Journal articles: 'Plasma morphine'

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Yu, Yinghao, Alan Bohan He, Michelle Liou, Chenyin Ou, Anna Kozłowska, Pingwen Chen, and Andrew Chihwei Huang. "The Paradoxical Effect Hypothesis of Abused Drugs in a Rat Model of Chronic Morphine Administration." Journal of Clinical Medicine 10, no. 15 (July 21, 2021): 3197. http://dx.doi.org/10.3390/jcm10153197.

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A growing body of studies has recently shown that abused drugs could simultaneously induce the paradoxical effect in reward and aversion to influence drug addiction. However, whether morphine induces reward and aversion, and which neural substrates are involved in morphine’s reward and aversion remains unclear. The present study first examined which doses of morphine can simultaneously produce reward in conditioned place preference (CPP) and aversion in conditioned taste aversion (CTA) in rats. Furthermore, the aversive dose of morphine was determined. Moreover, using the aversive dose of 10 mg/kg morphine tested plasma corticosterone (CORT) levels and examined which neural substrates were involved in the aversive morphine-induced CTA on conditioning, extinction, and reinstatement. Further, we analyzed c-Fos and p-ERK expression to demonstrate the paradoxical effect—reward and aversion and nonhomeostasis or disturbance by morphine-induced CTA. The results showed that a dose of more than 20 mg/kg morphine simultaneously induced reward in CPP and aversion in CTA. A dose of 10 mg/kg morphine only induced the aversive CTA, and it produced higher plasma CORT levels in conditioning and reacquisition but not extinction. High plasma CORT secretions by 10 mg/kg morphine-induced CTA most likely resulted from stress-related aversion but were not a rewarding property of morphine. For assessments of c-Fos and p-ERK expression, the cingulate cortex 1 (Cg1), prelimbic cortex (PrL), infralimbic cortex (IL), basolateral amygdala (BLA), nucleus accumbens (NAc), and dentate gyrus (DG) were involved in the morphine-induced CTA, and resulted from the aversive effect of morphine on conditioning and reinstatement. The c-Fos data showed fewer neural substrates (e.g., PrL, IL, and LH) on extinction to be hyperactive. In the context of previous drug addiction data, the evidence suggests that morphine injections may induce hyperactivity in many neural substrates, which mediate reward and/or aversion due to disturbance and nonhomeostasis in the brain. The results support the paradoxical effect hypothesis of abused drugs. Insight from the findings could be used in the clinical treatment of drug addiction.

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Kalman, Sigga, Kerstin Metcalf, and Christina Eintrei. "Morphine, Morphine-6-Glucuronide, and Morphine-3-Glucuronide in Cerebrospinal Fluid and Plasma After Epidural Administration of Morphine." Regional Anesthesia: The Journal of Neural Blockade in Obstetrics, Surgery, & Pain Control 22, no. 2 (March 1997): 131–36. http://dx.doi.org/10.1136/rapm-00115550-199722020-00005.

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Background and ObjectivesIt has been suggested that the potency of epidural morphine might be explained by spinal metabolism to the active and potent metabolite morphine-6-glucuronide (M6G). The main objective of this study was to describe the early pharmacokinetics of epidurally administered, morphine with special attention to the appearance of the glucuronated metabolites in cerebrospinal fluid (CSF).MethodsMorphine was administered epidurally to eight patients scheduled for major abdominal surgery. The concentrations of morphine and its 6-glucuronide and 3-glucuronide metabolites were monitored in blood and CSF at 10, 30, 60, and 120 minutes and 10 and 24 hours. Postoperative pain was estimated on a visual analog scale, and analgesia requirements (administered by a patient-controlled techique) were recorded.ResultsOnly traces of the metabolites were found in CSF and in only two patients throughout the 24 hours. Both metabolites appeared rapidly (within 30 minutes) in plasma in all patients and were found in plasma throughout the study period. Morphine concentration peaked in CSF within 30 minutes at a very high level; in plasma, it peaked at 10 minutes. No correlation was seen between initial or later concentrations of morphine in CSF and postoperative pain or morphine requirements.ConclusionsNo evidence of spinal metabolism of morphine could be found. Rapid distribution of morphine to CSF and plasma occurred after epidural administration. No value of initial CSF morphine concentrations for prediction of analgesic requirements could be demonstrated.

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May, Clive N., Ian W. Ham, Kirsten E. Heslop, Frances A. Stone, and Christopher J. Mathias. "Intravenous morphine causes hypertension, hyperglycaemia and increases sympatho-adrenal outflow in conscious rabbits." Clinical Science 75, no. 1 (July 1, 1988): 71–77. http://dx.doi.org/10.1042/cs0750071.

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1. In conscious rabbits, intravenous morphine (3 mg/kg) caused hypertension, bradycardia, hyperglycaemia and sedation. These changes were accompanied by large increases in plasma adrenaline and smaller increases in plasma noradrenaline. 2. These effects of morphine were prevented by intravenous naloxone, demonstrating their dependence on stimulation of opiate receptors. 3. Pretreatment with the antihistamines cimetidine and chlorpheniramine enhanced the morphine-induced rise in blood pressure, excluding a role for histamine release in the hypertensive action of morphine. 4. The centrally acting α2-adrenergic agonist clonidine prevented the morphine-induced hypertension and rise in plasma catecholamines, suggesting that these effects are exerted via central pathways. Clonidine alone reduced blood pressure and heart rate and produced hyperglycaemia. 5. α-Adrenergic blockade with phenoxybenzamine reduced the increase in blood pressure after morphine, although the increase in plasma catecholamines was augmented. 6. Pentobarbitone anaesthesia prevented the morphine-induced cardiovascular changes, the increase in plasma catecholamines and the hyperglycaemia. 7. These findings indicate, that in conscious rabbits, morphine induces hypertension by stimulation of opiate receptors leading to increased sympatho-adrenal activity. The hyperglycaemia appears to be in response to secretion of adrenaline. These effects probably result from a central action of morphine.

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D'Honneur, G., A. Gilton, P. Sandouk, J. M. Scherrmann, and P. Duvaldestin. "Plasma and Cerebrospinal Fluid Concentrations of Morphine and Morphine Glucuronides after Oral Morphine." Anesthesiology 81, no. 1 (July 1, 1994): 87–93. http://dx.doi.org/10.1097/00000542-199407000-00013.

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PORTENOY, R. K., K. M. FOLEY, J. STULMAN, E. KHAN, J. ADELHARDT, M. LAYMAN, D. F. CERBONE, and C. E. INTURRISI. "Plasma Morphine and Morphine-6-Glucuronide During Chronic Morphine Therapy for Cancer Pain." Survey of Anesthesiology 36, no. 4 (June 1992): 251. http://dx.doi.org/10.1097/00132586-199206000-00045.

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PORTENOY, R. K., K. M. FOLEY, J. STULMAN, E. KHAN, J. ADELHARDT, M. LAYMAN, D. F. CERBONE, and C. E. INTURRISI. "Plasma Morphine and Morphine-6-Glucuronide During Chronic Morphine Therapy for Cancer Pain." Survey of Anesthesiology 36, no. 4 (August 1992): 250???251. http://dx.doi.org/10.1097/00132586-199208000-00050.

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Meissner, Konrad, Michael J. Avram, Viktar Yermolenka, Amber M. Francis, Jane Blood, and Evan D. Kharasch. "Cyclosporine-inhibitable Blood–Brain Barrier Drug Transport Influences Clinical Morphine Pharmacodynamics." Anesthesiology 119, no. 4 (October 1, 2013): 941–53. http://dx.doi.org/10.1097/aln.0b013e3182a05bd3.

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Abstract Background: The blood–brain barrier is richly populated by active influx and efflux transporters influencing brain drug concentrations. Morphine, a drug with delayed clinical onset, is a substrate for the efflux transporter P-glycoprotein in vitro and in animals. This investigation tested whether morphine is a transporter substrate in humans. Methods: Fourteen healthy volunteers received morphine (0.1 mg/kg, 1-h IV infusion) in a crossover study without (control) or with the infusion of validated P-glycoprotein inhibitor cyclosporine (5 mg/kg, 2-h infusion). Plasma and urine morphine and morphine glucuronide metabolite concentrations were measured by mass spectrometry. Morphine effects were measured by miosis and analgesia. Results: Cyclosporine minimally altered morphine disposition, increasing the area under the plasma morphine concentration versus time curve to 100 ± 21 versus 85 ± 24 ng/ml·h (P < 0.05) without changing maximum plasma concentration. Cyclosporine enhanced (3.2 ± 0.9 vs. 2.5 ± 1.0 mm peak) and prolonged miosis, and increased the area under the miosis–time curve (18 ± 9 vs. 11 ± 5 mm·h), plasma effect-site transfer rate constant (ke0, median 0.27 vs. 0.17 h−1), and maximum calculated effect-site morphine concentration (11.5 ± 3.7 vs. 7.6 ± 2.9 ng/ml; all P < 0.05). Analgesia testing was confounded by cyclosporine-related pain. Conclusions: Morphine is a transporter substrate at the human blood–brain barrier. Results suggest a role for P-glycoprotein or other efflux transporters in brain morphine access, although the magnitude of the effect is small, and unlikely to be a major determinant of morphine clinical effects. Efflux may explain some variability in clinical morphine effects.

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Takahashi, Masahiko, Takeshi Ohara, Hiroyuki Yamanaka, Akira Shimada, Toshimichi Nakaho, and Makoto Yamamuro. "The oral-to-intravenous equianalgesic ratio of morphine based on plasma concentrations of morphine and metabolites in advanced cancer patients receiving chronic morphine treatment." Palliative Medicine 17, no. 8 (December 2003): 673–78. http://dx.doi.org/10.1191/0269216303pm824oa.

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To provide additional pharmacokinetic evidence for the oral-to-parenteral relative potency ratio of 1:2 to 1:3 for chronic morphine use in a palliative care setting, we determined the plasma concentrations of morphine and its major metabolites, morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G), in hospitalized advanced cancer patients maintained on long-term oral or intravenous morphine. There were significant linear correlations between daily doses of morphine and plasma concentrations (molar base) of morphine, M3G and M6G for both routes of administration. The oral-to-intravenous relative ratios of the regression coefficients were 2.9 for morphine and 1.8 for morphine» / M6G. The morphine kinetic variables were not significantly influenced by any hepato-renal biochemical markers. These results support the commonly used oral-to-intravenous relative potency ratio of 1:2 to 1:3 in patients with cancer pain receiving chronic morphine treatment.

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May, Clive N., Catherine J. Whitehead, Kirsten E. Heslop, and Christopher J. Mathias. "Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits." Clinical Science 76, no. 4 (April 1, 1989): 431–37. http://dx.doi.org/10.1042/cs0760431.

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1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium. 2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist. 3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished. 4. Adrenaline infused intravenously to mimic the levels that occurred after morphine caused a similar degree of hyperglycaemia but only a small increase in blood pressure. 5. Pretreatment with intracerebroventricular naloxone prevented the morphine-induced hypertension, hyperglycaemia, increase in plasma catecholamines, respiratory depression and sedation. 6. These results demonstrate that, in conscious rabbits, intravenous morphine causes hypertension by increasing sympathetic vasoconstrictor nerve activity and elevating plasma adrenaline levels; the latter alone produces the hyperglycaemia. Vasopressin release is not involved in the hypertensive response to morphine. The effects of morphine appear to result from stimulation of central opiate receptors leading to enhanced sympathoadrenal outflow.

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Schneider, JJ, PJ Ravenscroft, JD Cavenagh, AM Brown, and JP Bradley. "Plasma morphine-3-glucuronide, morphine-6-glucuronide and morphine concentrations in patients receiving long-term epidural morphine." British Journal of Clinical Pharmacology 34, no. 5 (November 1992): 431–33. http://dx.doi.org/10.1111/j.1365-2125.1992.tb05651.x.

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Lotsch, Jorn, Michel Weiss, Gabi Ahne, Gerd Kobal, and Gerd Geisslinger. "Pharmacokinetic Modeling of M6G Formation after Oral Administration of Morphine in Healthy Volunteers." Anesthesiology 90, no. 4 (April 1, 1999): 1026–38. http://dx.doi.org/10.1097/00000542-199904000-00016.

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Background Morphine is metabolized to two major metabolites, morphine-3-glucuronide and morphine-6-glucuronide (M6G). Under the conditions of long-term oral morphine administration, the accumulation of M6G may contribute to the analgesic effects, but it may also cause respiratory depression. Methods Five healthy male volunteers (ages 25-34 yr) received 90 mg MST (morphine sulfate 5H2O sustained-released tablet, equivalent to 67.8 mg oral morphine). Multiple plasma and urine samples were taken for as long as 14 and 36 h, respectively. Individual pharmacokinetics after intravenous administration of morphine and M6G were available from a previous investigation. A new model that considers the M6G-plasma profile as a sum of the input from the first-pass metabolism of morphine and the input from systemically available morphine was applied to the plasma concentration versus time curves of M6G. The concentrations of M6G at the effect site after long-term morphine administration were simulated. Results The fraction of morphine absorbed from the gut was 82+/-14%. Of this, 42+/-8% passed through the liver, resulting in an oral bioavailability of morphine of 34+/-9%. Of the total amount of M6G, 71+/-7% was formed during the first-pass metabolism, and 29+/-7% was formed by metabolism of systemic morphine. After 36 h, the amounts of M6G and morphine excreted in the urine were 92+/-17% and 9+/-3%, respectively. Simulation of effect-site concentrations of M6G indicated that after multiple oral dosing of morphine in patients with normal liver and renal function, M6G might reach concentrations two times greater than that of morphine. Conclusions M6G may contribute to the analgesic and side effects seen with long-term morphine treatment. The current model of morphine and M6G pharmacokinetics after oral administration of morphine may serve as a pharmacokinetic basis for experiments evaluating the analgesic contribution of M6G with long-term oral dosing of morphine.

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Kitabata, Yuji, Naonori Morita, Tetsuji Yamanishi, Masanobu Ozaki, Shiroh Kishioka, and Hiroyuki Yamamoto. "Negative correlation of plasma morphine concentration with plasma corticosterone level during morphine withdrawal in rats." Japanese Journal of Pharmacology 58 (1992): 74. http://dx.doi.org/10.1016/s0021-5198(19)48720-9.

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Öğütman, Ç., T. Özben, G. Şadan, A. Trakya, and M. İsbir. "Morphine Increases Plasma Immunoreactive Atrial Natriuretic Peptide Levels in Humans." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 27, no. 1 (January 1990): 21–24. http://dx.doi.org/10.1177/000456329002700105.

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Plasma immunoreactive α-atrial natriuretic peptide (IR α-ANP) levels were determined before, and at 5 and 10 min after bolus intravenous administration of morphine (0·15 or 0·30 mg/kg) in 21 otherwise healthy human subjects who underwent elective surgery. Five min after injection IR α-ANP levels had nearly doubled in response to both doses of morphine. At 10 min, plasma IR α-ANP concentrations were lower than at 5 min in the 0·15 mg/kg group suggesting that IR α-ANP levels peak shortly after morphine administration. Morphine has been widely used in the treatment of acute left ventricular failure and ANP is a recently discovered hormone which possesses unique favourable effects in patients with congestive heart failure when administered exogenously. The combination of these data suggests an important potential role for ANP in the mechanism of action of morphine in the treatment of acute left ventricular failure.

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Newby, N. C., M. P. Wilkie, and E. D. Stevens. "Morphine uptake, disposition, and analgesic efficacy in the common goldfish (Carassius auratus)." Canadian Journal of Zoology 87, no. 5 (May 2009): 388–99. http://dx.doi.org/10.1139/z09-023.

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The purposes of the present study were to examine the rate of morphine uptake in goldfish ( Carassius auratus (L., 1758)) when administered via the water, to calculate the pharmacokinetics of morphine when administered intraperitoneally, and to determine whether morphine could act as an analgesic. When administered via the water, morphine uptake was very slow, and the concentration accumulated in the plasma was <1% of that in water after 2 h. Furthermore, changing water pH or hardness caused small changes in morphine uptake from the water, but plasma levels remained <1% of water concentrations after 2 h exposure. The pharmacokinetics of morphine administered intraperitoneally (40 mg/kg) revealed a half-time for elimination of 37 h and a mean residence time of 56 h. Finally, morphine acted as an analgesic when administered via the water as demonstrated by significantly decreased rubbing behaviour in response to the presence of a noxious stimulus (subcutaneous injection of 0.7% acetic acid). Although morphine appeared to have analgesic properties in goldfish, morphine administered via ambient water is not recommended because of its slow rate of uptake.

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KALMAN, S., K. METCALF, and C. EINTREI. "Morphine, morphine-6-glucuronide, and morphine-3-glucuronide in cerebrospinal fluid and plasma after epidural administration of morphine." Regional Anesthesia and Pain Medicine 22, no. 2 (March 1997): 131–36. http://dx.doi.org/10.1016/s1098-7339(06)80031-3.

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KUKANICH, B., B. D. X. LASCELLES, and M. G. PAPICH. "Pharmacokinetics of morphine and plasma concentrations of morphine-6-glucuronide following morphine administration to dogs." Journal of Veterinary Pharmacology and Therapeutics 28, no. 4 (August 2005): 371–76. http://dx.doi.org/10.1111/j.1365-2885.2005.00661.x.

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SAMUELSSON, H., T. HEDNER, R. VENN, and A. MICHALKIEWICZ. "CSF and Plasma Concentrations of Morphine and Morphine Glucuronides in Cancer Patients Receiving Epidural Morphine." Survey of Anesthesiology 39, no. 6 (December 1993): 317. http://dx.doi.org/10.1097/00132586-199312000-00008.

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Samuelsson, Håkan, Thomas Hedner, Richard Venn, and Andrew Michalkiewicz. "CSF and plasma concentrations of morphine and morphine glucuronides in cancer patients receiving epidural morphine." Pain 52, no. 2 (February 1993): 179–85. http://dx.doi.org/10.1016/0304-3959(93)90129-d.

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Collins, SallyL, ClaraC Faura, R. Andrew Moore, and HenryJ McQuay. "Peak Plasma Concentrations After Oral Morphine." Journal of Pain and Symptom Management 16, no. 6 (December 1998): 388–402. http://dx.doi.org/10.1016/s0885-3924(98)00094-3.

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Gutkowska, Jolanta, Karoly Racz, Raul Garcia, Gaétan Thibault, Otto Kuchel, Jacques Genest, and Marc Cantin. "The morphine effect on plasma ANF." European Journal of Pharmacology 131, no. 1 (November 1986): 91–94. http://dx.doi.org/10.1016/0014-2999(86)90519-4.

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Kumar, Rakesh, Cynthia Torres, Yasuhiro Yamamura, Idia Rodriguez, Melween Martinez, Silvija Staprans, Robert M. Donahoe, Edmundo Kraiselburd, Edward B. Stephens, and Anil Kumar. "Modulation by Morphine of Viral Set Point in Rhesus Macaques Infected with Simian Immunodeficiency Virus and Simian-Human Immunodeficiency Virus." Journal of Virology 78, no. 20 (October 15, 2004): 11425–28. http://dx.doi.org/10.1128/jvi.78.20.11425-11428.2004.

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ABSTRACT Six rhesus macaques were adapted to morphine dependence by injecting three doses of morphine (5 mg/kg of body weight) for a total of 20 weeks. These animals along with six control macaques were infected intravenously with mixture of simian-human immunodeficiency virus KU-1B (SHIVKU-1B), SHIV89.6P, and simian immunodeficiency virus 17E-Fr. Levels of circulating CD4+ T cells and viral loads in the plasma and the cerebrospinal fluid were monitored in these macaques for a period of 12 weeks. Both morphine and control groups showed precipitous loss of CD4+ T cells. However this loss was more prominent in the morphine group at week 2 (P = 0.04). Again both morphine and control groups showed comparable peak plasma viral load at week 2, but the viral set points were higher in the morphine group than that in the control group. Likewise, the extent of virus replication in the cerebral compartment was more pronounced in the morphine group. These results provide a definitive evidence for a positive correlation between morphine and levels of viral replication.

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Bragg, P., M. S. Zwass, M. Lau, and D. M. Fisher. "Opioid pharmacodynamics in neonatal dogs: differences between morphine and fentanyl." Journal of Applied Physiology 79, no. 5 (November 1, 1995): 1519–24. http://dx.doi.org/10.1152/jappl.1995.79.5.1519.

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Clinical experience and laboratory studies suggest that neonates are more sensitive than adults to the ventilatory depressant effects of morphine. Similar sensitivity has been cited, but not demonstrated, for fentanyl. To examine this issue, we determined ventilatory pharmacodynamics of morphine and fentanyl in 28 dogs aged 2–35 days. During isohypercapnia, morphine or fentanyl was infused to depress minute ventilation by > 50% and arterial plasma opioid concentrations were measured. For each drug, an effect compartment pharmacodynamic model was fit to the values for minute ventilation to determine the steady-state opioid plasma concentration depressing ventilation by 50% (C50) and the rate constant for equilibration between plasma concentration and effect (keo). For morphine, there was a marked age-related increase in C50 but no change in keo. For fentanyl, there was a small maturational increase in C50 and no change in keo. We conclude that there are marked maturational changes in the ventilatory depressant effects of morphine resulting from maturational changes in sensitivity rather than in equilibration. Maturational changes in the ventilatory effects of fentanyl are much smaller in magnitude than those for morphine.

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Somogyi, Andrew A., Roger L. Nation, Charles Olweny, Panagiotis Tsirgiotis, Jacoba van Crugten, Robert W. Milne, James F. Cleary, Catherine Danz, and Felix Bochner. "Plasma Concentrations and Renal Clearance of Morphine, Morphine-3-Glucuronide and Morphine-6-Glucuronide in Cancer Patients Receiving Morphine." Clinical Pharmacokinetics 24, no. 5 (May 1993): 413–20. http://dx.doi.org/10.2165/00003088-199324050-00005.

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Muraki, Takamura, Teruko Nomoto, and Ryuichi Kato. "Developmental changes in the effects of carbachol and morphine on cGMP contents of plasma, heart, and lung of mice." Canadian Journal of Physiology and Pharmacology 67, no. 10 (October 1, 1989): 1283–87. http://dx.doi.org/10.1139/y89-204.

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It is considered that carbachol increases plasma cGMP levels by acting on muscarinic receptors and morphine increases these levels by acting on opioid receptors, followed by stimulation of muscarinic receptors. We investigated the ability of carbachol and morphine to increase cGMP contents of plasma, heart, and lung and the guanylate cyclase activity of heart and lung homogenate in 1-, 2-, 3-, and 7-week-old mice. The increase in plasma cGMP levels induced by carbachol showed a peak at 2 and 3 weeks of age. The basal cGMP contents in heart and lung and their rise induced by carbachol, as well as the guanylate cyclase activity of these organs, were decreased in 7-week-old mice. The effects of morphine on the cGMP contents showed a similar developmental change, except for no effect in 1-week-old mice. These changes in the effects of carbachol and morphine may be the result of developmental changes of the muscarinic receptor – guanylate cyclase system and opioid receptors.Key words: cGMP, mouse development, carbachol, morphine.

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Lötsch, Jörn, Michael Zimmermann, Jutta Darimont, Claudia Marx, Rafael Dudziak, Carsten Skarke, and Gerd Geisslinger. "Does the A118G Polymorphism at the μ-opioid Receptor Gene Protect against Morphine-6-Glucuronide Toxicity?" Anesthesiology 97, no. 4 (October 1, 2002): 814–19. http://dx.doi.org/10.1097/00000542-200210000-00011.

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Background Some, but not all, patients with renal dysfunction suffer from side effects after morphine administration because of accumulation of the active metabolite morphine-6-glucuronide (M6G). The current study aims to identify genetic causes that put patients at risk for, or protect them from, opioid side effects related to high plasma M6G. Candidate genetic causes are the single nucleotide polymorphism (SNP) A118G of the mu-opioid-receptor gene (OPRM1), which has recently been identified to result in decreased potency of M6G, and mutations in the MDR1-gene coding P-glycoprotein, of which morphine and M6G might be a substrate. Methods Two men, aged 87 and 65 yr, with renal failure (creatinine clearance of 6 and 9 ml/min) received 30 mg/day oral morphine for pain treatment. Both patients had sufficient analgesia from morphine. However, while one patient tolerated morphine well despite high plasma M6G of 1735 nM, in the patient with M6G plasma concentrations of 941 nM it caused severe sleepiness and drowsiness. Patients were genotyped for known SNPs of the OPRM1 and MDR1 genes. Results The patient who tolerated morphine well despite high plasma M6G was a homozygous carrier of the mutated G118 allele of the mu-opioid-receptor gene, which has been previously related to decreased M6G potency. In contrast, the patient who suffered from side effects was "wild-type" for this mutation. No other differences were found between the OPRM1 and MDR1 genes. Conclusions The authors hypothesize that the A118G single nucleotide polymorphism of the mu-opioid-receptor is among the protective factors against M6G-related opioid toxicity. The observation encourages the search for pharmacogenetic reasons that cause interindividual variability of the clinical effects of morphine.

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Hand, C. W., R. A. Moore, H. J. McQuay, M. C. Allen, and J. W. Sear. "Analysis of Morphine and its Major Metabolites by Differential Radioimmunoassay." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 24, no. 2 (March 1987): 153–60. http://dx.doi.org/10.1177/000456328702400205.

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The analysis of morphine, morphine-3-glucuronide (M-3-G) morphine-6-glucuronide (M-6-G) by differential radioimmunoassay using idodinated label and three different antisera is described. These methods were used to measure concentrations of morphine and its conjugated metabolites in human plasma, over a 3-h period, following a single 10 mg intravenous dose. In 13 patients peak concentrations of M-3-G (739 nmol/L±73.7 SEM) were approximately 10 times greater than those of M-6-G (71-3 nmol/L±8-6 SEM). Times to reach these peaks were similar for both metabolites. Decay of morphine from plasma followed a biexponential pattern with a mean terminal half-life of 59.3 min (±81 SEM, n=11). Accurate determination of the half-lives of the glucuronides was not possible due to the short sampling period, but M-6-G seemed to have a similar half-life to morphine, while M-3-G was eliminated more slowly.

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Natalini, Cláudio Corrêa. "Plasma and cerebrospinal fluid alfentanil, butorphanol, and morphine concentrations following caudal epidural administration in horses." Ciência Rural 36, no. 5 (October 2006): 1436–43. http://dx.doi.org/10.1590/s0103-84782006000500014.

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This study was conducted with the objective of determining the plasma and cerebrospinal fluid (CSF) concentrations after epidurally administered alfentanil, butorphanol, and morphine in horses. Five clinically healthy adult horses were studied. Morphine 0.1mg kg-1, alfentanil 0.02mg kg-1, and butorphanol 0.08mg kg-1 in equal volumes (20ml) were epidurally injected. A 10-ml sample of CSF and blood were drawn at sampling times before the epidural administration and at 5, 10, 20, 30, 40, 50, 60 and 120 minutes, and hourly for 24 hours Enzyme-linked immonosorbent assay (ELISA) was used as the screening test to detect the injected opioids. ANOVA and Bonferroni’s test were used with a P values <0.05 considered significant. The ELISA method was used and seemed to be efficient to detect plasma and CSF epidurally administered alfentanil, butorphanol, and morphine in horses. Epidurally administered alfentanil produces fast cerebrospinal fluid levels that are higher than plasma levels. Less lipid soluble drugs such as morphine and butorphanol produce higher plasma levels than CSF levels for the same time point.

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Hoskin, P. J., O. Alsayed-Omar, G. W. Hanks, A. Johnston, and P. Turner. "The Influence of Blood Sample Preparation on Measured Levels of Morphine and its Major Metabolites." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 26, no. 2 (March 1989): 182–84. http://dx.doi.org/10.1177/000456328902600216.

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The effect of six different methods of blood sample preparation on concentrations of morphine (M), morphine-3-glucuronide (M3G) and morphine-6–glucuronide (M6G) have been investigated using a specific high performance liquid chromatography assay. No difference between glass or plastic tubes was seen in concentrations of M, M3G, or M6G; and no difference between plasma and serum in M and M6G concentrations. M3G concentrations, however, were significantly lower in plasma compared with serum. Heparin had no effect on M, M6G or M3G, whereas citrate in a glass tube produced consistently lower concentrations of M, M3G and M6G. Standardization of sample collection using plasma samples in plastic heparin tubes is recommended for future studies.

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Dongen, RT, BJ Crul, PM Koopman-Kimenai, and TB Vree. "Morphine and morphine-glucuronide concentrations in plasma and CSF during long-term administration of oral morphine." British Journal of Clinical Pharmacology 38, no. 3 (September 1994): 271–73. http://dx.doi.org/10.1111/j.1365-2125.1994.tb04352.x.

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30

Portenoy, R. K., E. Khan, M. Layman, J. Lapin, M. G. Malkin, K. M. Foley, H. T. Thaler, D. J. Cerbone, and C. E. Inturrisi. "Chronic morphine therapy for cancer pain: Plasma and cerebrospinal fluid morphine and morphine-6-glucuronide concentrations." Neurology 41, no. 9 (September 1, 1991): 1457. http://dx.doi.org/10.1212/wnl.41.9.1457.

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31

Chapman, D. J., M. J. Cross, S. P. Joel, and G. W. Aherne. "A Specific Radioimmunoassay for the Determination of Morphine-6-Glucuronide in Human Plasma." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 32, no. 3 (May 1995): 297–302. http://dx.doi.org/10.1177/000456329503200306.

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A specific antiserum for morphine-6-glucuronide (M6G) has been raised in a rabbit in response to immunization with a novel hapten: Protein conjugate (N-aminobutylnormorphine-6-glucuronide-thyroglobulin). Cross-reactivity with morphine and structurally related compounds was found to be negligible as expected from the nature of this immunogen. Using this antiserum, a simple, rapid and robust radioimmunoassay (RIA) has been developed for determination of M6G in samples of human plasma. The assay has a sensitivity of 0·05 ng/mL using 100 μL sample volumes and affords complete recovery of M6G over the range 2–200 ng/mL. The presence of morphine or morphine-3-glucuronide at concentrations up to 100 times the levels of M6G did not result in any measurable interference. Close agreement was obtained between M6G results obtained using the RIA and a specific high-performance liquid chromatography assay. This RIA offers an attractive alternative to existing methods for the determination of M6G in human plasma and will facilitate further metabolic and pharmacokinetic studies of morphine and M6G in the clinical setting.

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32

Rasmussen, Natalie Ann, and Lynne A. Farr. "Effects of Morphine and Time of Day on Pain and Beta-Endorphin." Biological Research For Nursing 5, no. 2 (October 2003): 105–16. http://dx.doi.org/10.1177/1099800403257166.

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Clients report more pain at some times of day than at others due, in part, to the temporal variation of the body's inhibitory pain response. The analgesic effectiveness of morphine varies with the time of day, perhaps due to the inhibiting or enhancing effects of the drug on plasma beta-endorphin (BE). This experiment was designed to examine the timed effects of morphine on the pain-induced BE response. Six groups of treatment mice (injected with morphine sulfate) and 6 groups of control mice (injected with saline) were exposed to an acute pain stimulus at 4-h intervals, and blood was collected. Plasma BE was analyzed using radioimmunoassay. Control mice showed a robust cir-cadian BE-response rhythm with a peak at 0000 and a nadir at 1200, whereas the BE response of mice that received morphine was arrhythmic. Animals that received morphine tolerated the noxious stimulus longer, but the analgesia varied with time of day. These results indicate that morphine abolishes the rhythmic BE response to pain and does not inhibit pain equally at all times of day. Morphine doses should be titrated to maximize the endogenous pain control system while achieving analgesia with decreased dosages.

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33

Beck, D. H., M. Schenk, U. Doepfmer, and W. J. Kox. "Relation of morphine consumption and morphine plasma concentration during patient-controlled analgesia." European Journal of Anaesthesiology 17, Supplement 19 (2000): 193. http://dx.doi.org/10.1097/00003643-200000002-00633.

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34

Faura, Clara C., R. Andrew Moore, JoséF Horga, Christopher W. Hand, and Henry J. McQuay. "Morphine and morphine-6-glucuronide plasma concentrations and effect in cancer pain." Journal of Pain and Symptom Management 11, no. 2 (February 1996): 95–102. http://dx.doi.org/10.1016/0885-3924(95)00148-4.

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35

Venn, R. F., A. Michalkieaicz, P. Hardy, and C. Wells. "Concentrations of morphine, morphine metabolites and peptides in human CSF and plasma." Pain 41 (January 1990): S188. http://dx.doi.org/10.1016/0304-3959(90)92512-o.

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Chen, Z. R., R. Ritchie, R. J. Irvine, F. Bochner, and A. Somogyi. "Plasma morphine concentration-analgesic relationship in the rat after codeine and morphine." Pain 41 (January 1990): S193. http://dx.doi.org/10.1016/0304-3959(90)92522-r.

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37

Gourlay, Geoffrey K., John L. Plummer, and David A. Cherry. "Chronopharmacokinetic variability in plasma morphine concentrations following oral doses of morphine solution." Pain 61, no. 3 (June 1995): 375–81. http://dx.doi.org/10.1016/0304-3959(94)00204-r.

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38

Zhou, Y., R. Spangler, CE Maggos, XM Wang, JS Han, A. Ho, and MJ Kreek. "Hypothalamic-pituitary-adrenal activity and pro-opiomelanocortin mRNA levels in the hypothalamus and pituitary of the rat are differentially modulated by acute intermittent morphine with or without water restriction stress." Journal of Endocrinology 163, no. 2 (November 1, 1999): 261–67. http://dx.doi.org/10.1677/joe.0.1630261.

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Acute administration of morphine stimulates the secretion of hypothalamic-pituitary-adrenal (HPA) hormones, ACTH, beta-endorphin and corticosterone in the rat. In this study we investigated the effects of repeated multiple-dose morphine on HPA activity under two different conditions: without or with water restriction stress. Rats received six intermittent injections of morphine (6.25 mg/kg per injection, s.c.) every 2 h and were killed 30 min after the last injection. The results were as follows. (1) Morphine significantly elevated plasma ACTH and corticosterone levels; water restriction also significantly increased ACTH secretion, but with no significant increase of plasma corticosterone levels. In contrast, rats treated with morphine under the water restriction condition failed to show any increases of either ACTH or corticosterone levels. (2) Morphine did not change pro-opiomelanocortin (POMC) mRNA levels in the anterior pituitary; whereas water restriction significantly increased the POMC mRNA levels. The water restriction-induced increases of POMC mRNA in the anterior pituitary were absent in the rats which received morphine. (3) Morphine significantly increased POMC mRNA levels in the hypothalamus; water restriction had no effect. The morphine-induced increases in POMC mRNA in the hypothalamus were absent in the rat under the water restriction condition. These findings, that the effects of morphine on HPA activation or POMC mRNA expression depend on the presence of stress, suggest a counter-regulatory role of opiates on a stress response and opioid gene expression.

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39

Trudeau, V. L., J. C. Meijer, D. F. M. van de Wiel, M. M. Bevers, and J. H. F. Erkens. "Effects of morphine and naloxone on plasma levels of LH, FSH, prolactin and growth hormone in the immature male pig." Journal of Endocrinology 119, no. 3 (December 1988): 501–8. http://dx.doi.org/10.1677/joe.0.1190501.

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ABSTRACT The effects of acute i.v. administration of gonadotrophin-releasing hormone (GnRH; 0·1 μg/kg), morphine (3 mg/kg) and/or naloxone (0·5 mg/kg) on LH and FSH secretion was evaluated in young male pigs (approximately 6 weeks old) with venous brachiocephalic cannulae. The effects of morphine and/or naloxone treatments on prolactin and GH were also evaluated. The influence of morphine on hypophysial hormone secretion was also examined 2 days after castration. Animals treated with morphine and/or naloxone were compared with saline-injected control animals. Injection of GnRH induced 400 and 50% increases in LH and FSH respectively. Morphine and/or naloxone did not influence LH secretion in intact or castrated animals. Morphine suppressed (P < 0·01) FSH levels 40–60 min after injection whereas naloxone had no effect. Castration eliminated morphine-induced suppression of FSH. Injection of morphine followed by naloxone resulted in acutely raised (P < 0·05) FSH concentrations. Morphine induced a threefold increase (P < 0·01) in prolactin within 30 min of injection and naloxone inhibited the effect of morphine. Levels of GH were increased (P < 0·01) 20 min after morphine treatment and this increase was delayed when naloxone was given immediately after morphine. Naloxone alone did not affect prolactin or GH secretion. Castration caused increases in LH (P < 0·05) and FSH (P < 0·01), did not influence prolactin or GH, and reduced plasma testosterone to undetectable (< 1·0 nmol/l) levels. These results suggest that in young male pigs the hypothalamic-hypophysial axis is responsive to GnRH and gonadal negative feedback. The opiate/LH pathway appears to be non-functional or incomplete, while the opiate/FSH pathway seems to be active. Morphine stimulated the release of prolactin probably via a naloxone-sensitive opiate receptor. J. Endocr. (1988) 119, 501–508

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40

Moore, R. A., H. J. McQuay, R. E. S. Bullingham, D. Baldwin, and M. C. Allen. "Systemic Availability of Oral Slow-Release Morphine in Man." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 22, no. 3 (May 1985): 226–31. http://dx.doi.org/10.1177/000456328502200303.

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In a within-patient crossover study on twelve patients we investigated plasma morphine concentrations for 48 hours after administration of intravenous morphine sulphate followed 24 hours later by oral MST Continus [MST]. Patients received either 10 mg i.v. morphine followed by 10 mg MST or 20 mg i.v. morphine followed by 2×10 mg MST tablets. Systemic clearance of morphine was low, being about 3 ml/min/kg after both intravenous and oral administration. The ratio of the areas under the concentration–time curve for MST relative to that for i.v. morphine was about 1:1 for 20 mg doses, but was significantly greater than 1:1 for 10 mg doses. The results suggest high oral systemic availability for morphine and low hepatic morphine metabolism.

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41

Lagas, Jurjen S., Jiri FP Wagenaar, Alwin DR Huitema, Michel JX Hillebrand, Cornelis HW Koks, Victor EA Gerdes, Desiderius PM Brandjes, and Jos H. Beijnen. "Lethal morphine intoxication in a patient with a sickle cell crisis and renal impairment: Case report and a review of the literature." Human & Experimental Toxicology 30, no. 9 (November 5, 2010): 1399–403. http://dx.doi.org/10.1177/0960327110388962.

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Morphine-6-glucuronide, the active metabolite of morphine, and to a lesser extent morphine itself are known to accumulate in patients with renal failure. A number of cases on non-lethal morphine toxicity in patients with renal impairment report high plasma concentrations of morphine-6-glucuronide, suggesting that this metabolite achieves sufficiently high brain concentrations to cause long-lasting respiratory depression, despite its poor central nervous system penetration. We report a lethal morphine intoxication in a 61-year-old man with sickle cell disease and renal impairment, and we measured concentrations of morphine and morphine-6-glucuronide in blood, brain and cerebrospinal fluid. There were no measurable concentrations of morphine-6-glucuronide in cerebrospinal fluid or brain tissue, despite high blood concentrations. In contrast, the relatively high morphine concentration in the brain suggests that morphine itself was responsible for the cardiorespiratory arrest in this patient. Given the fatal outcome, we recommend to avoid repeated or continuous morphine administration in renal failure.

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42

Sheward, W. J., J. E. Coombes, R. J. Bicknell, G. Fink, and J. A. Russell. "Release of oxytocin but not corticotrophin-releasing factor-41 into rat hypophysial portal vessel blood can be made opiate dependent." Journal of Endocrinology 124, no. 1 (January 1990): 141–50. http://dx.doi.org/10.1677/joe.0.1240141.

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ABSTRACT The effects of morphine dependence and abrupt opiate withdrawal on the release of oxytocin and corticotrophin-releasing factor-41 (CRF-41) into hypophysial portal vessel blood in rats anaesthetized with urethane were investigated. Adult female Sprague–Dawley rats were made dependent upon morphine by intracerebroventricular infusion of morphine for 5 days; abrupt opiate withdrawal was induced by injection of the opiate antagonist naloxone. The basal concentrations of oxytocin in portal or peripheral plasma from morphine-dependent rats did not differ significantly from those in control, vehicle-infused rats. In rats in which the pituitary gland was not removed after stalk section, the i.v. injection of naloxone hydrochloride (5 mg/kg) resulted in a large and sustained increase in the concentration of oxytocin in both portal and peripheral plasma in control and morphine-dependent rats. The i.v. injection of naloxone resulted in a threefold increase in the secretion of oxytocin into portal blood in acutely hypophysectomized rats infused with morphine, but did not alter oxytocin secretion in vehicle-infused hypophysectomized rats. The concentration of oxytocin in peripheral plasma in both vehicle- and morphine-infused hypophysectomized rats was at the limit of detection of the assay and was unchanged by the administration of naloxone. There were no significant differences in the secretion of CRF-41 into portal blood in vehicle- or morphine-infused hypophysectomized rats either before or after the administration of naloxone. These data show that, as for oxytocin release from the neurohypophysis into the systemic circulation, the mechanisms which regulate oxytocin release into the portal vessel blood can also be made morphine dependent. The lack of effect of morphine or naloxone on the release of CRF-41 or other stress neurohormones suggests that the effect of opiate dependence and withdrawal is selective for oxytocin and is not simply a non-specific response to 'stress'. Journal of Endocrinology (1990) 124, 141–150

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43

Karbownik, Agnieszka, Danuta Szkutnik-Fiedler, Tomasz Grabowski, Anna Wolc, Joanna Stanisławiak-Rudowicz, Radosław Jaźwiec, Edmund Grześkowiak, and Edyta Szałek. "Pharmacokinetic Drug Interaction Study of Sorafenib and Morphine in Rats." Pharmaceutics 13, no. 12 (December 16, 2021): 2172. http://dx.doi.org/10.3390/pharmaceutics13122172.

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A combination of the tyrosine kinase inhibitor—sorafenib—and the opioid analgesic—morphine—can be found in the treatment of cancer patients. Since both are substrates of P-glycoprotein (P-gp), and sorafenib is also an inhibitor of P-gp, their co-administration may affect their pharmacokinetics, and thus the safety and efficacy of cancer therapy. Therefore, the aim of this study was to evaluate the potential pharmacokinetic drug–drug interactions between sorafenib and morphine using an animal model. The rats were divided into three groups that Received: sorafenib and morphine (ISOR+MF), sorafenib (IISOR), and morphine (IIIMF). Morphine caused a significant increase in maximum plasma concentrations (Cmax) and the area under the plasma concentration–time curves (AUC0–t, and AUC0–∞) of sorafenib by 108.3 (p = 0.003), 55.9 (p = 0.0115), and 62.7% (p = 0.0115), respectively. Also, the Cmax and AUC0–t of its active metabolite—sorafenib N-oxide—was significantly increased in the presence of morphine (p = 0.0022 and p = 0.0268, respectively). Sorafenib, in turn, caused a significant increase in the Cmax of morphine (by 0.5-fold, p = 0.0018). Moreover, in the presence of sorafenib the Cmax, AUC0–t, and AUC0–∞ of the morphine metabolite M3G increased by 112.62 (p < 0.0001), 46.82 (p = 0.0124), and 46.78% (p = 0.0121), respectively. Observed changes in sorafenib and morphine may be of clinical significance. The increased exposure to both drugs may improve the response to therapy in cancer patients, but on the other hand, increase the risk of adverse effects.

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44

TANČIN, VLADIMIR, WOLF-DIETER KRAETZL, and DIETER SCHAMS. "Effects of morphine and naloxone on the release of oxytocin and on milk ejection in dairy cows." Journal of Dairy Research 67, no. 1 (February 2000): 13–20. http://dx.doi.org/10.1017/s0022029999003945.

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The aim of this study was to investigate the action of opioids (the μ receptor agonist morphine) and the antagonist naloxone on inhibition of oxytocin release and milk let-down in response to milking in dairy cows. In the first experiment, cows were injected with 0, 21, 70 and 210 mg morphine 10 min before milking on four successive days. Plasma oxytocin levels after 1 min manual stimulation of the udder were reduced by 70 and 210 mg morphine, and milk let-down was inhibited at the latter dose. In the second experiment, cows were injected after a control milking with 210 mg morphine (or 350 mg at 10 min before milking the following day if not effective) to inhibit milk flow. On the following day the inhibiting dose of morphine was given with 210 mg naloxone. Naloxone injection given before morphine had no effect on plasma oxytocin concentrations, but abolished the inhibition of oxytocin release by morphine and potentiated oxytocin release in response to milking. Naloxone alone injected the day after control milking increased oxytocin levels during milking, suggesting involvement of the opioid system in milking. A model has been developed for the control of opioid effects during milking. Morphine suppressed oxytocin release during milking in a dose-dependent manner and the effect was reversible by naloxone.

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45

Somogyi, A. A., R. L. Nation, C. Olweny, J. Cleary, P. Tsirgiotis, R. W. Milne, C. van Crugten, and F. Bochner. "Plasma concentrations and renal clearances of morphine-6- and morphine-3-glucuronide in cancer patients receiving morphine." Pain 41 (January 1990): S193. http://dx.doi.org/10.1016/0304-3959(90)92523-s.

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46

Curley, Taylor L., Douglas H. Thamm, Sam W. Johnson, and Pedro Boscan. "Effects of morphine on histamine release from two cell lines of canine mast cell tumor and on plasma histamine concentrations in dogs with cutaneous mast cell tumor." American Journal of Veterinary Research 82, no. 12 (December 2021): 1013–18. http://dx.doi.org/10.2460/ajvr.20.08.0137.

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Abstract OBJECTIVE To determine the effects of morphine on histamine release from 2 canine mast cell tumor (MCT) cell lines and on plasma histamine concentrations in dogs with cutaneous MCTs. ANIMALS 10 dogs with cutaneous MCT and 10 dogs with soft tissue sarcoma (STS). PROCEDURES The study consisted of 2 phases. First, 2 canine MCT cell lines were exposed to 3 pharmacologically relevant morphine concentrations, and histamine concentrations were determined by an ELISA. Second, dogs with MCT or STS received 0.5 mg of morphine/kg, IM, before surgery for tumor excision. Clinical signs, respiratory rate, heart rate, arterial blood pressure, rectal temperature, and plasma histamine concentrations were recorded before and 5, 15, 30, and 60 minutes after morphine administration but prior to surgery. Data were compared by use of a 2-way ANOVA with the Sidak multiple comparisons test. RESULTS In the first phase, canine MCT cell lines did not release histamine when exposed to pharmacologically relevant morphine concentrations. In the second phase, no differences were noted for heart rate, arterial blood pressure, and rectal temperature between MCT and STS groups. Plasma histamine concentrations did not significantly differ over time within groups and between groups. CONCLUSIONS AND CLINICAL RELEVANCE No significant changes in histamine concentrations were noted for both in vitro and in vivo study phases, and no hemodynamic changes were noted for the in vivo study phase. These preliminary results suggested that morphine may be used safely in some dogs with MCT.

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Hand, C. W., R. A. Moore, and J. W. Sear. "Comparison of Whole Blood and Plasma Morphine." Journal of Analytical Toxicology 12, no. 4 (July 1, 1988): 234–35. http://dx.doi.org/10.1093/jat/12.4.234.

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Nordberg, G., L. Borg, T. Hedner, and T. Mellstrand. "CSF and plasma pharmacokinetics of intramuscular morphine." European Journal of Clinical Pharmacology 27, no. 6 (1985): 677–81. http://dx.doi.org/10.1007/bf00547048.

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49

Hammoud, Hala Abou, Guy Aymard, Philippe Lechat, Nicolas Boccheciampe, Bruno Riou, and Frédéric Aubrun. "Relationships between plasma concentrations of morphine, morphine-3-glucuronide, morphine-6-glucuronide, and intravenous morphine titration outcomes in the postoperative period." Fundamental & Clinical Pharmacology 25, no. 4 (September 6, 2010): 518–27. http://dx.doi.org/10.1111/j.1472-8206.2010.00867.x.

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50

Portenoy, Russell K., Kathleen M. Foley, James Stulman, Elizabeth Khan, Jean Adelhardt, Mary Layman, Daniel F. Cerbone, and Charles E. Inturrisi. "Plasma morphine and morphine-6-glucuronide during chronic morphine therapy for cancer pain: plasma profiles, steady-state concentrations and the consequences of renal failure." Pain 47, no. 1 (October 1991): 13–19. http://dx.doi.org/10.1016/0304-3959(91)90005-i.

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Journal articles on the topic 'Plasma morphine'

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