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Journal articles on the topic 'Opiate effects on humans'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

PFEIFFER, A., V. BRANTL, A. HERZ, and H. M. EMRICH. "Kappa-opiate receptors mediate psychotomimetic effects in humans." Acta Endocrinologica 113, no. 1_Suppl (August 1986): S157—S158. http://dx.doi.org/10.1530/acta.0.111s157.

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2

Specker, S., Winai Wananukul, Dorothy Hatsukami, Kim Nolin, Lyn Hooke, Mary Jeanne Kreek, and Paul R. Pentel. "Effects of dynorphin A(1-13) on opiate withdrawal in humans." Psychopharmacology 137, no. 4 (June 17, 1998): 326–32. http://dx.doi.org/10.1007/s002130050626.

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3

Kabalak, Ayla A., Oytun O. Senel, and Nermin Gogus. "The Effects of Transcranial Electrical Stimulation on Opiate-Induced Analgesia in Rats." Pain Research and Management 9, no. 4 (2004): 203–6. http://dx.doi.org/10.1155/2004/416016.

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BACKGROUND AND OBJECTIVES:Recent experiments have shown that transcranial electrical stimulation significantly increases the potency and duration of the analgesic effects of opioids in humans and rats. In the present study, the influence of transcranial electrical stimulation (TCES) on the analgesic effect of remifentanil hydrochloride (HCl) in rats was determined.METHODS:Experiments were performed on 80 albino male Wistar rats. Rats were randomly assigned to four groups: remifentanil HCl, remifentanil HCl and TCES, TCES, and control (n=20/group). Remifentanil HCl was injected on the 55th minute. Analgesia was assessed using the wet tail-flick latency test.RESULTS:In the remifentanil HCl group, analgesia (10.85±1.04 s) was reached at the fifth minute, and the analgesia was high for the first 10 min. In the remifentanil HCl and TCES group, the latency time peaked (16.60±1.19 s) at the fifth minute. This peak was 150% higher than that for the remifentanil HCl group, and 251% higher than the control or TCES groups. Analgesia in the remifentanil HCl and TCES group was sustained for 20 min at a statistically higher rate than the other treatment groups (P<0.001).CONCLUSIONS:TCES markedly increased the duration and analgesic potency of remifentanil HCl in rats. This effect appeared to be related to the release of enkephalins from brain structures, thus enhancing opioid analgesia.

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4

Yaksh, Tony L., and Xiao-Ying Hua. "Spinal Tolerance and Dependence: Some Observations on the Role of SpinalN-Methyl-D-Aspartate Receptors and Phosphorylation in the Loss of Opioid Analgesic Responses." Pain Research and Management 5, no. 1 (2000): 33–39. http://dx.doi.org/10.1155/2000/514020.

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The continuous delivery of opiates can lead to a reduction in analgesic effects. In humans, as in other animals, some component of this change in sensitivity seems likely to have a strong pharmacodynamic component. Such loss of effect, deemed to be tolerance in the present article, can be readily demonstrated in animals with repeated bolus and continuous intrathecal infusion of mu and delta opioids and alpha-2 adrenergic agonists. Research has shown that this loss of effect can be diminished by concurrent treatment withN-methyl-D-aspartate (NMDA) receptor antagonists and by the suppression of the activity of spinal protein kinase C (PKC). This suggests in part the probable role of PKC-mediated phosphorylation in the right shift in the dose-effect curves observed with continuous opiate or adrenergic exposure. Importantly, this right shift is seen to occur in parallel with an increase in the phosphorylating activity in the dorsal horn and in the expression of several PKC isozymes. The target of this phosphorylation is not certain. Phosphorylation of the NMDA receptor enhances its functionality, while phosphorylation of the opioid receptor or associated channels seems to diminish their activity or to enhance internalization. While the focus is on several specific components, the accumulating data emphasize the biological complexity of these changes in spinal drug reactivity.

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5

HU, Huankai, Seiji MIYAUCHI, Christy C. BRIDGES, Sylvia B. SMITH, and Vadivel GANAPATHY. "Identification of a novel Na+- and Cl−-coupled transport system for endogenous opioid peptides in retinal pigment epithelium and induction of the transport system by HIV-1 Tat." Biochemical Journal 375, no. 1 (October 1, 2003): 17–22. http://dx.doi.org/10.1042/bj20031059.

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The endogenous opioid peptides enkephalins, dynorphins and endorphins consist of five or more amino acids. These peptides participate in a multitude of biological functions in mammalian cells by interacting with different subtypes of opiate receptors located on the plasma membrane and in the nucleus. Here we report on the identification of a new peptide transport system in the human retinal pigment epithelial (RPE) cells that transports a variety of endogenous opioid peptides with high affinity. We identified this novel, hitherto unrecognized, transport system when we were analysing the differential effects of Tat, the transacting factor encoded by HIV-1, on various transport processes in RPE cells. This transport system is markedly induced by Tat. This opioid transport system is energized by transmembrane Na+ and Cl− gradients and is distinct from any of the previously identified transport systems for opioid peptides in mammalian cells. Free amino acids, dipeptides, tripeptides and non-peptide opiate receptor antagonists are excluded by this newly identified transport system. The affinities of endogenous opioid peptides for this system are in the range of 0.4–40 μM. The identification of the high-affinity Na+- and Cl−-coupled transport system in mammalian cells that is specific for endogenous opioid peptides and is induced by HIV-1 Tat is of significance not only to the biology of opioid peptides but also to the pathology of HIV-1 infection in humans.

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6

Tabibi, Zahra, David C. Schwebel, Abolfazl Mohammadzadeh Moghaddam, Javad Salehi Fadardi, and Sara Mirzaei Feizabadi. "Differential effects of stimulant versus opiate drugs on driving performance." Accident Analysis & Prevention 150 (February 2021): 105885. http://dx.doi.org/10.1016/j.aap.2020.105885.

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7

Murphy, D. B., J. A. Sutton, L. F. Prescott, and M. B. Murphy. "Opioid-induced Delay in Gastric Emptying." Anesthesiology 87, no. 4 (October 1, 1997): 765–70. http://dx.doi.org/10.1097/00000542-199710000-00008.

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Background Opioids delay gastric emptying, which in turn may increase the risk of vomiting and pulmonary aspiration. Naloxone reverses this opiate action on gastric emptying, but it is not known whether this effect in humans is mediated by central or peripheral opiate antagonism. The importance of peripheral opioid receptor antagonism in modulating opioid-induced delay in gastric emptying was evaluated using methylnaltrexone, a quaternary derivative of the opiate antagonist naltrexone, which does not cross the blood-brain barrier. Methods In a randomized, double-blind, crossover placebo-controlled study, 11 healthy volunteers were given either placebo (saline), 0.09 mg/kg morphine, or 0.09 mg/kg morphine plus 0.3 mg/kg methylnaltrexone on three separate occasions before ingesting 500 ml deionized water. The rate of gastric emptying was measured by two methods: a noninvasive epigastric bioimpedance technique and the acetaminophen absorption test. Results The epigastric bioimpedance technique was sufficiently sensitive to detect opioid-induced changes in the rate of gastric emptying. The mean +/- SD time taken for the gastric volume to decrease to 50% (t0.5) after placebo was 5.5 +/- 2.1 min. Morphine prolonged gastric emptying to (t0.5) of 21 +/- 9.0 min (P < 0.03). Methylnaltrexone given concomitantly with morphine reversed the morphine-induced delay in gastric emptying to a t0.5 of 7.4 +/- 3.0 (P < 0.04). Maximum concentrations and area under the concentration curve from 0 to 90 min of serum acetaminophen concentrations after morphine were significantly different from placebo and morphine administered concomitantly with methylnaltrexone (P < 0.05). No difference in maximum concentration or area under the concentration curve from 0 to 90 min was noted between placebo and methylnaltrexone coadministered with morphine. Conclusions The attenuation of morphine-induced delay in gastric emptying by methylnaltrexone suggests that the opioid effect is mediated outside the central nervous system. Methylnaltrexone may have the potential to decrease the side effects of opioid medications, which are mediated peripherally, while maintaining the central analgesia effect of the opioid.

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8

Drago, F., G. Panissidi, F. Bellomio, A. Dal Belle, E. Aguglia, and G. Gorgone. "EFFECTS OF OPIATES AND OPIOIDS ON INTRAOCULAR PRESSURE OF RABBITS AND HUMANS." Clinical and Experimental Pharmacology and Physiology 12, no. 2 (April 1985): 107–13. http://dx.doi.org/10.1111/j.1440-1681.1985.tb02312.x.

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9

Dahan, Albert MD, Elise Sarton, Luc Teppema, and Cees Olievier. "Sex-related Differences in the Influence of Morphine on Ventilatory Control in Humans." Anesthesiology 88, no. 4 (April 1, 1998): 903–13. http://dx.doi.org/10.1097/00000542-199804000-00009.

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Background Opiate agonists have different analgesic effects in male and female patients. The authors describe the influence of sex on the respiratory pharmacology of the mu-receptor agonist morphine. Methods The study was placebo-controlled, double-blind, and randomized. Steady-state ventilatory responses to carbon dioxide and responses to a step into hypoxia (duration, 3 min; oxygen saturation, approximately 82%; end-tidal carbon dioxide tension, 45 mmHg) were obtained before and during intravenous morphine or placebo administration (bolus dose of 100 microg/kg, followed by a continuous infusion of 30 microg x kg(-1) x h(-1)) in 12 men and 12 women. Results In women, morphine reduced the slope of the ventilatory response to carbon dioxide from 1.8 +/- 0.9 to 1.3 +/- 0.7 l x min(-1) x mmHg(-1) (mean +/- SD; P < 0.05), whereas in men there was no significant effect (control = 2.0 +/- 0.4 vs. morphine = 1.8 +/- 0.4 l x min(-1) x mmHg(-1)). Morphine had no effect on the apneic threshold in women (control = 33.8 +/- 3.8 vs. morphine = 35.3 +/- 5.3 mmHg), but caused an increase in men from 34.5 +/- 2.3 to 38.3 +/- 3 mmHg, P < 0.05). Morphine decreased hypoxic sensitivity in women from 1.0 +/- 0.5 l x min(-1) x %(-1) to 0.5 +/- 0.4 l x min(-1) x %(-1) (P < 0.05) but did not cause a decrease in men (control = 1.0 +/- 0.5 l x min(-1) x %(-1) vs. morphine = 0.9 +/- 0.5 l x min(-1) x %(-1)). Weight, lean body mass, body surface area, and calculated fat mass differed between the sexes, but their inclusion in the analysis as a covariate revealed no influence on the differences between men and women in morphine-induced changes. Conclusions In both sexes, morphine affects ventilatory control. However, we observed quantitative and qualitative differences between men and women in the way morphine affected the ventilatory responses to carbon dioxide and oxygen. Possible mechanisms for the observed sex differences in the respiratory pharmacology of morphine are discussed.

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10

Sallam, Hanaa S., and Jiande D. Z. Chen. "The Prokinetic Face of Ghrelin." International Journal of Peptides 2010 (February 10, 2010): 1–11. http://dx.doi.org/10.1155/2010/493614.

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This review evaluated published data regarding the effects of ghrelin on GI motility using the PubMed database for English articles from 1999 to September 2009. Our strategy was to combine all available information from previous literature, in order to provide a complete structured review on the prokinetic properties of exogenous ghrelin and its potential use for treatment of various GI dysmotility ailments. We classified the literature into two major groups, depending on whether studies were done in health or in disease. We sub-classified the studies into stomach, small intestinal and colon studies, and broke them down further into studies done in vitro, in vivo (animals) and in humans. Further more, the reviewed studies were presented in a chronological order to guide the readers across the scientific advances in the field. The review shows evidences that ghrelin and its (receptor) agonists possess a strong prokinetic potential to serve in the treatment of diabetic, neurogenic or idiopathic gastroparesis and possibly, chemotherapy-associated dyspepsia, postoperative, septic or post-burn ileus, opiate-induced bowel dysfunction and chronic idiopathic constipation. Further research is necessary to close the gap in knowledge about the effect of ghrelin on the human intestines in health and disease.

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11

Camilleri, M., J. R. Malagelada, V. Stanghellini, A. R. Zinsmeister, P. C. Kao, and C. H. Li. "Dose-related effects of synthetic human beta-endorphin and naloxone on fed gastrointestinal motility." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 1 (July 1, 1986): G147—G154. http://dx.doi.org/10.1152/ajpgi.1986.251.1.g147.

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In humans, plasma beta-endorphin levels rise during application of acute stressful stimuli (vertigo, cold pain, and transcutaneous electrical stimulation) that induce gut motor disturbances. Whereas it is possible that circulating beta-endorphin participates in the mediation of these central effects on gut motility, its role cannot be established solely on the basis of changes in plasma levels. Therefore, we designed the present study to investigate 1) the dose-related effects of intravenous synthetic human beta-endorphin and naloxone on gastrointestinal pressure activity in fed healthy individuals; and 2) the interactions of the opiate agonist and antagonist. Infusion of beta-endorphin increased pyloric phasic pressure activity (P less than 0.001) and induced intestinal bursts of rhythmic activity (P less than 0.05) which interrupted normal fed motility. These effects were dose related, with the pyloric dose-response profile being essentially linear. The effects in the proximal intestine were obtained with doses of beta-endorphin at 250 ng X kg-1 X min-1 or greater. In the antrum, there was an overall reduction in phasic pressure activity (P less than 0.02), which was predominantly an effect of the highest dose of beta-endorphin infused (2,500 ng X kg-1 X min-1). Naloxone by itself had no significant effect on fed upper gut motility. However, naloxone significantly inhibited the effect of the lower doses of beta-endorphin on the pylorus. In addition, naloxone significantly reduced the probability of beta-endorphin, triggering intestinal bursts of rhythmic activity. These data suggest that beta-endorphin may play a humoral role in the stimulation of fed pyloric contraction at physiological levels.(ABSTRACT TRUNCATED AT 250 WORDS)

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12

Fischman, M. W., and R. W. Foltin. "Stimulant-opiate interactions in humans." European Neuropsychopharmacology 6 (June 1996): 229. http://dx.doi.org/10.1016/0924-977x(96)88381-7.

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13

Souied, Osama, Hassan Baydoun, Zahraa Ghandour, and Neville Mobarakai. "Levamisole-Contaminated Cocaine: An Emergent Cause of Vasculitis and Skin Necrosis." Case Reports in Medicine 2014 (2014): 1–3. http://dx.doi.org/10.1155/2014/434717.

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The prevalence of cocaine adulterated with levamisole-induced vasculitis is increasing and physicians should be aware of this unique entity. There have been many reports of cutaneous vasculitis syndrome caused by cocaine which is contaminated with levamisole. Levamisole was used as an antihelminth drug and later was rescinded from use in humans due to adverse effects. Through this paper, we will report a 39-year-old crack cocaine user who presented with purpuric rash and skin necrosis of his ear lobes. Levamisole-induced vasculitis syndrome was suspected. A urine toxicology screen was positive for cocaine, opiates, and marijuana. Blood work revealed positive titres of ANA and p-ANCA, as well as anti-cardiolipin antibody. Biopsy taken from the left ear showed focal acute inflammation, chronic inflammation with thrombus formation, and extravasated blood cells. Treatment was primarily supportive with wound care.

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Shimizu, Mikiko, Michael Tropak, Roberto J. Diaz, Fumiaki Suto, Harinee Surendra, Elena Kuzmin, Jing Li, et al. "Transient limb ischaemia remotely preconditions through a humoral mechanism acting directly on the myocardium: evidence suggesting cross-species protection." Clinical Science 117, no. 5 (August 3, 2009): 191–200. http://dx.doi.org/10.1042/cs20080523.

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rIPC (remote ischaemic preconditioning) is a phenomenon whereby short periods of ischaemia and reperfusion of a tissue or organ (e.g. mesentery, kidney) can protect a distant tissue or organ (e.g. heart) against subsequent, potentially lethal, ischaemia. We, and others, have shown that transient limb ischaemia can provide potent myocardial protection experimentally and clinically during cardiac surgery. Nonetheless, our understanding of the signal transduction from remote stimulus to local effect remains incomplete. The aim of the present study was to define the humoral nature of rIPC effector(s) from limb ischaemia and to study their local effects in isolated heart and cardiomyocyte models. Using a Langendorff preparation, we show that infarct size after coronary artery ligation and reperfusion was substantially reduced by rIPC in vivo, this stimulus up-regulating the MAPKs (mitogen-activating protein kinases) p42/p44, and inducing PKCε (protein kinase Cε) subcellular redistribution. Pre-treatment with the plasma and dialysate of plasma (obtained using 15 kDa cut-off dialysis membrane) from donor rabbits subjected to rIPC similarly protected against infarction. The effectiveness of the rIPC dialysate was abrogated by passage through a C18 hydrophobic column, but eluate from this column provided the same level of protection. The dialysate of rIPC plasma from rabbits and humans was also tested in an isolated fresh cardiomyocyte model of simulated ischaemia and reperfusion. Necrosis in cardiomyocytes treated with rIPC dialysate was substantially reduced compared with control, and was similar to cells pre-treated by ‘classical’ preconditioning. This effect, by rabbit rIPC dialysate, was blocked by pre-treatment with the opiate receptor blocker naloxone. In conclusion, in vivo transient limb ischaemia releases a low-molecular-mass (<15 kDa) hydrophobic circulating factor(s) which induce(s) a potent protection against myocardial ischaemia/reperfusion injury in Langendorff-perfused hearts and isolated cardiomyocytes in the same species. This cardioprotection is transferable across species, independent of local neurogenic activity, and requires opioid receptor activation.

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Salmanzadeh, Hamed, S. Mohammad Ahmadi-Soleimani, Maryam Azadi, Robert F. Halliwell, and Hossein Azizi. "Adolescent Substance Abuse, Transgenerational Consequences and Epigenetics." Current Neuropharmacology 19, no. 9 (September 14, 2021): 1560–69. http://dx.doi.org/10.2174/1570159x19666210303121519.

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Adolescence is the transitional period between childhood and adulthood and a critical period in brain development. Adolescence in humans is also associated with increased expression of risk-taking behaviors. Epidemiological and clinical studies, for example, show a surge of drug abuse and raise the hypothesis that the adolescent brain undergoes critical changes resulting in diminished control. Determining how substance abuse during this critical period might cause longterm neurobiological changes in cognition and behavior is therefore critically important. The present work aims to provide an evaluation of the transgenerational and multi-generational phenotypes derived from parent animals exposed to drugs of abuse only during their adolescence. Specifically, we will consider changes found following the administration of cannabinoids, nicotine, alcohol and opiates. In addition, epigenetic modifications of the genome following drug exposure will be discussed as emerging evidence of the underlying adverse transgenerational effects. Notwithstanding, much of the new data discussed here is from animal models, indicating that future clinical studies are much needed to better understand the neurobiological consequences and mechanisms of drug actions on the human brains’ development and maturation.

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Lyu, Kaddour, Kopcho, Panzner, Shouman, Kim, Martinson, et al. "Human Immunodeficiency Virus (HIV) Infection and Use of Illicit Substances Promote Secretion of Semen Exosomes that Enhance Monocyte Adhesion and Induce Actin Reorganization and Chemotactic Migration." Cells 8, no. 9 (September 3, 2019): 1027. http://dx.doi.org/10.3390/cells8091027.

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Semen exosomes (SE) from HIV-uninfected (HIV−) individuals potently inhibit HIV infection in vitro. However, morphological changes in target cells in response to SE have not been characterized or have the effect of HIV infection or the use of illicit substances, specifically psychostimulants, on the function of SE been elucidated. The objective of this study was to evaluate the effect of HIV infection, psychostimulant use, and both together on SE-mediated regulation of monocyte function. SE were isolated from semen of HIV− and HIV-infected (HIV+) antiretroviral therapy (ART)-naive participants who reported either using or not using psychostimulants. The SE samples were thus designated as HIV−Drug−, HIV−Drug+, HIV+Drug−, and HIV+Drug+. U937 monocytes were treated with different SEs and analyzed for changes in transcriptome, morphometrics, actin reorganization, adhesion, and chemotaxis. HIV infection and/or use of psychostimulants had minimal effects on the physical characteristics of SE. However, different SEs had diverse effects on the messenger RNA signature of monocytes and rapidly induced monocyte adhesion and spreading. SE from HIV infected or psychostimulants users but not HIV−Drug− SE, stimulated actin reorganization, leading to the formation of filopodia-like structures and membrane ruffles containing F-actin and vinculin that in some cases were colocalized. All SE stimulated monocyte chemotaxis to HIV secretome and activated the secretion of matrix metalloproteinases, a phenotype exacerbated by HIV infection and psychostimulant use. SE-directed regulation of cellular morphometrics and chemotaxis depended on the donor clinical status because HIV infection and psychostimulant use altered SE function. Although our inclusion criteria specified the use of cocaine, humans are poly-drug and alcohol users and our study participants used psychostimulants, marijuana, opiates, and alcohol. Thus, it is possible that the effects observed in this study may be due to one of these other substances or due to an interaction between different substances.

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17

Frost, J. James, Helen S. Mayberg, Bernard Sadzot, Robert F. Dannals, John R. Lever, Hayden T. Ravert, Alan A. Wilson, Henry N. Wagner, and Jonathan M. Links. "Comparison of [11C]Diprenorphine and [11C]Carfentanil Binding to Opiate Receptors in Humans by Positron Emission Tomography." Journal of Cerebral Blood Flow & Metabolism 10, no. 4 (July 1990): 484–92. http://dx.doi.org/10.1038/jcbfm.1990.90.

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The kinetics and regional distribution of [11C]carfentanil, a μ-selective opiate receptor agonist, and [11C]diprenorphine, a nonselective opiate receptor antagonist, were compared using paired positron emission tomography studies in two normal volunteers. Kinetics of total radioactivity (counts/mCi/pixel) was greater for [11C]diprenorphine than [11C]carfentanil in all regions. [11C]Carfentanil binding (expressed as the total/nonspecific ratio) reached near equilibrium at ∼40 min, whereas [11C]diprenorphine showed a linear increase until ∼60 min. Kinetics of specific binding demonstrated significant dissociation of [11C]carfentanil from opiate receptors, whereas little dissociation of [11C]diprenorphine was observed during the 90-min scan session. Regional distributions of [11C]carfentanil and [11C]diprenorphine were qualitatively and quantitatively different: Relative to the thalamus (a region with known predominance of μ-receptors), [11C]diprenorphine displayed greater binding in the striatum and cingulate and frontal cortex compared to [11C]carfentanil, consistent with labeling of additional, non-μ sites by [11C]diprenorphine. We conclude from these studies that [11C]diprenorphine labels other opiate receptor subtypes in addition to the μ sites selectively labeled by [11C]carfentanil. The nonselective nature of diprenorphine potentially limits its usefulness in defining abnormalities of specific opiate receptor subtypes in various diseases. Development of selective tracers for the δ- and κ-opiate receptor sites, or alternatively use of unlabeled inhibitors to differentially displace μ, δ, and κ subtypes, will help offset these limitations.

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Given, Michael B., Gary E. Sander, and Thomas D. Giles. "Non-opiate and peripheral-opiate cardiovascular effects of morphine in conscious dogs." Life Sciences 38, no. 14 (April 1986): 1299–303. http://dx.doi.org/10.1016/0024-3205(86)90423-6.

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19

Miller, N. S., T. Swiney, and R. Barkin. "Effects of opiate prescription analgesic medication." European Psychiatry 23 (April 2008): S315. http://dx.doi.org/10.1016/j.eurpsy.2008.01.1083.

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Hall, F. S., X. F. Li, M. Goeb, S. Roff, H. Hoggatt, I. Sora, and G. R. Uhl. "Congenic C57BL/6 µ opiate receptor (MOR) knockout mice: baseline and opiate effects." Genes, Brain and Behavior 2, no. 2 (March 21, 2003): 114–21. http://dx.doi.org/10.1034/j.1601-183x.2003.00016.x.

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Masood, Ramoona, and Kianoush Khosravi-Darani. "Biopeptides in Milk: Opiate and Antithrombotic Effects." Mini-Reviews in Medicinal Chemistry 15, no. 10 (June 19, 2015): 872–77. http://dx.doi.org/10.2174/1389557515666150519104219.

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22

Giagnoni, G., L. Basilico, T. Rubino, L. Donin, and E. Gori. "Influence of ω-conotoxin on opiate effects." Pharmacological Research 22 (September 1990): 229. http://dx.doi.org/10.1016/s1043-6618(09)80263-6.

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Coyle, M. G. "Neurobehavioral effects of treatment for opiate withdrawal." Archives of Disease in Childhood - Fetal and Neonatal Edition 90, no. 1 (January 1, 2005): F73—F74. http://dx.doi.org/10.1136/adc.2003.046276.

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24

Drain, Cecil B. "The Opiate Crisis: Effects on Perianesthesia Nursing." Journal of PeriAnesthesia Nursing 35, no. 1 (February 2020): 99–100. http://dx.doi.org/10.1016/j.jopan.2019.12.001.

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Kim, Woong Mo. "Tramadol Induced Paradoxical Hyperalgesia." Pain Physician 1;16, no. 1;1 (January 14, 2013): 41–44. http://dx.doi.org/10.36076/ppj.2013/16/41.

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Opioids have been the mainstay analgesics for postoperative, cancerous, and chronic noncancerous pain. Common concerns regarding the use of opioids include the development of physical dependence and addiction. However, as a potential complication of opioid therapy, opioid-induced hyperalgesia (OIH) is often overlooked. That is, patients receiving opioids to control their pain may paradoxically become more sensitive to pain as a consequence of opioid therapy. OIH is a very important issue because it may complicate the clinical course of pain treatment and even worsen the suffering of patients receiving opioids because of the development of excruciating pain. Three OIH types were defined: 1) in the context of maintenance dosing and withdrawal, 2) at very high or escalating doses, and 3) at ultra-low doses. In the literature, most attention has been paid to the first 2 forms, and almost all cases of reported OIH have been ascribed to morphine administration. The third form of OIH has not been documented in humans, although it has been observed in animals. We present 2 cases of OIH resulting from administration of tramadol, which is a synthetic analogue of codeine and exhibits 10-fold less affinity for mu-opioid receptors, in patients suffering from chronic pain. The 2 cases presented herein imply the importance of recognizing OIH in patients medicated with tramadol if analgesic effects are lost in the context of dose titration, when generalized pain is reported without any evidence of disease exacerbation. While OIH associated with ultra-low dose opiates seems to be quite rare, if it is suspected, switching to other drugs and an appropriate treatment should be considered. Key words: Opioid-induced hyperalgesia, opioids, chronic pain, serotonin syndrome, tramadol, ketamine

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26

Nader, Karim, and Derek van der Kooy. "Clonidine antagonizes the aversive effects of opiate withdrawal and the rewarding effects of morphine only in opiate withdrawn rats." Behavioral Neuroscience 110, no. 2 (1996): 389–400. http://dx.doi.org/10.1037/0735-7044.110.2.389.

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27

Ong-Lam, M., and S. Basic. "Opiate sparing effects of cannabinoid in CRPS patients." Journal of Pain 10, no. 4 (April 2009): S57. http://dx.doi.org/10.1016/j.jpain.2009.01.300.

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GREEN, LYNETTE, and MICHAEL GOSSOP. "Effects of Information on the Opiate Withdrawal Syndrome." Addiction 83, no. 3 (March 1988): 305–9. http://dx.doi.org/10.1111/j.1360-0443.1988.tb00472.x.

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Molina, P. E., Vande C. Stowe, and J. Lu. "IMMUNOMODULATORY EFFECTS OF OPIATE ANALGESIA IN TRAUMA/HEMORRHAGE." Shock 19, Supplement (June 2003): 52. http://dx.doi.org/10.1097/00024382-200306001-00154.

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Kosten, Thomas R., and Brett S. Rayford. "Effects of ethnicity on low-dose opiate stabilization." Journal of Substance Abuse Treatment 12, no. 2 (March 1995): 111–16. http://dx.doi.org/10.1016/0740-5472(94)00069-4.

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Sufka, Kenneth J., Richard A. Hughes, Tammy M. McCormick, and James L. Borland. "Opiate effects of isolation stress in domestic fowl." Pharmacology Biochemistry and Behavior 49, no. 4 (December 1994): 1011–15. http://dx.doi.org/10.1016/0091-3057(94)90257-7.

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Zvartu, �. �., and V. S. Kovalenko. "Secondary reinforcing effects of opiate agonists in mice." Neuroscience and Behavioral Physiology 17, no. 5 (September 1987): 379–86. http://dx.doi.org/10.1007/bf01188726.

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Higgins, Stephen T., Maxine L. Stitzer, George E. Bigelow, and Ira A. Liebson. "Contingent methadone delivery: Effects on illicit-opiate use." Drug and Alcohol Dependence 17, no. 4 (July 1986): 311–22. http://dx.doi.org/10.1016/0376-8716(86)90080-3.

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Li, Yuai, Greg A. Looney, Bruce F. Kimler, and A. Hurwitz. "Opiate effects on 5-fluorouracil disposition in mice." Cancer Chemotherapy and Pharmacology 39, no. 3 (December 2, 1996): 273–77. http://dx.doi.org/10.1007/s002800050572.

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Price, Donald D., and David J. Mayer. "Evidence for endogenous opiate analgesic mechanisms triggered by somatosensory stimulation (including acupuncture) in humans." Pain Forum 4, no. 1 (March 1995): 40–43. http://dx.doi.org/10.1016/s1082-3174(11)80074-7.

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Jonassaint, Charles R., Jude C. Jonassaint, Allison Ashley-Koch, Soheir S. Adam, Marilyn J. Telen, and Laura M. De Castro. "The Effects of Chronic Opiates Pain Therapy in Sickle Cell Anemia." Blood 110, no. 11 (November 16, 2007): 3404. http://dx.doi.org/10.1182/blood.v110.11.3404.3404.

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Abstract Sickle cell disease (SCD) patients experience high rates of morbidity and early mortality. Hydroxyurea (HU) therapy is associated with decreased morbidity and mortality as well as improved patient health outcomes (Charache et al, 1995 and Steinberg et al, 2003). However, the effect of chronic opiate pain management on HU treatment outcomes is unknown. In the current study, we evaluated the effects of HU and chronic long acting opiate therapy-OxyContin, methadone, fentanyl and MS Contin-on the following laboratory parameters: white blood cell count (WBC), hemoglobin (Hb), and mean corpuscular volume (MCV). Changes in these variables are known to be linked with HU effects on morbidity and mortality in SCD. 142 homozygous sickle cell anemia patients (75 females and 67 males) from the outpatient clinic at Duke University Medical Center were included in this study. Clinical data were collected by patient interview as well as review of medical records after informed consent. Patients were classified in 4 groups based on report of chronic daily use of long acting opiates and/or HU (current therapy with HU) as follows: No HU or opiates (None); opiates only; HU only; and HU and opiates. ANOVAs were used to identify combined effects of opiate therapy, HU therapy and the 3 laboratory parameters. Overall, we found that patients on HU (n=76, 54%), had lower WBC and higher Hb and MCV than the no HU patients (n=66, 46%), with p<.01 for all associations, as could be expected. In contrast to the positive effects of HU, patients on opiates had higher WBC than non opiate patients (p<.01). Surprisingly, when adjusting for gender and age, opiate therapy appeared to moderate the effect of HU treatment on WBC (p=.05) and MCV (p=.04). Patients who were on HU and opiates concurrently exhibited 17% higher WBC and 6% lower MCV than patients who were on HU alone, suggesting that opiate therapy may be attenuating the positive effects of HU. The findings from the current study confirm that HU treatment is associated with better patient health indices, i.e. lower WBC, higher Hb and MCV. In contrast, chronic opiate pain management, often a concomitant therapy with HU, was associated with poorer patient laboratory indices, both with or without concurrent HU treatment. Overall, these data indicate that the chronic use of opiates may decrease the efficacy of HU treatment in this patient population. Further studies are needed to study the mechanism of drug interaction between opiate and HU in SCD patients. The previously suggested inhibitory effect of HU on the cytochrome P450 CYP3A, an important cytochrome in the metabolism of some opiates (Reardon et al, 2005), should be considered for future studies of drug-drug interaction in SCD. Figure Figure

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Pfeiffer, D. G., A. Pfeiffer, O. F. X. Almeida, and A. Herz. "Opiate suppression of LH secretion involves central receptors different from those mediating opiate effects on prolactin secretion." Journal of Endocrinology 114, no. 3 (September 1987): 469–76. http://dx.doi.org/10.1677/joe.0.1140469.

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ABSTRACT The involvement of μ- and κ-opiate receptors in the regulation of LH and prolactin secretion was investigated in long-term ovariectomized rats using selective opiate receptor agonists and antagonists. The μ-agonists morphine and [d-Ala2,MePhe4,Gly5-ol]-enkephalin (DAGO) suppressed LH levels in a dose-related manner. The benzomorphane (−)-5,9-dimethyl-2′-hydroxy-2-(tetrahydrofurfuryl)-6,7-benzomorphan tartrate (MR 2034; a designated κ-agonist) also suppressed LH levels, whereas another benzomorphane κ-agonist (−)-5,9-dimethyl-2′-hydroxy-2-(2-methoxy-propyl)-6,7-benzomorphan hydrobromide (MRZ 2549) had no effect on the levels of this hormone. Pretreatment with the highly selective μ-antagonist β-funaltrexamine (β-FNA), the fumarate methyl ester derivative of naltrexone, blocked the actions of both μ-agonists and MR 2034, indicating that opiate suppression of LH secretion is mediated by μ-receptors. This was further confirmed by in-vitro studies: the KCl-induced release of LHRH from perifused hypothalami obtained from ovariectomized rats was significantly reduced by DAGO but not by MRZ 2549. Prolactin secretion was stimulated in a dose-dependent manner by both μ- and κ-agonists. The stimulation caused by morphine and DAGO was antagonized by β-FNA, whereas that caused by the κ-agonists MR 2034 and MZR 2549 was resistant to blockade by β-FNA but not by naloxone (an antagonist which blocks all classes of opiate receptors when given in high doses). Thus prolactin secretion seems to be regulated by both μ- and κ-opiate receptors, whereas the effects on LH secretion seem to involve μ-receptors only. J. Endocr. (1987) 114, 469–476

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Mendelsohn, Mortimer L. "Antimutagenic effects in humans." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 267, no. 2 (June 1992): 257–64. http://dx.doi.org/10.1016/0027-5107(92)90070-i.

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Locke, Robin L., Linda L. Lagasse, Ronald Seifer, Barry M. Lester, Seetha Shankaran, Henrietta S. Bada, and Charles R. Bauer. "Effects of prenatal substance exposure on infant temperament vary by context." Development and Psychopathology 28, no. 2 (June 3, 2015): 309–26. http://dx.doi.org/10.1017/s0954579415000504.

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AbstractThis was a prospective longitudinal multisite study of the effects of prenatal cocaine and/or opiate exposure on temperament in 4-month-olds of the Maternal Lifestyle Study (N= 958: 366 cocaine exposed, 37 opiate exposed, 33 exposed to both drugs, 522 matched comparison). The study evaluated positivity and negativity during The Behavior Assessment of Infant Temperament (Garcia Coll et al., 1988). Parents rated temperament (Infant Behavior Questionnaire; Rothbart, 1981). Cocaine-exposed infants showed less positivity overall, mainly during activity and threshold items, more negativity during sociability items, and less negativity during irritability and threshold items. Latent profile analysis indicated individual temperament patterns were best described by three groups:low/moderate overall reactivity, high social negative reactivity,andhigh nonsocial negative reactivity. Infants with heavy cocaine exposure were more likely in high social negative reactivity profile, were less negative during threshold items, and required longer soothing intervention. Cocaine- and opiate-exposed infants scored lower on Infant Behavior Questionnaire smiling and laughter and duration of orienting scales. Opiate-exposed infants were rated as less respondent to soothing. By including a multitask measure of temperament we were able to show context-specific behavioral dysregulation in prenatally cocaine-exposed infants. The findings indicate flatter temperament may be specific to nonsocial contexts, whereas social interactions may be more distressing for cocaine-exposed infants.

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Mellstrand, Tore. "Loperamide—an Opiate Receptor Agonist with Gastrointestinal Motility Effects." Scandinavian Journal of Gastroenterology 22, sup130 (January 1987): 65–66. http://dx.doi.org/10.3109/00365528709091001.

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Dyakonova, Varya, F. W. Schürmann, and D. A. Sakharov. "Effects of opiate ligands on intraspecific aggression in crickets." Peptides 23, no. 5 (May 2002): 835–41. http://dx.doi.org/10.1016/s0196-9781(02)00007-4.

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Goddard, Kashmir. "Pregnancy and its effects on opiate and alcohol use." Drugs and Alcohol Today 9, no. 4 (December 11, 2009): 18–21. http://dx.doi.org/10.1108/17459265200900037.

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Downs, David A. "Methadone, buprenorphine and naltrexone effects on opiate self-administration." Pharmacology Biochemistry and Behavior 36, no. 2 (June 1990): 425. http://dx.doi.org/10.1016/0091-3057(90)90443-l.

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Filipović, D., V. Ivetić, N. Naumović, and A. Kelemen. "P241 Electroencephalographic study of opiate epileptogenic effects in rabbits." Electroencephalography and Clinical Neurophysiology 99, no. 4 (October 1996): 327. http://dx.doi.org/10.1016/0013-4694(96)88367-2.

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Kapur, S., and A. Pal. "FC03-03 - Opiate receptor alleles and alcohol dependence." European Psychiatry 26, S2 (March 2011): 1824. http://dx.doi.org/10.1016/s0924-9338(11)73528-3.

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Alcohol use is a major cause of morbidity and mortality and is less understood than other addictive disorders. Humans vary in alcohol responses which could be related to genetic susceptibility for alcoholism. The objective of the present study was to examine the prevalence of OPRM1 polymorphisms in addicts. The opioid receptor mu1 (OPRM1) mediates the action of morphine and is a major determinant of striatal dopamine responses to alcohol. Two polymorphism, C17T and A11G of exon I were screened in subjects with addiction to alcohol and opioids and compared with subjects without a history of any sort of drug addiction using restriction fragment length polymorphism, which was further validated by DNA sequencing. The allelic frequencies between the two groups were compared and the difference was found to be of statistical significant (p < 0.0001), with the 17T allele having a 3.06-fold higher risk of alcohol addiction (risk ratio (RR) = 3.069, 95%CI of RR = 2.0339 to 4.6127, odds ratio (OR) = 3.9554; 95%CI of OR = 2.4175 to6.4718) and 118G allele having a 1.81-fold higher risk of alcohol addiction (risk ratio (RR) = 1.8096, 95%CI of RR = 13459 to 2.433, odds ratio (OR) = 2.2025; 95%CI of OR = 1.479 to 3.2799). Similar differences were observed in the case of opiate addiction, RR = 1.1369 to 2.7647, OR = 1.9367; 95%CI = 1.1625 to 3.2263 and RR = 1.7363, 95%CI of RR = 1.3043 to 2.3112, OR = 2.0725; 1.42 to 3.0248) for 17T and 118G respectively. Further studies to unravel the epigenetic control of expression of these candidate genes are underway.

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Khazraee, Emad, and Kristene Unsworth. "Social media: The new opiate of the masses?" International Review of Information Ethics 18 (December 1, 2012): 49–59. http://dx.doi.org/10.29173/irie303.

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This study argues that the relationship between new information and communication technologies (ICT) and social movements should be done from a socio-technical perspective. In the present study, we broaden this perspective and use Actor-Network Theory (ANT) to better understand the relationship between social media (as a new ICT) and social movements. From the perspective of ANT, one cannot define unidirectional causal relationships between the social and the technical. New technical developments create opportunities to change the social order and in the meantime technologies are transformed and are adapted differently by humans. Preliminary findings examining the use of Facebook among Iranians, applying the aforementioned relational sociology perspective based on ANT, suggest that the role new ICTs play in social movements and social change is not linear and constant through time. The impact of new ICTs might be different considering different stages in a social movement timeline. In fact, there may be a stage where ICTs actually function as a sort of pressurerelease value, allowing individuals to remain content within the status quo rather than choosing to pursue more radical goals. We propose the utilization of the two concepts of “durability” and “mobility”, from ANT literature, to better understand the potential of online social networking technologies for social change. We suggest three different time stages as short (emergence of movements), mid (development or decline of movements), and late stage (the movement’s continuation, survival or disappearance through time) to be considered in the study of relationship between social media and social change.

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Streel, Emmanuel, Bernard Dan, Valérie Antoniali, Béatrice Clement, Salvatore Campanella, Catherine Hanak, Philippe Vanderlinden, Isy Pelc, and Paul Verbanck. "Effects of anaesthetic agents in interference of naloxone-induced opiate-withdrawal are dose-dependent in opiate-dependent rats." Life Sciences 77, no. 6 (June 2005): 650–55. http://dx.doi.org/10.1016/j.lfs.2004.11.035.

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McAuliffe, William E., Mary Rohman, Barry Feldman, and Elaine K. Launer. "The Role of Euphoric Effects in the Opiate Addictions of Heroin Addicts, Medical Patients and Impaired Health Professionals." Journal of Drug Issues 15, no. 2 (April 1985): 203–24. http://dx.doi.org/10.1177/002204268501500204.

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Although the importance of euphoria-seeking in opiate addiction has been debated by leading drug abuse theorists including Lindesmith, Wikler, Brill, Bejerot and others, few researchers have heretofore collected systematic data on the issue. Statistical and case study data obtained over the past few years show that euphoria-seeking is a major cause of opiate addiction for most nontherapeutic addicts but for only a few therapeutic addicts. Theoretical analysis and empirical data indicate that euphoria-seeking is also a key component in the causation of many of the secondary problems of nontherapeutic addiction, including crime, unemployment, death, and disease. In the absence of euphoria-seeking, opiate addiction would be a much less severe public health and social problem.

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McLemon, Erin, and Rose Chesworth. "Cannabinoid treatment of opiate addiction." Neuroanatomy and Behaviour 3 (June 12, 2021): e14. http://dx.doi.org/10.35430/nab.2021.e14.

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Opioid abuse is a growing global problem. Current therapies for opioid abuse target withdrawal symptoms and have several adverse side effects. There are no treatments to address opioid-induced neural adaptations associated with abuse and addiction. Preclinical research demonstrates interactions between the endogenous opioid and cannabinoid systems, suggesting that cannabinoids may be used to treat opioid addiction and dependence. The aim of this review is to assess how cannabinoids affect behavioural and molecular measures of opioid dependence and addiction-like behaviour in animal models. It appears that cannabidiol and cannabinoid receptor 1 (CB1R) antagonists have potential for treating drug-craving and drug-seeking behaviour, based on evidence from preclinical animal models. Ligands which inhibit the action of cannabinoid degradation enzymes also show promise in reducing opioid withdrawal symptoms and opioid self-administration in rodents. Agonists of CB1R could be useful for treating symptoms of opioid withdrawal; however, the clinical utility of these drugs is limited by side effects, the potential for cannabinoid addiction and an increase in opiate tolerance induced by cannabinoid consumption. The mechanisms by which cannabinoids reduce opioid addiction-relevant behaviours include modulation of cannabinoid, serotonin, and dopamine receptors, as well as signalling cascades involving ERK-CREB-BDNF and peroxisome proliferator-activated receptor-α. Identifying the receptors involved and their mechanism of action remains a critical area of future research.

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Weinberger, S. E., R. A. Steinbrook, D. B. Carr, E. R. von Gal, J. E. Fisher, D. E. Leith, V. Fencl, and M. Rosenblatt. "Endogenous opioids and ventilatory responses to hypercapnia in normal humans." Journal of Applied Physiology 58, no. 5 (May 1, 1985): 1415–20. http://dx.doi.org/10.1152/jappl.1985.58.5.1415.

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Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.

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