac). Compared with placebo, NSAIDs probably resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (moderate SOE). For other interventions, we included 135 RCTs and 6 comparative observational studies (37,653 patients). Compared with placebo, antiemetics (low SOE), dihydroergotamine (moderate to high SOE), ergotamine plus caffeine (moderate SOE), and acetaminophen (moderate SOE) reduced acute pain. Opioids were evaluated in 15 studies (2,208 patients).Butorphanol, meperidine, morphine, hydromorphone, and tramadol in combination with acetaminophen may reduce pain at 2 hours and 1 day, compared with placebo (low SOE). Some opioids may be less effective than some antiemetics or dexamethasone (low SOE). No studies evaluated instruments for predicting risk of opioid misuse, opioid use disorder, or overdose, or evaluated risk mitigation strategies to be used when prescribing opioids for the acute treatment of episodic migraine. Calcitonin gene-related peptide (CGRP) receptor antagonists improved headache relief at 2 hours and increased the likelihood of being headache-free at 2 hours, at 1 day, and at 1 week (low to high SOE). Lasmiditan (the first approved 5-HT1F receptor agonist) restored function at 2 hours and resolved pain at 2 hours, 1 day, and 1 week (moderate to high SOE). Sparse and low SOE suggested possible effectiveness of dexamethasone, dipyrone, magnesium sulfate, and octreotide. Compared with placebo, several nonpharmacologic treatments may improve various measures of pain, including remote electrical neuromodulation (moderate SOE), magnetic stimulation (low SOE), acupuncture (low SOE), chamomile oil (low SOE), external trigeminal nerve stimulation (low SOE), and eye movement desensitization re-processing (low SOE). However, these interventions, including the noninvasive neuromodulation devices, have been evaluated only by single or very few trials. Conclusions. A number of acute treatments for episodic migraine exist with varying degrees of evidence for effectiveness and harms. Use of triptans, NSAIDs, antiemetics, dihydroergotamine, CGRP antagonists, and lasmiditan is associated with improved pain and function. The evidence base for many other interventions for acute treatment, including opioids, remains limited.