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Biomedical subjects

R M Swift

Publications and source records attributed to R M Swift.

12 recordsLinked to original sources
PubMed1992

The relationship between craving, anxiety, and other symptoms in opioid withdrawal.

Craving and anxiety share many similar attributes including comparable responses to pharmacological agents. To better characterize the relationship among craving, anxiety, and other opioid withdrawal signs and symptoms, we examined 32 opioid-dependent subjects undergoing clonidine-assisted opioid withdrawal. A 13-item analog scale measured subjective withdrawal symptoms. Statistical analyses of separate subscale items, using craving as the dependent variable, showed that the highest positive correlations occur for craving and anxiety. The high correlation between craving and anxiety suggests common mechanisms underlying both.

Anxiety↗
PubMed1992

Studies on a wearable, electronic, transdermal alcohol sensor.

The measurement of alcohol consumption over long time periods is important for monitoring treatment outcome and for research applications. Giner, Inc. has developed a wearable device that senses ethanol vapor at the surface of the skin, using an electrochemical cell that produces a continuous current signal proportional to ethanol concentration. A thermistor monitors continuous contact of the sensor with the skin, and a data-acquisition/logic circuit stores days of data recorded at 2- to 5-min intervals. Testing of this novel ethanol sensor/recorder was conducted on nonalcoholic human subjects consuming known quantities of ethanol and on intoxicated alcoholic subjects. The transdermal sensor signal closely follows the pattern of the blood alcohol concentration curve, although with a delay. This paper describes the concept of electrochemical ethanol measurement and presents some of the clinical data collected in support of the sensor/recorder development.

Adult↗
PubMed1992

Ethanol exposure results in a transient decrease in human platelet cAMP levels: evidence for a protein kinase C mediated process.

At concentrations between 2 and 32 mM, ethanol is shown to depress human platelet cAMP levels. The effect is biphasic, maximal at 30 sec, with platelet concentrations of cAMP returning to baseline values at higher ethanol concentrations and at longer incubation times. The cAMP lowering effect of ethanol can be blocked by a phosphodiesterase (PPDE) inhibitor, 3-isobutyl-1-methyl-xanthine (IBMX), at a concentration of 2 mM, suggesting that an increase in PPDE activity may be responsible for this effect. Exposure of platelets to 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7), a protein kinase C (PKC) inhibitor, blocks the ethanol-induced decrease in platelet cAMP, suggesting ethanol may be acting through activation of PKC.

Alcoholism↗
PubMed1991

Benzodiazepine requirements during alcohol withdrawal syndrome: clinical implications of using a standardized withdrawal scale.

An accurate characterization of the severity of the alcohol withdrawal syndrome is likely to provide clear guidelines for drug therapy in this disorder. We studied (retrospectively) the usefulness of a standardized withdrawal scale on benzodiazepine drug requirements for patients undergoing alcohol detoxification in a general hospital. One hundred thirty-three patients received the revised Clinical Institute withdrawal Assessment Scale for Alcohol and were medicated only if the score was greater than 10. A comparison group of 117 patients was treated without reference to the scale. The groups were evenly matched with respect to age, sex, concurrent drug use, and laboratory abnormalities. Subjects treated according to the scale required less benzodiazepine (median dose, 50 mg diazepam equivalent compared with 75 mg) (p = 0.04). Rates of complications, discharge against medical advice, and length of stay did not differ between the groups. Rank correlation coefficients revealed a closer relationship between the degree of alcohol exposure (as determined by admitting blood alcohol levels, creatine phosphokinase, and SGOT) and benzodiazepine requirements during withdrawal for the group treated with the scale. Findings suggest that when the scale is used, patients with a greater degree of physical dependence receive (appropriately) a higher dose of benzodiazepine and those with a lesser degree of dependence receive (appropriately) a lower dose of benzodiazepine. Use of the scale appears to minimize both under- and overdosing with benzodiazepine for alcohol withdrawal syndrome.

Administration, Oral↗
PubMed1990

Human leukocyte beta-adrenergic stimulated cyclic AMP in ethanol intoxication and withdrawal.

The effects of ethanol were examined on cyclic AMP production in intact human leukocytes in vitro. In leukocytes isolated from alcohol abstinent subjects, ethanol enhances isoproterenol-stimulated and prostaglandin E1-stimulated cyclic AMP formation. Without agonist, ethanol is able to stimulate cyclic AMP production at concentrations of 160 mM and above. Leukocytes isolated from subjects undergoing alcohol detoxification showed increases in basal levels of leukocyte cyclic AMP, in isoproterenol-stimulated cyclic AMP, and in ethanol-stimulated cyclic AMP on the 2nd or 3rd day of withdrawal in comparison to the first day of withdrawal and in comparison to abstinent subjects. The data suggest that increased beta-adrenergic activity seen in alcohol withdrawal may be in part due to an increased responsiveness of beta-adrenergic stimulated cyclic AMP in tissues.

Adrenergic beta-Agonists↗
PubMed1989

Altered methadone pharmacokinetics in pregnancy: implications for dosing.

Lower plasma methadone levels have been reported in pregnant women receiving methadone maintenance for heroin addiction. Methadone pharmacokinetics was examined in a 24-year-old woman 8 months pregnant with twins, who experienced severe withdrawal symptoms beginning 10-12 hours after her daily 30 mg methadone dose. Methadone plasma concentration-time data were fit to a one-compartment pharmacokinetic model by extended least-squares regression. Estimated half-life for methadone was 8.1 hours, which is much shorter than the usual methadone half-life (greater than 24 hours). Plasma methadone concentrations were estimated for the cases of a) increasing the 30 mg methadone dose by 50% and administering it once daily and b) continuing the 30 mg methadone dose but administering it at 12-hour intervals. Although the model is derived from a single subject, the simulations performed clearly suggest a need for altered methadone dosing in pregnancy. More sustained plasma methadone levels are achieved with twice-daily dosing of methadone than are achieved by administering an increased methadone dose once daily. Twice-daily dosing would be expected to produce fewer withdrawal symptoms and, ultimately, improved compliance with treatment.

Adult↗
PubMed1979

Morphine and endorphins modulate dopamine turnover in rat median eminence.

The is evidence that some of the actions of both endogenous and exogenous opioids (e.g., stimulation of prolactin release) are mediated by interaction with catecholaminergic systems. Morphine (1.67, 5, and 15 mg/kg of body weight, intraperitoneally) altered dopamine turnover as measured by the alpha-methyl-p-tyrosine method in the median eminence, neostriatum, and frontal cortex of male Sprague-Dawley rats. The turnover rate of dopamine was reduced in the median eminence and frontal cortex but accelerated in the neostriatum. In the frontal cortex all doses were effective in decreasing dopamine turnover; however, in the median eminence the lowest dose of morphine did not significantly alter dopamine turnover. All three doses accelerated dopamine turnover in the neostriatum. Naloxone effectively reversed the effects of morphine at all doses in all brain areas, whereas it had no effect on turnover when given alone. In the median eminence, neostriatum, and frontal cortex, intraventricular injection of [D-Ala2,D-Leu5]-enkephalin (25 micrograms) or beta-endorphin (15 micrograms) produced the same effects on dopamine turnover as morphine. The actions of these peptides were blocked by naloxone. It is hypothesized that opiates and opioid peptides increase prolactin release by reducing the activity of the tuberoinfundibular dopaminergic system.

Animals↗