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Biomedical subjects

W Hope

Publications and source records attributed to W Hope.

At least 19 recordsLinked to original sources
PubMed2002

Increase in prevalence of nosocomial non-Candida albicans candidaemia and the association of Candida krusei with fluconazole use.

Candida is an important nosocomial pathogen. This study was undertaken to provide information on the rate of candidaemia, to define the risks for candidaemia and to describe and account for the epidemiology of candidaemia at our institution between 1992 and 1999. The overall rate was 0.052 per 1000 patient days and 0.27 per 1000 discharges. The major risks for candidaemia were colonization at a non-sterile site (OR 3.85, 95%CI 1.80-9.09), total parenteral nutrition (TPN) in the absence of neutropenia (OR 11.8, 95%CI 4.5-35.4, P<0.001) and neutropenia in the absence of TPN (OR 3.7, 95%CI 1.8-7.7, P<0.001). There was no change in the overall incidence of candidaemia but there was a steady decline in the rate of C. albicans with a corresponding rise in the incidence of non- C. albicans species. C. krusei was highly associated with fluconazole exposure (chi(2)=20.78, P<0.001). There was no evidence of spread of C. krusei using random amplification of polymorphic DNA, suggesting the appearance of this organism was due to the selection pressure exerted by fluconazole.

Antifungal Agents↗
PubMed2000

Shared governance--nurses making a difference.

AIM: This paper aims to describe how shared governance can be successfully integrated into existing management structures in a large medical directorate. It will show how the shared governance philosophy can lead to the creation of a culture where nurses feel important and valued and also consider its use as a foundation for the implementation of the nursing strategy. BACKGROUND: The hospital adopted shared governance in 1995 with the setting up of councils led by staff nurses. Shared governance advocates claim it broadens involvement of clinically-based nurses in the process of change through devolved decision-making thereby enhancing clinical practice and increasing staff moral and self-esteem. Key issues Shared governance is a cultural change that will develop the leadership and management skills of all grades of staff. Shared governance is not a quick fix for the profession; involvement of all staff needs time, persistence, determination and a strong commitment to training and development. CONCLUSION: The national nursing strategy puts nurses in a position to positively influence health care for the advantage of patients, however, for nurses to grasp this opportunity cultural change is required. This practical example of shared governance demonstrates how it can be used to create a proactive culture, focused on improving patient care. The nurturing and developing of clinically-based nurses provides them with the knowledge and skills to challenge the status quo and lead change. Thus, shared governance is an excellent foundation from which to develop the nursing strategy.

Decision Making, Organizational↗
PubMed1999

Role of endogenous adenosine in the expression of opiate withdrawal in rats.

Samples of extracellular fluid from striatum and nucleus accumbens of anaesthetised rats undergoing opiate withdrawal were collected using microdialysis and then analysed for adenosine and its metabolites using high performance liquid chromatography (HPLC) and ultraviolet (UV) detection. Although the amount of adenosine present in the dialysate from either brain region was below the limit of detection by 90 min after probe placement, the metabolites could still be detected. Samples of dialysates collected from the nucleus accumbens contained significantly higher concentrations of hypoxanthine and inosine following naloxone challenge. The data are compatible with the hypothesis that endogenous adenosine might be involved in the expression of the opiate abstinence syndrome.

Adenosine↗
PubMed1998

A study on seasonal variation in the development of morphine dependence in rats.

The possibility that naloxone-precipitated opiate withdrawal behaviors varied qualitatively over the course of the year was investigated. The experiments were carried out at monthly intervals over a 2-year period using rats treated with a morphine-containing slow-release emulsion. The results obtained from these experiments were equivocal, neither providing support for seasonal variance in the expression of the opiate abstinence syndrome, nor showing a complete lack of time-related differences. Although some behavioral signs of opiate abstinence showed seasonally related alterations in frequency over one of the years, this was not consistent from one year to another. It was therefore concluded that no significant relationship between the severity of the abstinence syndrome and the time of the year in which the experiment carried out could be demonstrated.

Animals↗
PubMed1998

Absorption of morphine from a slow-release emulsion used to induce morphine dependence in rats.

This study was performed to measure absorption of morphine from the injection site following treatment of rats with slow-release emulsions formulated with morphine hydrochloride and morphine base. Samples of emulsion were collected from the injection site of halothane anesthetized animals at 24 and 48 h following emulsion treatment and concentrations of morphine remaining in the emulsion were analyzed using high-performance liquid chromatography (HPLC). In another group of morphine-treated rats, at times equivalent to collecting samples of emulsion, the intensity of naloxone-precipitated withdrawal behaviors was monitored. Both morphine base- and hydrochloride-containing emulsions induced a high degree of physical dependence in animals treated over 48 h. Release of morphine from emulsions containing morphine base was slower than that from the hydrochloride formulations. In the 24-h morphine base-treated animals, approximately 45% was absorbed from the injection site as opposed to 99% in the 24-h morphine hydrochloride-treated animals. These results suggest that morphine base containing emulsions provide a more sustained exposure to the opioid.

Administration, Cutaneous↗
PubMed1997

Effect of adenosine receptor agonists and antagonists on the expression of opiate withdrawal in rats.

The effects of the selective A1 adenosine receptor agonist N6-cyclopentyladenosine (CPA) and the selective A2a agonist 2-[p-(2-carboxethyl)phenylethyl-ethylamino]-5'-ethylcarboxamidoade nosine (CGS 21680) (each at 0.03, 0.1 and 0.3 mg/kg, SC) as well as the selective A1 adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), non-selective antagonists 3-isobutyl-1-methylxanthine (IBMX), aminophylline, 3,7-dimethyl-1-propargyl-xanthine (DMPX) and 8(p-sulfophenyl)-theophylline (8-SPT) were investigated (each at 5, 10 and 30 mg/kg, SC) for their ability to alter the naloxone-precipitated opiate withdrawal syndrome in morphine-dependent rats. Effects of CPA and CGS 21680 on opiate withdrawal in the presence of aminophylline were also investigated. Both CPA and CGS 21680, caused a significant reduction in the incidence of body shakes, teeth chatter and paw shakes and decreased the amount of faecal matter produced. DPCPX, IBMX, DMPX, 8-SPT and aminophylline significantly increased the incidence of jumps and decreased the amount of faecal matter produced. The incidence of body shakes was significantly increased by DMPX, 8-SPT and IBMX. Neither CPA nor CGS 21680 were able to reverse the significant increase in the incidence of jumps caused by aminophylline. These data suggest that there is a role for endogenous adenosine in the modulation of the opiate abstinence syndrome and both A1 and A2a adenosine receptors are involved in this phenomenon.

Animals↗
PubMed1997

Role of morphine glucuronide metabolites in morphine dependence in the rat.

Concentrations of morphine and its 3- and 6-glucuronide metabolites (M3G and M6G) in plasma, brain, and urine of rats exposed to morphine for either 24 or 48 h were measured using high-performance liquid chromatography. In another group of morphine-treated rats, the intensity of naloxone-precipitated withdrawal behaviours was monitored at 24 and 48 h. The behavioural effects of M3G in opiate-naive and opiate-dependent rats were also investigated. Morphine was present in plasma, urine, and brain at 24 and 48 h, whereas M3G was detected in plasma and urine only. M6G was not present in detectable quantities in either plasma, urine, or brain. Although plasma concentrations of M3G were similar in both time groups, rats treated for 48 h had significantly larger quantities of M3G in their urine than did the other treatment groups. The incidence of withdrawal behaviour was significantly higher in animals exposed to morphine for 48 h than in those with only 24 h of exposure, M3G had no behavioural effects in the opiate-naive rats and did not precipitate an opiate-abstinence syndrome in morphine-dependent rats. From these results, it was concluded that although M3G is the major product formed by morphine breakdown in rats, it is unlikely that it is involved in the development of morphine dependence in this species.

Animals↗
PubMed1997

Analysis of buprenorphine in rat plasma using a solid-phase extraction technique and high-performance liquid chromatography with electrochemical detection.

A solid-phase extraction method and sensitive reversed phase high-performance liquid chromatography analysis with electrochemical detection of buprenorphine and its metabolite, norbuprenorphine, in rat plasma is described. Adequate separation of the compounds of interest was achieved on a Phenomenex C18 reversed-phase column using a mobile phase comprising phosphate buffer: acetonitrile (75:25, pH 3.0) and 0.25 mM 1-octane-sulfonic acid, at a flow rat of 1 ml/min. Electrochemical detection was performed at a potential of 0.75 V and sensitivity of 2 nA. Buprenorphine and norbuprenorphine were extracted from plasma by solid-phase extraction technique using naltrindole as an internal standard (IS). Recoveries of buprenorphine and norbuprenorphine following the extraction method were high (70%-89%) over the concentration range used (25-100 ng/ml) and no endogenous substances in plasma interfered with any of the sample components. The retention times for norbuprenorphine, IS, and buprenorphine were 8, 12.5, and 30.5 min, respectively. The limits of detection of buprenorphine and norbuprenorphine in spiked plasma samples were 25 and 5 ng/ml, respectively. Using this method, buprenorphine was detected in rat plasma in animals acutely treated with the drug (5 mg/kg, s.c.).

Animals↗
PubMed1996

The induction and quantitation of methadone dependence in the rat.

Slow-release emulsion (SRE) formulations of methadone were used to induce dependence in rats. Animals were exposed to total methadone doses of either 0, 15, 31.25, 62.5, or 125 mg/kg over 48 h. Withdrawal was induced following intraperitoneal challenge with either naloxone (3 mg/kg) or saline (control), and dependence was assessed in terms of the presence/absence of 13 nominated withdrawal behaviors. Three scoring systems to quantify dose-response relationships for withdrawal are described: (1) using the mean number of withdrawal behaviors per animal within each treatment group; (2) using the sum of the percentage of animals within a treatment group displaying each of the withdrawal behaviors; and (3) a modification of these, to further isolate the naloxone-induced component of the withdrawal score, that is, subtraction of data obtained from saline-challenged animals from those of naloxone-challenged rats. In SRE-treated rats, schemes (1) and (2) gave rise to positive dose-response relationships, while scheme (3) resulted in bell-shaped dose-response curves. To validate the proposed scoring systems, each was applied to data obtained from animals made dependent to methadone via administration in the drinking water. The most appropriate system was that utilizing the mean number of withdrawal behaviors; the method is simple, robust, and amenable to statistical analysis.

Animals↗
PubMed1996

Functional characterization of adenosine receptors in the nucleus tractus solitarius mediating hypotensive responses in the rat.

1. The aim of this study was to characterize adenosine receptors located in the nucleus tractus solitarius (NTS) that mediate decreases in blood pressure in the anaesthetized rat. To determine the adenosine receptor subtype involved, a range of selective agonists and antagonists were studied and their relative potencies evaluated. 2. The rank order of agonist potency in inducing decreases in diastolic blood pressure was N6-cyclopentyladenosine (CPA) > N6-cyclohexyladenosine (CHA) > N-ethyl-carboxamidoadenosine (NECA) > or = 2-phenylaminoadenosine (CV1808) > 2-p-(carboxyethyl)phenethylamino-5' N-ethylcarboxamidoadenosine (CGS 21680) > N6-(2-(4-aminophenyl)ethyl)-adenosine (APNEA). 3. The hypotensive action of CPA following microinjection into the NTS was antagonized by i.v. infusions (50 micrograms kg-1 min-1) of adenosine receptor antagonists, 8-cyclopentyl-1,3 dipropylxanthine (DPCPX), 8-phenyltheophylline (8-PT), 8-(p-sulphophenyl)theophylline (8-SPT), and 1,3-dipropyl-8-N-(2-diethylamino)ethyl)-N methyl-4-(2,3,6,7-tetrahydro-2,6-dioxo) benzenesulphonamidexanthine (PD 115199). The antagonist potency order was DPCPX > PD115199 > or = 8-PT. Intravenous infusion of 8-SPT had no effect on blood pressure responses to microinjection of CPA into the NTS. 4. The results suggest that adenosine A1 receptors in the NTS mediate hypotensive responses in the anaesthetized rat preparation.

Adenosine↗
PubMed1995

Changes in adenosine receptors mediating hypotension in morphine-dependent rats.

The hypotensive actions of morphine have been shown to be mediated by adenosine. Since tolerance has been reported to the hypotensive effects of morphine, this study was designed to determine whether morphine dependence altered adenosine receptor-mediated decreases in blood pressure in the Hooded Wistar rat. Following the induction of morphine dependence, the effects of adenosine receptor agonists and antagonists were studied in intact and pithed rat preparations. The hypotensive effects of adenosine were significantly less in morphine-dependent rats when compared to opiate naive rats. The adenosine A1 receptor agonist cyclohexyladenosine induced decreases in diastolic blood pressure which were significantly reduced in morphine-dependent rats when compared to opiate naive rats. However, the adenosine A2A receptor agonist 2-p-(carboxyethyl)-phenylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680) had a greater effect on blood pressure in morphine-dependent rats compared to opiate naive rats. The effects of adenosine receptor antagonists 8-cyclopentyl-1,3-dipropylxanthine, 8-phenyltheophylline, 8-(p-sulfophenyl)theophylline and 3,7-dimethyl-1-propargylxanthine infused at 50 micrograms/kg per min on the hypotensive actions of adenosine were studied in opiate naive and morphine-dependent rats. In intact rats the induction of morphine dependence reduced the potency of these antagonists at inhibiting adenosine-induced decreases in blood pressure. The same series of experiments was conducted in the pithed rat preparation. In this case the hypotensive actions of both cyclohexyladenosine and CGS 21680 were greater in morphine-dependent rats than opiate naive rats. In pithed rats, morphine dependence did not change the potencies of adenosine receptor antagonists on the hypotensive actions of adenosine. These results suggest that adenosine A1 receptors are downregulated in morphine-dependent rats, and that adenosine A2 receptors are upregulated in morphine-dependent rats.

Adenosine↗
PubMed1995

The role of adenosine in the hypotensive actions of morphine.

The role of adenosine in the hypotensive action of morphine was examined in the pentobarbitone anaesthetized or pithed rat preparations. Adenosine (10-300 micrograms/kg) induced dose-dependent decreases in diastolic blood pressure in the anaesthetized rat preparation. These effects were attenuated by infusion of 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 50 micrograms/kg/min), 8-phenyltheophylline (8PT; 50 micrograms/kg) also induced dose-dependent decreases in diastolic blood pressure. Guanethidine (16 micrograms/kg/min), atropine (1 mg/kg), DPCPX and 8 PT reduced the effect of morphine on diastolic blood pressure, whilst DMPX (50 micrograms/kg/min) was inactive. In the pithed rat preparation morphine was inactive at doses up to 10 mg/kg. The results suggest that the hypotensive effect of morphine is mediated at least in part by the release of adenosine which then acts on centrally located adenosine receptors to induce changes in autonomic control of blood pressure.

Adenosine↗
PubMed1994

Methadone levels in plasma, urine, and amniotic fluid of methadone-treated pregnant rats.

Methadone was administered in the form of a slow release emulsion to nonpregnant rats and pregnant animals at early, middle, or late gestation. Following a 48-h treatment period, plasma, urine, and amniotic fluid were analyzed for methadone and its two major metabolites using solid-phase extraction and reversed-phase HPLC. Methadone and its primary metabolite were detected in plasma and urine of all rats with levels of both compounds comparable at all stages of gestation. No significant difference was found for either methadone or its primary metabolite between gestation groups and nonpregnant animals. Amniotic fluid collected in middle and late gestation groups contained methadone and primary metabolite at levels similar to that of maternal plasma. These data show that methadone can be detected in plasma, urine, and amniotic fluid following short-term treatment of pregnant rats with the opiate. Methadone levels did not alter during pregnancy and were, in fact, similar to that of nonpregnant animals. These results indicate that the fetal environment contains methadone levels comparable to that of the maternal circulation.

Amniotic Fluid↗
PubMed1992

Effect of adenosine analogues on the expression of opiate withdrawal in rats.

The aim of this study was to test whether convergent dependence occurs in vivo. The adenosine A1 receptor agonist N6-[(R)-1-methyl-2-phenylethyl]adenosine (R-PIA), the A2 agonist 2-(phenylamino)adenosine (CV-1808), the nonselective A1, A2 agonist (adenosine-5'-ethylcarboxamide (NECA), and the alpha 2-adrenoceptor agonist clonidine were screened (each at 30, 100, and 300 micrograms/kg, SC) for their ability to alter naloxine-precipitated withdrawal signs in morphine-dependent rats. The results indicate that there is convergent dependence involving opioid and adenosine A1 receptors on those effects expressed by withdrawal diarrhoea, paw-shakes, teeth-chattering, body-shakes, and jumping. Further, dependence expressed by body-shakes involves convergence involving A1 receptors, as well as alpha 2-adrenoceptors; while A1 receptors are involved in dependence expressed by jumping, stimulation of alpha 2-adrenoceptors augments this sign. Adenosine analogues may be of clinical value for detoxification of opiate addicts.

Adenosine↗
PubMed1992

Determination of methadone and its metabolites by high performance liquid chromatography following solid-phase extraction in rat plasma.

This paper describes a rapid, quantitative liquid chromatographic analysis and extraction of methadone and its two major metabolites from rat plasma, using difenoxin as the internal standard. Using a C18 column, resolution of all sample components and the internal standard is achieved with a mobile phase of 25:75 acetonitrile-0.08% diethylamine in 1000 mL water, pH 2.3, at a flow rate of 1.5 mL/min. The injection volume is 100 microL. Standards are linear over the range 25-100 ng, with a lower limit of detection for methadone of 0.25 ng. Within- and between-run coefficients of variation (CV) are 1.24% and 2.94%, respectively. Extraction of methadone and its metabolites from rat plasma uses a solid-phase extraction technique that is highly efficient. Extraction efficiencies of 90.3%, 99.6%, 85.9% and 93.8% were achieved for methadone, its primary and secondary metabolites, and difenoxin, respectively.

Animals↗
PubMed1990

Evidence that A2 purinoceptors are involved in endothelium-dependent relaxation of the rat thoracic aorta.

1. The effect of adenosine and some adenosine analogues on the isolated thoracic aorta from rats was compared with the effect of adenosine 5'-triphosphate (ATP) and adenosine 5'-diphosphate (ADP). 2. Both ATP and adenosine analogues caused relaxation of the noradrenaline (30 nM)-contracted thoracic aorta. 3. The order of potency for adenosine analogues was 5'-(N-ethyl) carboxamidoadenosine (NECA) greater than L-N6-phenylisopropyladenosine (L-PIA), adenosine 5'-monophosphate (AMP), adenosine indicating the presence of adenosine A2 receptors. 4. Removal of the endothelium or prior treatment with haemoglobin (10 microM) attenuated relaxant responses to both ATP and NECA, attenuation being greater for ATP than NECA. 5. 8-Phenyltheophylline (10 microM) reduced relaxant responses to NECA but not to ATP in the intact tissue. 6. These results provide evidence that there are two components to relaxation of the rat thoracic aorta induced by purinoceptor agonists. The first is an endothelium-dependent mechanism involving release of endothelium-derived relaxant factor (EDRF) and the second is due to a direct effect on smooth muscle.

Adenosine↗