PubMed · 11644888
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Margaret Mary O'Connor. 1996. Nurses and euthanasia -- some issues.. https://pubmed.ncbi.nlm.nih.gov/11644888/
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A method for the determination of the synthetic narcotic analgesic piritramide in human serum utilizing high-performance liquid chromatography with atmospheric pressure chemical ionization two-stage mass spectrometry (HPLC-APCI-MS-MS) is presented. Pipamperone is used as the internal standard. Serum samples are prepared by liquid-liquid extraction under basic conditions with 1-chlorobutane. The chromatographic separation is achieved on an RP-18 stationary phase applying gradient elution with methanol-0.02% trifluoroacetic acid in water. Detection is carried out in the MS-MS single reaction monitoring mode of the ion-trap mass spectrometer. The limit of detection is 0.3 ng/ml and the calibration covers the range of 1-80 ng/ml. The intra-day RSDs are 6.1 to 7.3% over the calibration range, whereas the inter-day RSDs are 9.6 to 12.8%.
To establish pharmacokinetic/pharmacodynamic relationships, a selective and specific high-performance liquid chromatographic method was developed for the quantitation of remifentanil and its metabolite in dog plasma. The assay involves a solid-phase extraction and a reversed-phase chromatographic separation with ultraviolet detection (lambda=210 nm). The calibration curves are linear in the range of 7.89-1500 ng ml(-1). Intra-day assay variability is less than 7% for all standards evaluated. Good recovery, linearity, accuracy, and precision were achieved with the assay that proved readily applicable to pharmacokinetic studies in dogs.
Chronic cocaine administration produces alterations in mu and kappa opioid receptor density as well as striatal and accumbens opioid-regulated adenylyl cyclase activity, suggesting a psychostimulant responsive interaction between opioidergic and dopaminergic systems. Stimulation of G-protein-coupled opioid receptors inhibits adenylyl cyclase production of cyclic AMP. The present study employed in situ [(35)S]GTPgammaS binding to measure opioid receptor-stimulated activation of G-proteins in response to acute and chronic cocaine exposure. Male Fischer rats received acute (1 or 3 days) or chronic (14 days) binge pattern cocaine administration. Three and 14 days of cocaine injections resulted in greater increases in the ability of the mu receptor agonist DAMGO to stimulate [(35)S]GTPgammaS binding in both the core and the shell of the nucleus accumbens, all regions of the caudate putamen and the cingulate cortex compared with saline-matched controls. The greatest increases in DAMGO-stimulated [(35)S]GTPgammaS binding were observed in the dorsal areas of the caudate putamen in animals that received 14 days of cocaine. No significant changes in delta (DPDPE), or kappa (dynorphin A(1-17)) receptor-stimulated [(35)S]GTPgammaS binding were found in any brain region in response to cocaine administration. These results demonstrate that binge pattern cocaine administration induce changes in mu but not delta or kappa opioid receptor-mediated G-protein activity. This study provides support for the hypothesis that the addictive properties of both psychostimulants and opiates may share common neurochemical signaling substrates.