Готові списки джерел за темами / Plasma morphine

Добірка наукової літератури з теми "Plasma morphine"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "Plasma morphine"

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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Дисертації з теми "Plasma morphine"

Athanasos, Peter. "Opioid maintained subjects and the effects of high dose morphine and adjuvant analgesics." Thesis, 2013. http://hdl.handle.net/2440/83272.

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Research has shown that maintenance on methadone and buprenorphine for the treatment of opioid addiction can produce the effects of hyperalgesia. This presents difficulties in the management of moderate to severe acute pain in this population. The situation is complicated by a dearth of evidence-based guidelines for pain management. The main aims of the four studies described in this thesis were to examine whether very high intravenous morphine doses alone (55.2 mg)(targeting plasma morphine concentrations of 180 ng/ml), or in combination with ketorolac (185.4 mg)(targeting plasma ketorolac concentrations of 4000 ng/ml), tramadol (229 mg)(targeting plasma tramadol concentrations of 1000 ng/ml) or S(+)-Ketamine (S-ketamine) (14.5 mg)(targeting plasma S-ketamine concentrations of 60 ng/ml) (opioid adjuvants) produced antinociception or respiratory effects in methadone maintained subjects (methadone subjects) and buprenorphine maintained subjects (buprenorphine subjects). The antinociceptive tests of the cold pressor and electrical stimulation were utilised. The effects of different maintenance doses of methadone and buprenorphine were also examined. Methadone maintained subjects were stratified into once daily dose groups of 11-45 (n=6), 46-80 (n=6) and 81-115 (n=6) mg per day. Buprenorphine maintained subjects were stratified into once daily dose groups of 2 to 8 (n=4), 9 to 15 (n=4) and 16-22 (n=4) mg per day. A healthy control group was administered lower doses of morphine alone (11.95 mg), and with adjuvants. The same doses of adjuvants were used in each instance. In the first study high dose morphine failed to provide antinociception for the methadone subjects. High dose morphine significantly decreased respiration rate, but only by an average of 2 breaths per minute. Methadone subjects were hyperalgesic in the cold pressor test. There were no differences in the antinociceptive responses of the different stratified methadone groups to the high dose morphine. Methadone subjects maintained on the highest doses had the highest respiratory depression. In the second study buprenorphine subjects performed similarly to methadone subjects in at least three respects: firstly, high dose morphine had little antinociceptive effect; secondly, this dose significantly decreased respiration rate; and thirdly, buprenorphine and methadone subjects were similarly hyperalgesic in the cold pressor test. There were also no differences in the antinociceptive responses of the different buprenorphine groups to the high dose morphine. In the third study tramadol and ketorolac, when combined with high dose morphine, failed to provide antinociception in either the cold pressor or electrical stimulation tests to methadone subjects. The combination of S-ketamine and high dose morphine provided statistically but not clinically significant improvement in antinociception in the cold pressor test. In the fourth study ketorolac and high dose morphine did not provide antinociception in buprenorphine maintained subjects. While the combinations of S-ketamine or tramadol and high dose morphine provided statistically significant antinociception for buprenorphine maintained subjects in the cold pressor test, it was not clear whether this change represented a clinically significant improvement. High dose morphine alone, or combined with opioid adjuvants at these concentrations is unlikely to provide pain relief in this population. The use of higher concentrations of adjuvants in combination with high dose morphine needs to be further evaluated. Other strategies should also be explored that may provide effective pain relief in patients maintained on opioids for the treatment of opioid dependence.
Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2013

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Vošahlíková, Miroslava. "Modulační vliv monovalentních iontů na δ-opioidní receptory". Doctoral thesis, 2014. http://www.nusl.cz/ntk/nusl-342333.

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The exact role of opioid receptors in drug addiction and modulatory mechanism of action of monovalent cations on these receptors are still not fully understood. Our results support the view that the mechanism of addiction to morphine is primarily based on desensitization of μ- and δ-opioid receptors. Desenzitization of agonist response proceeds already at the level of G protein functional activity. Long-term exposure of rats to morphine resulted in increase of number of δ-opioid receptors and change of their sensitivity to sodium ions. Analysis of the effect of different monovalent ions on agonist binding in δ-OR- Gi1α (Cys351 -Ile351 )-HEK293 cell line confirmed the preferential sensitivity of δ-opioid receptor to sodium ions. We have distinguished the high- and low-affinity Na+ sites. Biophysical analysis of interaction of lithium, sodium, potassium and cesium ions with plasma membranes isolated from HEK293 cells with the help of fluorescent probes indicated that monovalent ions interact, in low-affinity manner, with the polar, membrane-water interface of membrane bilayer. Key words: morphine, forebrain cortex, opioid receptors, G proteins, monovalent ions, plasma membrane, fluorescence spectroscopy.

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Ujčíková, Hana. "Morfiem navozené změny membránových a solubilních bílkovin frontální mozkové kůry potkana." Doctoral thesis, 2014. http://www.nusl.cz/ntk/nusl-342324.

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The aim of this Ph.D. thesis was to analyze the morphine-induced changes of frontal brain cortex protein composition in rats exposed to increasing doses of morphine (10-50 mg/kg) for prolonged period of time (10 days). The first part of this work was oriented to the analysis of the phenomenon of hypersensitization/superactivation of adenylyl cyclase (AC), which is regarded as one of the crucial molecular mechanisms causing drastic pathological consequences of drug addiction. The increase of AC activity represents a "compensatory" response and is functionally related to the desensitization of G protein response to prolonged morphine exposure of target cells. The clear desensitization of µ-OR- and δ-OR-stimulated G protein response by morphine was demonstrated in our laboratory by analysis of the dose-response curves of DAMGO and DADLE-stimulated, high-affinity [35 S] GTPγS binding in plasma membranes isolated from frontal brain cortex of rats exposed to morphine according to the same protocol as that used in my Ph.D. thesis (10-50 mg/kg, 10 days). The κ-OR-stimulated [35 S] GTPγS binding was unchanged. It has been determined the amount of all AC isoforms (AC I-IX) in plasma membranes (PM) isolated from control and morphine-treated rats which were sacrificed 24 hours since the last dose of morphine....

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Книги з теми "Plasma morphine"

Dodds, Chris, Chandra M. Kumar, and Frédérique Servin. Anaesthetic pharmacology in the elderly. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198735571.003.0003.

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The importance of the changes and variability in pharmacology with ageing and the risks these pose in the elderly are emphasized. Detailed descriptions are given of the pharmacokinetic aspects of distribution, initial volume of distribution, and plasma binding; elimination affected by hepatic and renal clearance changes; and effect site variability. The pharmacodynamics changes are then reviewed. Specific anaesthetic agents are then described, covering the induction agents thiopentone, propofol, etomidate, ketamine, and midazolam. The volatile anaesthetics sevoflurane and desflurane, and nitrous oxide are discussed. The opioid analgesics fentanyl, alfentanil, sufentanil, and remifentanil are described followed by the opiate morphine. The much slower onset and offset of muscle relaxants in the elderly is explained, and the differences between steroid and benzylisoquinolinium compounds are described. Finally, the reversal agents, including sugammadex, are reviewed.

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Частини книг з теми "Plasma morphine"

Dahn, Tim, Josh Gunn, Scott Kriger, and Andrea R. Terrell. "Quantitation of Morphine, Codeine, Hydrocodone, Hydromorphone, Oxycodone, Oxymorphone, and 6-Monoacetylmorphine (6-MAM) in Urine, Blood, Serum, or Plasma Using Liquid Chromatography with Tandem Mass Spectrometry Detection." In Methods in Molecular Biology, 411–22. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-459-3_40.

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Park, Gilbert, and Maire P. Shelly. "Sedation and analgesia in the critically ill." In Oxford Textbook of Medicine, 3153–57. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.1707.

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Nearly all critically ill patients need analgesia, anxiolysis, hypnosis, or measures to help them tolerate their tracheal tube. Although making the patient unconscious may appear the easiest way to achieve this, it is fraught with hazards. Pain relief and tube tolerance—these are the first priority, and usually involves giving opioids. Morphine, which has both analgesic and sedative effects, is the opioid against which others are judged. Remifentanil is a relatively new agent that has properties useful in critically ill patients: fast onset of action, a predictable short half-life (10–21 min), and it is broken down by a nonspecific enzyme system present in plasma such that accumulation does not occur, and the drug wears off rapidly, even after prolonged infusions and in renal or hepatic failure....

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Тези доповідей конференцій з теми "Plasma morphine"

Nielsen, T. H., H. K. Nielsen, S. E. Husted, S. L. Hansen, and K. H. Olsen. "PLATELET FUNCTION AND ENDOCRINE STRESS RESPONSE DURING BUPIVACAINE EPIDURAL ANALGESIA. THE EFFECT OF MORPHINE ADDITION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644887.

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Platelet aggregation plays a central role in thromboembolism. Epidural analgesia can diminish the formation of deep venous thrombosis. In a randomized study twenty patients admitted to transartliroscopic meniscectomy were allocated to epidural analgesia with or without morphine epidurally. S-cortisol, s-thromboxane -B2(s-T2 B2) and platelet aggregation were measured before premedication, when epidural block extended from S3to T5, just before skin closure and exsufflation of tne thigh tourniquet, and the last sample was taken ten min after exsufflation. Aggregability was measured in platelet-rich plasma and expressed as the treshold concentration of collagen. Cortisol and T Bp were measured by RIA.S-cortisol decreased duringxanalgesia in the morphine group (p<o.o5), and during operation in both groups (p<o.o5) being significant lower in the morphine group (p<o.o5).S-TxB2 decreased significantly in the morphine group during analgesia, but there was no significant difference in s-TxB2 between the two groups. Treshold concentration of Collagen for aggregation of platelets showed an insignificant increase for both groups during analgesia, but did not differ between the two groups. Removal of the tourniquet did not influence any of the measurements. It is concluded that additionof morphine to bupivaca- ine epidural analgesia further decrease activity of the adrenocortical system, and the combined regime seems to inhibit platelet function in the same manner as monotherapy with local anaesthetics.

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NAKASHIMA, K., Y. OGATA, MN NAKASHIMA, and M. WADA. "HPLC WITH FLUORESCENCE DETECTION OF MORPHINE IN RAT PLASMA USING 4-(4,5-DIPHENYL-1H-IMIDAZOL-2-YL)BENZOYL CHLORIDE AS A LABEL." In Proceedings of the 13th International Symposium. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702203_0060.

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Arena, Maurizio, Matteo Chiatto, Francesco Amoroso, Rosario Pecora, and Luigi de Luca. "Feasibility studies for the installation of Plasma Synthetic Jet Actuators on the skin of a morphing wing flap." In Active and Passive Smart Structures and Integrated Systems XII, edited by Alper Erturk. SPIE, 2018. http://dx.doi.org/10.1117/12.2300512.

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Wang, Xiang, Rinze Benedictus, and Roger M. Groves. "Plasmon resonance spectral peak shift due to morphing of gold nanoparticles for strain sensing." In Optical Sensing and Detection VII, edited by Francis Berghmans and Ioanna Zergioti. SPIE, 2022. http://dx.doi.org/10.1117/12.2619170.

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Clark, Robert A., Nicholas Plewacki, Pritheesh Gnanaselvam, Jeffrey P. Bons, and Vaishak Viswanathan. "The Effect of Thermal Barrier Coating Surface Temperature on the Adhesion Behavior of CMAS Deposits." In ASME Turbo Expo 2020: Turbomachinery Technical Conference and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/gt2020-15544.

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Abstract The interaction of thermal barrier coating’s surface temperature with CMAS (calcium magnesium aluminosilicate) like deposits in gas turbine hot flowpath hardware is investigated. Small Hastelloy X coupons were coated in TBC using the air plasma spray (APS) method and then subjected to a thermal gradient via back-side impingement cooling and front-side impingement heating using the High Temperature Deposition Facility (HTDF) at The Ohio State University (OSU). A 1-D heat transfer model was used to estimate TBC surface temperatures and correlate them to intensity values taken from infrared (IR) images of the TBC surface. TBC frontside surface temperatures were varied by changing back-side mass flow (kept at a constant temperature), while maintaining a constant hot-side gas temperature and jet velocity representative of modern commercial turbofan high-pressure turbine (HPT) inlet conditions (approximately 1600K and 200 m/s, or Mach 0.25). In this study, Arizona Road Dust (ARD) was utilized to mimic the behavior of CMAS attack on TBCs. To identify the minimum temperature at which particles adhere, the back-side cooling mass flow was set to the maximum amount allowed by the test setup, and trace amounts of 0–10 μm ARD particles were injected into the hot-side flow to impinge on the TBC surface. The TBC surface temperature was increased through coolant reduction until noticeable deposits formed, as evaluated through an IR camera. Accelerated deposition tests were then performed where approximately 1 gram of ARD was injected into the hot side flow while the TBC surface temperature was held at various points above the minimum observed deposition temperature. Surface deposition on the TBC coupons was evaluated using an infrared camera and a backside thermocouple. Coupon cross sections were also evaluated under a scanning electron microscope for any potential CMAS ingress into the TBC. Experimental results of the impact of surface temperature on CMAS deposition and deposit evolution and morphology are presented. In addition, an Eulerian-Lagrangian solver was used to model the hot-side impinging jet with particles at four TBC surface temperatures and deposition was predicted using the OSU Deposition model. Comparisons to experimental results highlight the need for more sophisticated modeling of deposit development through conjugate heat transfer and mesh morphing of the target surface. These results can be used to improve physics-based deposition models by providing valuable data relative to CMAS deposition characteristics on TBC surfaces, which modern commercial turbofan high pressure turbines use almost exclusively.

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Звіти організацій з теми "Plasma morphine"

Thomas, Thommey P., Baohua Huang, Ankur Desai, Hong Zong, Xue-Min Cheng, Alina Kotlyar, Pascale R. Leroueil, et al. Plasma-Mediated Release of Morphine from Synthesized Prodrugs. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada577469.

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