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Morphine in blood

Spiehler, V., Brown, R., Unconjugated Morphine in Blood by radioimmunoassay and gas chroma-tography/mass spectrometry, J. Forensic Sci., 32, 906, 1987. [Pg.117]

Klein L, Ailes N, Fackelman G E 1989 Postanesthetic equine myopathy suggestive of malignant hyperthermia. A case report. Veterinary Surgery 18 479-482 Kollias-Baker C, Sams R 2002 Detection of morphine in blood and urine samples from horses administered poppy seeds and morphine sulfate orally. Journal of Analytical Toxicology 26 81-86... [Pg.304]

Anders and Mannering introduced on-column derivatization of morphine with propionic anhydride and obtained only one peak. They believed that it was dipropionylmorphine. Von Meyer et al. made use of the same derivatization reaction for the quantitative determination of morphine in blood, but they found that the monopropionyl derivatives of morphine and nalorphine (used as an internal standard) were found in the proportion 99 1, as compared with the... [Pg.124]

V Spiehler, et al. Unconjugated morphine in blood by radioimmunoassay and gas chromatography mass spectrometry. J Forensic Sci 32 906, 1987. [Pg.313]

A person ingests a morphine overdose. The half-life of morphine in blood is about 3.0 h. If the blood plasma concentration 5.0 h after ingestion was 6.0 mg dm of blood, estimate the peak concentration of morphine at the time of ingestion. [Pg.425]

Instrument qualification. This step is a means of measuring an instrument s quality and ensures that we have consistent instrument performance. This is of prime importance in forensic science analyses because we need to be sure that the results that we are reporting are consistent. For example, consider that we have obtained a value for the presence of morphine in blood that is indicative of a lethal concentration later that day, we run the sample again, on the same instrument, and find that the value we have determined on this occasion is half that of the original. This is a very extreme scenario nonetheless, we must be able to show that the instrument we are using for our analyses will give us the same results each time we carry out the work (an acceptable level of error will usually be associated with the value that we report and be outlined in an SOP). A number of steps are involved in instrument qualification design qualification (DQ), operation qualification (OQ), and performance qualification (PQ) these are explained in Chapter 8. [Pg.181]

Several examples of the applications of polarography in these fields have been already mentioned in Chapters VI and VII, viz. determinations of benzene, toluene, naphthalene and phenols in the atmosphere, breath, blood or urine, of amino acids (with particular interest to tyrosine, tryptophane, phenylalanine, histidine and histamine), of ketoacids, ketosteroids, carbon disulphide in air and blood, ethanol, acetoin, sugars and morphine in blood, of lactic acid, mandelic acid in bile and urine, adrenaline and thyroxine in iodinated proteins and last, but not least, of thiol compounds, both soluble and bound in biological materials. A few further examples will be given here. [Pg.192]

When an analyte is fluorescent, direct fluorometric detection is possible by means of a spectrofluorometer operating at appropriate excitation and observation wavelengths. This is the case for aromatic hydrocarbons (e.g. in crude oils), proteins (e.g. in blood serum, in cow milk), some drugs (e.g. morphine), chlorophylls, etc. Numerous fields of applications have been reported analysis of air and water pollutants, oils, foods, drugs monitoring of industrial processes monitoring of species of clinical relevance criminology etc. [Pg.15]

Lee H-M, Lee C-W. 1991. Determination of morphine and codeine in blood and bile by gas chromatography with a derivatization procedure. J Anal Toxicol 15 182. [Pg.15]

In retrospect, the reason for this is not all that obscure. Most of the soldiers were in hypo-volaemic shock with low blood pressure, low blood volume, and as part of the shock syndrome, systemic circulation was minimal with intense vasoconstriction - hence the poor therapeutic effect. The repeated doses of morphine were usually given intramuscularly into the buttock or thigh but their clearance into the systemic circulation was minimal until resuscitation occurred and the peripheral circulation was restored. Blood flow to the muscle increased and all the morphine injected became available - all at once. This was the reason for the morphine overdoses and the occasional death. Thereafter it has become standard practice to give morphine in emergency directly into the veins and not into poorly perfused muscles. [Pg.154]

In hypotensive states, more fall in blood pressure occurs due to morphine. [Pg.78]

Nearly all opioids induce bradycardia (Bowdle, 1998), most likely mediated via central stimulation of the vagus nerve. Cardiovascular depression associated with most opioids is moderate and only the stronger opioids of the fentanyl group induce a more severe effect. Morphine and some of its analogs induce a non-opioid receptor-mediated release of histamine, which can result in a decrease in blood pressure and compensatory... [Pg.144]

Pereira et al. (1993) evaluated postoperative pain relief and incidence of side-effects of the combination of epidural morphine (0.5 mg) and sublingual nifedipine (10 mg). In this double-blind, placebo-controlled study 36 women were submitted to elective operations (hysterectomy and colpoperineoplasty). The nifedipine-treated group showed a significant drop in blood pressure which was controlled by rehydration. The results indicate that epidural morphine-induced postoperative pain relief may be enhanced by systemic administration of nifedipine with easily controlled side-effects. [Pg.370]

The metabolic effects of morphine are not marked and are clinically unimportant. The metaholic rale may be decreased slightly due to the lowered activity and tone of the skeletal muscles resulting front the central depression. A rise in blood sugar may be observed after the injection of... [Pg.1041]

M3G is the predominant metabolite in young children. The total body morphine clearance is 80% of an adult at 6 months of age.23 When the brains of experimental animals are directly injected with M3G, neuroexcitatory and anti-analgesic responses result, although this does not happen after system administration. Nonetheless, small amounts of M3G do cross the blood-brain barrier, and this may account for some reports of neuroexcitatory responses to morphine in humans. Attempts at correlating M3G plasma concentrations or M3G morphine or M3G M6G concentration ratios with the clinical activity of M3G have sometimes been successful, and sometimes not. To date, there are only two published studies describing the effects of injecting M3G directly into humans both studies yielded equivocal results.24... [Pg.52]

D. L. Allen, K. S. Scott and J. S. Oliver, Comparison of sohd-phase extraction and supercritical fluid extraction for the analysis of morphine in whole blood , J. Anal. Toxicol. 23 216-218 (1999). [Pg.300]

He YJ, Brockmoller J, Schmidt H, Roots I, Kirchheiner J (2008) CYP2D6 ultrarapid metabolism and morphine/codeine ratios in blood was it codeine or heroin J Anal Toxicol 32 178-182... [Pg.141]

Actions Meperidine causes a depression of respiration similar to that of morphine, but there is no significant cardiovascular action when the drug is given orally. On intravenous (IV) administration, meperidine produces a decrease in peripheral resistance and an increase in peripheral blood flow, and may cause an increase in cardiac rate. As with morphine, meperidine dilates cerebral vessels, increases cerebrospinal fluid pressure, and contracts smooth muscle (the latter to a lesser extent than does morphine). In the gastrointestinal tract, meperidine impedes motility, and chronic use results in constipation. Meperidine does not cause pinpoint pupils, but rather causes the pupils to dilate because of an atropine-like activity. [Pg.149]

Heroin [HAIR o in] does not occur naturally but is produced by acetylation of morphine, which leads to a three-fold increase in its potency. Its greater lipid solubility allows it to cross the blood-brain barrier more rapidly than morphine, causing a more exaggerated euphoria when the drug is taken by injection. Heroin is converted to morphine in the body, but lasts about half as long. It has no accepted medical use in the United States. [Pg.151]

Although buprenorphine [byou preh NOR feen] is classified as a partial agonist acting at the p receptor, it behaves like morphine in naive patients. However, it can also antagonize morphine. Buprenorphine is administered parenterally and has a long duration of action because of its tight binding to the receptor. It is metabolized by the liver and excreted in the bile and urine. Adverse effects include respiratory depression, decrease (or, rarely, increase) in blood pressure, nausea and dizziness. [Pg.152]


See other pages where Morphine in blood is mentioned: [Pg.281]    [Pg.425]    [Pg.208]    [Pg.281]    [Pg.425]    [Pg.208]    [Pg.486]    [Pg.408]    [Pg.263]    [Pg.907]    [Pg.89]    [Pg.14]    [Pg.1]    [Pg.233]    [Pg.325]    [Pg.42]    [Pg.131]    [Pg.186]    [Pg.51]    [Pg.53]    [Pg.424]    [Pg.464]    [Pg.213]    [Pg.570]    [Pg.209]    [Pg.378]    [Pg.112]    [Pg.237]    [Pg.152]    [Pg.550]    [Pg.552]    [Pg.4]    [Pg.50]    [Pg.173]   
See also in sourсe #XX -- [ Pg.118 , Pg.178 , Pg.192 ]




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Blood morphine

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