bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enough! or too much. What is ‘excessive’ kava use in Arnhem Land?
Authors: CLOUGH ALAN 
Published: November 2003

AbstractThe objective of the study was to describe parameters for use in monitoring health, social and economic effects of kava use in Arnhem Land Aboriginal communities in the Northern Territory (NT). Kava has been used mainly in eight communities (population > 200), and in smaller associated homeland areas since 1982 with a total population of approximately 6800, using cross‐sectional description and comparison using data from three kava‐using communities. Interview data combined with health worker assessments were compiled using: (1) a sample (n = 136) aged 16–34 years in one community in 2001–02; (2) a sample (n = 101) aged 16 years and over in 2000 where physical assessments and biochemical and haematological data were also collected; (3) participant‐observation in one community (133 people aged 18 years and over) during 1989–91. Kava, supplied illegally, was still being used in Arnhem Land in 2001–02. In 2000 dermopathy characteristic of heavy use, abnormally low body mass index (BMI), low blood lymphocytes and abnormally high γ‐glutamyl transferase (GGT) occurred more frequently with increased kava use. These acute effects emerge at average consumption levels of from 310–440 g/week of kava powder. When kava users in one community began to consume it at an average of 240–425 g/week from mid‐1990, 19% of available cash resources were spent on kava with 11% of cash resources leaving the local community economy. The proportion of men drinking kava reached 70% and women 62% from mid‐1990, with 20% of the population spending unprecedented amounts of time (14 + hours/week) in activities where kava was consumed. These parameters may be useful to monitor kava's adverse health, social and economic effects. Their association with increased kava use suggests that approaches to minimizing harm from its abuse may begin fruitfully with controlling supply.
Comparison of disulfiram and placebo in treatment of alcohol dependence of adolescents
Authors: NIEDERHOFER HELMUT , STAFFEN WOLFGANG 
Published: November 2003

AbstractAbout 50% of alcoholic patients relapse within 3 months of treatment. Previous studies have suggested that disulfiram may help to prevent such relapse. The aim of our study was to assess the efficacy and safety of long‐term disulfiram treatment in alcohol dependence of adolescents. In this double‐blind, placebo‐controlled study we recruited 26 adolescents, aged 16–19 years, with chronic or episodic alcohol dependence. Patients were allocated treatment randomly with disulfiram (200 mg daily) or placebo for 90 days. Patients were assessed on the day treatment started and on days 30 and 90 by interview, self‐report, questionnaire and laboratory screening. Patients were classified as abstinent, relapsing or non‐attending. Time to first treatment failure (relapse or non‐attendance) was the primary outcome measure. The disulfiram (n = 13) and placebo (n= 13) groups were well matched in terms of baseline demographic and alcohol‐related variables. Thirteen disulfiram‐treated and 13 placebo‐treated patients completed the treatment phase; seven (1 vs. 6) relapsed, five (3 vs. 2) refused to continue treatment, three (1 vs. 2) had concurrent illness and two (1 vs. 1) had adverse side effects. At the end of treatment, seven disulfiram‐treated and two placebo‐treated patients had been abstinent continuously (p = 0.0063). Mean cumulative abstinence duration was significantly greater in the disulfiram group than in the placebo group [68.5 (SD 37.5) vs. 29.7 (19.0) days; p = 0.012]. Apart from occasional diarrhoea, there was no difference in side effects between groups. In some cases, disulfiram may be an effective and well‐tolerated pharmacological adjunct to psychosocial and behavioural treatment programmes for treatment of adolescent alcohol‐dependent patients.
A prototype screening instrument for cannabis use disorder: the Cannabis Use Disorders Identification Test (CUDIT) in an alcohol‐dependent clinical sample
Authors: ADAMSON SIMON J. , SELLMAN J. DOUGLAS 
Published: November 2003

AbstractThe Cannabis Use Disorders Identification Test (CUDIT) was used for the first time as part of a randomized controlled trial for brief interventions in mild to moderate alcohol‐dependent out‐patients. This sample may be seen as a population at increased risk of cannabis use disorder. The CUDIT was developed by modifying the Alcohol Use Disorders Identification Test (AUDIT). The ability of the CUDIT to accurately screen for cannabis abuse or dependence was examined in the portion of the sample who reported some cannabis use over the preceding 6 months (n = 53), as was self‐reported frequency of cannabis use in the preceding 6 months. The CUDIT was superior to the frequency measure, achieving positive predictive power of 84.6% and sensitivity of 73.3% at a cut‐off of 8, compared to positive predictive power of 81.8% and sensitivity of 60.0% for 80 or more cannabis use‐days. These results indicate the viability of a screening measure for identifying cannabis use disorder in at risk populations.
A systematic review of the effectiveness of brief interventions with substance using adolescents by type of drug
Authors: TAIT ROBERT J. , HULSE GARY K. 
Published: November 2003

AbstractThe aim of this paper is to evaluate the effectiveness of brief interventions (BI) with adolescents (mean age < 20) in reducing alcohol, tobacco or other drug (ATOD) use by means of a systematic review of BI for adolescent substance use in the English language literature up to 2002. We identified 11 studies involving 3734 adolescents. Follow‐up ranged from 6 weeks to 24 months. Motivational interviewing was the predominant approach, underpinning eight studies: the remaining three provided personalized health information. Seven papers reported outcomes for alcohol interventions and four involved other substances (including one with separate alcohol outcomes). The overall effect size was d= 0.126 with borderline homogeneity (Q = 14.9, df = 9, p = 0.09). The effect size from the eight alcohol interventions (n = 1075) was classified as significant but “small” (d = 0.275). The remaining non‐alcohol studies were considered separately as interventions involving tobacco or multiple substance use. The two interventions with tobacco involved a substantial sample (n = 2626) but had a very small effect (d = 0.037), while the two interventions addressing multiple substances involved few participants (n = 110) but had a medium — large effect (d = 0.78). Across a diverse range of settings (dental clinic, schools, universities, substance treatment centres) and, therefore, probably diverse clients, BI conferred benefits to adolescent substance users. BI had a small effect on alcohol consumption and related measures. The data for tobacco interventions suggested a very small reduction, particularly with general community interventions. The effect of BI with multiple substances appears substantial but the small sample cautions against expansive generalization.
Groin tissue necrosis requiring skin graft following parenteral abuse of buprenorphine tablets
Authors: FEENEY G. F. X. , FAIRWEATHER P. 
Published: November 2003

AbstractIn May 2002 Buprenorphine (Subutex®) was listed on the Australian Pharmaceutical Benefits Schedule for treatment in opioid dependence. In addition to broadening treatment options, buprenorphine has the advantage of an improved safety profile. The risk of overdose is lessened but other risks remain due to diversion. French experience reports widespread deviation of buprenorphine sublingual tablets to intravenous injection. We report a case of attempted parenteral administration of buprenorphine tablets. Stringent protocols for dispensing are appropriate.
Human Chest Wall Function while Awake and during Halothane Anesthesia
Authors: Warner David O. , Warner Mark A. 
Published: November 2003

Background
Changes in the distribution of respiratory drive to different respiratory muscles may contribute to respiratory depression produced by halothane. The aim of this study was to examine factors that are responsible for halothane-induced depression of the ventilatory response to carbon dioxide rebreathing.

Methods
In six human subjects, respiratory muscle activity in the parasternal intercostal, abdominal, and diaphragm muscles was measured using fine-wire electromyography electrodes. Chest wall motion was determined by respiratory impedance plethysmography. Electromyography activities and chest wall motion were measured during hyperpnea produced by carbon dioxide rebreathing while the subjects were awake and during 1 MAC halothane anesthesia.

Results
Halothane anesthesia significantly reduced the slope of the response of expiratory minute ventilation to carbon dioxide (from 2.88 +/- 0.73 (mean +/- SE) to 2.01 +/- 0.45 l.min-1.mmHg-1). During the rebreathing period, breathing frequency significantly increased while awake (from 10.3 +/- 1.4 to 19.7 +/- 2.6 min-1, P < 0.05) and significantly decreased while anesthetized (from 28.8 +/- 3.9 to 21.7 +/- 1.9 min-1, P < 0.05). Increases in respiratory drive to the phrenic motoneurons produced by rebreathing, as estimated by the diaphragm electromyogram, were enhanced by anesthesia. Anesthesia attenuated the response of parasternal electromyography and accentuated the response of the transversus abdominis electromyography to rebreathing. The compartmental response of the ribcage to rebreathing was significantly decreased by anesthesia (from 1.83 +/- 0.58 to 0.48 +/- 0.13 l.min-1.mmHg-1), and marked phase shifts between ribcage and abdominal motion developed in some subjects. However, at comparable tidal volumes, the ribcage contribution to ventilation was similar while awake and anesthetized in four of the six subjects.

Conclusions
Halothane anesthesia enhances the rebreathing response of neural drive to the primary respiratory muscle, the diaphragm. These findings provide direct evidence that, at the dose examined in this study, halothane-induced respiratory depression is caused by alterations in the distribution and timing of neural drive to the respiratory muscles, rather than a global depression of respiratory motoneuron drive.
Quantitative Assessment of Differential Sensory Nerve Block after Lidocaine Spinal Anesthesia
Authors: Liu Spencer , Kopacz Dan J. , Carpenter Randall L. 
Published: November 2003

Background
Recent technology allows for quantitative and selective measurement of A beta, A delta, and C fiber nerve transmission. To gain further insight into the physiology of differential block after lidocaine spinal anesthesia, the function of these different fibers was quantitatively measured over time, and these measurements were correlated with regression of anesthesia to pinprick, touch, cold, and tolerance of tetanic electrical current (equivalent to surgical incision).

Methods
Six volunteers received lidocaine spinal anesthesia with 50 mg lidocaine (5% in dextrose). Cutaneous current perception thresholds at 2,000, 250, and 5 Hz, which stimulate A beta, A delta, and C fibers, respectively, were determined at L2-L3 (medial aspect above knee) before and every 10 min after spinal anesthesia. Dermatomal levels to pinprick, touch, and cold were assessed every 5 min after spinal anesthesia. Tolerance to tetanic electrical stimulus was assessed at L2-L3 every 10 min after spinal anesthesia.

Results
Differential block was demonstrated by the sequential return of sensation to touch, pinprick, and cold at L2-L3. Recovery of function of A beta, A delta, and C fibers correlated with return of sensation to touch (R2 = 0.7, p = 0.03), pinprick (R2 = 0.75, p = 0.02), and cold (R2 = 0.67, p = 0.04) respectively. Loss of tolerance of surgical anesthesia corresponded to return of A beta current perception thresholds to baseline, whereas current perception thresholds for A delta and C fibers were still increased to greater than baseline (p = 0.025).

Conclusions
Differential sensory block during spinal anesthesia is due to different recovery profiles of A beta, A delta, and C fibers. Return of A beta current perception thresholds to baseline correlated with duration of surgical anesthesia as assessed with an electrical stimulation model.
Carbachol, Norepinephrine, and Hypocapnia Stimulate Phosphatidylinositol Turnover in Rat Tracheal Slices
Authors: Shibata Osamu , Makita Tetsuji , Tsujita Toshiya , Tomiyasu Shiro , Fujigaki Toru , Nakamura Harumasa , Sumikawa Koji 
Published: November 2003

Background
The intracellular mechanisms involved in the alpha-adrenoceptor- or hyperventilation-induced bronchoconstriction remain unknown. Because there is a direct relationship between phosphatidylinositol (PI) metabolism and airway smooth muscle contraction induced by muscarinic agonists, the authors examined the effects of carbachol (CCh), norepinephrine (NE), and hypocapnia on PI turnover in the airway smooth muscle.

Methods
Rat tracheal slices were incubated in Krebs-Henseleit solution containing LiCl and [3H]myo-inositol in the presence of NE, CCh, or neither. The PCO2 in the solution was 36 +/- 3 mmHg (normocapnia), 19 +/- 2 mmHg (moderate hypocapnia), or 5 +/- 2 mmHg (severe hypocapnia), respectively. [3H]inositol monophosphate (IP1) formed was counted with a liquid scintillation counter.

Results
Basal IP1 formed was greater at severe hypocapnia than at normocapnia. Norepinephrine- and CCh-induced IP1 formation were also greater at hypocapnia than at normocapnia.

Conclusions
These results indicate that CCh, NE, and hypocapnia stimulate PI turnover in the airway smooth muscle, which would cause bronchoconstriction, and hypocapnia also augments NE- and CCh-induced PI turnover, which could cause worsening of exercise-induced asthma and vagotonic asthma, respectively.
Halothane Impairs the Hemodynamic Influence of Endothelium-derived Nitric Oxide
Authors: Sigmon David H. , Florentino-Pineda Ivan , Van Dyke Russell A. , Beierwaltes William H. 
Published: November 2003

Background
The endogenous vasodilator endothelium-derived nitric oxide (EDNO) contributes to the regulation of vascular tone and organ perfusion. It has been suggested that some volatile anesthetics may diminish the influence of EDNO and thereby decrease regional blood flow.

Methods
Radioactive microspheres were used to determine regional hemodynamics in rats. The authors tested the hypothesis that halothane inhibits EDNO and, therefore, should diminish the response to nitric oxide synthesis inhibition by NW-nitro-L-arginine methyl ester (L-NAME) compared with either conscious or barbiturate-anesthetized rats.

Results
NW-nitro-L-arginine methyl ester decreased blood flow to the brain by 23% (P < 0.005) in conscious rats to a level similar to that seen with either anesthetic agent. In both conscious and barbiturate-anesthetized rats, L-NAME increased blood pressure (BP) by 24 +/- 2 (P < 0.001) and 20 +/- 1 (P < 0.001) mmHg and total peripheral resistance (TPR) by 132% (P < 0.001) and 105% (P < 0.001), respectively. In contrast, during halothane anesthesia, both the pressor response (only 7 +/- 1 mmHg) and the increase in TPR (only 22%) were greatly diminished (P < 0.001). NW-nitro-L-arginine methyl ester decreased cardiac output (CO) by 47% (P < 0.001) and heart rate (HR) by 28% (P < 0.001) in conscious rats. In barbiturate-anesthetized rats, L-NAME decreased CO by 38% (P < 0.005) and HR by 13% (P < 0.001). In halothane-anesthetized rats, L-NAME changed neither CO nor HR. Thus halothane anesthesia largely eliminated the systemic response to EDNO synthesis inhibition. In conscious rats, L-NAME decreased blood flow to the heart (30%) and kidneys (47%). In barbiturate-anesthetized rats, L-NAME did not alter blood flow to the heart but decreased renal blood flow by 35% (P < 0.005). In halothane-anesthetized rats, L-NAME did not alter blood flow to either the heart or the kidneys. Overall, halothane blunted or blocked the systemic and regional hemodynamic responses to EDNO synthesis inhibition seen in conscious and barbiturate-anesthetized rats.

Conclusions
Halothane anesthesia greatly diminished or eliminated all systemic and regional hemodynamic responses to L-NAME. These data indicate that halothane anesthesia inhibits EDNO-mediated regulation of systemic and organ hemodynamics.
Effects of Opioid Microinjections in the Nucleus of the Solitary Tract on the Sleep-Wakefulness Cycle States in Cats
Authors: Reinoso-Barbero Francisco , de Andres Isabel 
Published: November 2003

Background
Previous studies have shown that the region of the nucleus of the solitary tract (NST) is involved in the control of electrocortical activity and in sleep mechanisms. It also is well known that this region contains the highest concentration of opioid receptors within the medullary brainstem. The involvement of the NST opioid system in sleep-wakefulness states were evaluated.

Methods
Ten cats were implanted with electrodes for chronic polygraphic recordings of their sleep-wakefulness states and provided with an implanted guide cannula stereotaxically aimed at the NST region. Microinjections of saline, morphine sulfate, morphiceptin (specific mu agonist), D-pen-2-D-pen-5-enkephalin (delta agonist), and U-50488H (kappa agonist) were given to the freely moving animals (doses 0.8-2.4 x 10(-9) M, in a volume of 0.05 microliters of saline). After microinjections, sleep-wakefulness recordings were obtained for 8 h.

Results
Morphine microinjections in NST provoked a dose-dependent enhancement of all the polygraphic and behavioral manifestations of slow wave sleep. This effect was blocked by the prior intraperitoneal administration of naloxone. The mu and delta agonists also produced a hypnotic effect by enhancing slow wave sleep. By contrast, the kappa agonist caused no changes in sleep-wakefulness states.

Conclusions
These results indicate that endogenous opioids could be involved in controlling electrocortical activity generated by NST and that activation of mu and delta NST opioid receptors enhanced the electroencephalographic synchronization associated with behavioral slow wave sleep in cats.
The Effects of Halothane on Cardiovascular Responses in the Neuraxis of Cats
Authors: Farber Neil E. , Samso Enric , Kampine John P. , Schmeling William T. 
Published: November 2003

Background
This study examined the effects of halothane on arterial pressure after central nervous system (CNS) pressor site stimulation in anesthetized cats, cats rendered unconscious by midcollicular transection, and conscious cats.

Methods
Two anesthetized groups and two nonanesthetized groups were used. Cats were anesthetized with either alpha-chloralose and urethane or pentobarbital. Nonanesthetized groups were cats with midcollicular transections or conscious cats with chronically implanted electrodes. Stimulating electrodes were placed into vasomotor areas of the hypothalamus (HYP), reticular formation (RF), and medulla, and arterial pressure responses to increasing stimulus currents were examined during different halothane concentrations. Two groups of cats were also anesthetized with either pentobarbital or urethane and underwent bilateral carotid artery occlusion.

Results
Stimulation at each CNS site produced increases in arterial pressure and heart rate. Halothane attenuated pressor responses evoked by stimulation of all loci in all groups of cats. The inhibition by halothane on these cardiovascular responses was greatest at HYP and RF sites, while the medulla was more resistant to the effects of halothane in the anesthetized animals. Midcollicular transection decreased this medullary resistance. The inhibition of pressor responses by halothane was also greater in pentobarbital-than chloralose urethane-anesthetized animals. In contrast, pressor responses elicited by bilateral carotid occlusion were attenuated by halothane similarly in both anesthetic groups. Reticular formation stimulation in conscious animals resulted in "altering responses" in addition to pressor effects, both of which were attenuated by halothane.

Conclusions
Modulation of CNS cardiovascular control centers contribute to halothane-induced hemodynamic alterations. Baseline anesthesia, CNS stimulation site, and the suprabulbar system influence the effects of halothane.
Halothane Inhibits Signaling through m1 Muscarinic Receptors Expressed in Xenopus Oocytes
Authors: Durieux Marcel E. 
Published: November 2003

Background
Interactions between volatile anesthetics and muscarinic acetylcholine receptors have been studied primarily in binding assays or in functional systems derived from tissues or cells, often containing multiple receptor subtypes. Because interactions with muscarinic signaling systems may explain some effects and side effects of anesthetics and form a model for anesthetic-protein interactions in general, the author studied anesthetic inhibition of muscarinic signaling in an isolated system.

Methods
mRNA encoding the m1 muscarinic receptor subtype was prepared in vitro and expressed in Xenopus oocytes. Effects of halothane on methylcholine-induced intracellular Ca2+ release was measured. Angiotensin II receptors were expressed to evaluate anesthetic effects on intracellular signaling.

Results
m1 Receptors expressed in oocytes were functional, and could be inhibited by atropine and pirenzepine. Halothane depressed m1 muscarinic signaling in a dose-dependent manner: half-maximal inhibition of 10(-7) M methylcholine was obtained with 0.3 mM halothane. The effect was reversible and could be overcome by high concentrations of muscarinic agonist. Angiotensin II signaling was unaffected by 0.34 mM halothane.

Conclusions
m1 Muscarinic signaling is inhibited by halothane, and lack of halothane effect on angiotensin signaling indicates that the intracellular signaling systems of Xenopus oocytes are unaffected. Therefore, the most likely site of halothane action is the receptor and/or G protein. Oocytes provide a versatile system for detailed investigation into the molecular mechanism of anesthetic-protein interactions.
Cerebral Metabolism during Propofol Anesthesia in Humans Studied with Positron Emission Tomography
Authors: Alkire Michael T. , Haier Richard J. , Barker Steven J. , Shah Nitin K. , Wu Joseph C. , Kao James Y. 
Published: November 2003

Background
Although the effects of propofol on cerebral metabolism have been studied in animals, these effects have yet to be directly examined in humans. Consequently, we used positron emission tomography (PET) to demonstrate in vivo the regional cerebral metabolic changes that occur in humans during propofol anesthesia.

Methods
Six volunteers each underwent two PET scans; one scan assessed awake-baseline metabolism, and the other assessed metabolism during anesthesia with a propofol infusion titrated to the point of unresponsiveness (mean rate +/- SD = 7.8 +/- 1.5 mg.kg-1.h-1). Scans were obtained using the 18fluorodeoxyglucose technique.

Results
Awake whole-brain glucose metabolic rates (GMR) averaged 29 +/- 8 mumoles.100 g-1.min-1 (mean +/- SD). Anesthetized whole-brain GMR averaged 13 +/- 4 mumoles.100 g-1.min-1 (paired t test, P < or = 0.007). GMR decreased in all measured areas during anesthesia. However, the decrease in GMR was not uniform. Cortical metabolism was depressed 58%, whereas subcortical metabolism was depressed 48% (P < or = 0.001). Marked differences within cortical regions also occurred. In the medial and subcortical regions, the largest percent decreases occurred in the left anterior cingulate and the inferior colliculus.

Conclusion
Propofol produced a global metabolic depression on the human central nervous system. The metabolic pattern evident during anesthesia was reproducible and differed from that seen in the awake condition. These findings are consistent with those from previous animal studies and suggest PET may be useful for investigating the mechanisms of anesthesia in humans.