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Biomedical subjects

A W Jones

Publications and source records attributed to A W Jones.

At least 19 recordsLinked to original sources
PubMed1992

Lack of effect of omeprazole, cimetidine, and ranitidine on the pharmacokinetics of ethanol in fasting male volunteers.

The effects of three gastric antisecretory drugs on the pharmacokinetics of ethanol have been studied in a randomized crossover experiment. Male medical students (n = 12) took ethanol 0.8 g/kg body weight at 08.00 h after an overnight fast. On seven successive days before drinking ethanol they were given omeprazole 20 mg, cimetidine 800 mg, ranitidine 300 mg, or no drug, with a period of at least 7 days between treatments. The peak blood ethanol concentration of 21.9 to 22.8 mmol.l-1 occurred at 64 to 70 min after the end of drinking. The rate of disappearance of ethanol from the blood ranged from 3.0 to 3.3 mmol.l-1.h-1 and the rate of removal from the whole body ranged from 8.0 to 8.5 g.h-1. The apparent volume of distribution of ethanol was almost the same for all four treatments: mean 0.68 l.kg-1, corresponding to a mean total body water of 44 l (59% body weight). Mean areas under the concentration-time profiles of ethanol ranged from 83 to 87 mmol.l-1.h for the four treatments. It is concluded that omeprazole, cimetidine and ranitidine do not alter the kinetics of a moderate dose of ethanol.

Adult↗
PubMed1992

Pharmacokinetics of ethanol in plasma and whole blood: estimation of total body water by the dilution principle.

The pharmacokinetics of ethanol in plasma and whole blood have been investigated and the results used to estimate the volume of total body water (TBW) by means of the dilution principle. Fifteen men (mean age 62 y) were given 0.6 g ethanol/kg body weight as an intravenous infusion over 1 h. The peak concentration of ethanol in plasma was 120 mg.dl-1 compared to 108 mg.dl-1 for whole blood. The disappearance rate of ethanol from plasma was 18.6 mg.dl-1.h-1 compared to 17.0 mg.dl-1.h-1 for the whole blood concentration-time data. The apparent volume of distribution of ethanol (Vz) was 0.54 l.kg-1 according to plasma kinetics compared to 0.59 l.kg-1 for the kinetics derived from whole blood. The mean area under the curve (AUC) was 294 mg.dl-1 x h for plasma kinetics compared to 266 mg.dl-1 x h for whole blood. The TBW was 40.9 l or 50.9% of body weight for the plasma concentration-time data. This agreed well with the 40.3 l or 50.1% of body weight obtained using whole blood.

Body Water↗
PubMed1992

Salivary duct carcinoma: report of a case and review of the literature.

Salivary duct carcinoma is a rare primary tumour of the salivary glands arising most frequently in the parotid gland. It has a male preponderance and occurs most often in patients over the age of 50 years. Its distinctive histological features include dilated ducts containing cells arranged in cribriform, papillary or solid patterns often with central necrosis and reminiscent of intraduct carcinoma of the breast. These features are associated with an obvious invasive component. It is an aggressive neoplasm and may metastasize widely, causing death in a high proportion of cases.

Carcinoma↗
PubMed1992

Activation of multiple mechanisms including phospholipase D by endothelin-1 in rat aorta.

This study investigated the cellular mechanisms underlying the endothelin-1 (ET-1)-induced contraction of rat aorta with focus on the involvement of phospholipase D (PLD). Preincubating rat aorta in Ca(2+)-free solution reduced the contraction by 80%, whereas diltiazem (10 microM), a voltage-operated Ca2+ channel blocker, caused only a small reduction (27%, P less than 0.05) of the contraction. In myo-[3H]inositol-labeled aorta, ET-1 stimulated the formation of [3H]inositol bisphosphate and [3H]inositol trisphosphate, indicating the activation of phospholipase C (PLC). In aorta labeled with 32PO4, [3H] myristic acid or [32P]lyso-platelet-activating factor followed by exposure to ethanol (0.5%), ET-1 stimulated phosphatidylethanol (PEt) production, suggesting that ET-1 activates PLD. The PEt response was not attenuated by staurosporine (ST, 0.1 microM), an inhibitor of protein kinase C (PKC) but was inhibited by removal of Ca2+. The ET-1-induced PEt response was at least additive to that induced by phorbol 12-myristate 13-acetate (1 microM). ET-1 also stimulated the release of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) into the tissue medium. Unlike the PEt responses, the 6-keto-PGF1 alpha response could be inhibited by ST. Removal of Ca2+ abolished the response. These results suggest that 1) ET-1 activates multiple cellular mechanisms including PLC, PLD, and the arachidonate cascade; 2) PKC activation may not be essential for the ET-1 activation of PLD but may play an important role in the ET-1 stimulation of 6-keto-PGF1 alpha release; and 3) Ca2+ is an important factor in the ET-1-induced PLD activity and 6-keto-PGF1 alpha release.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Ethanol monitoring of transurethral prostatic resection during inhaled anesthesia.

The purpose of this study was to examine the precision of a method of breath-alcohol analysis used to monitor absorption of irrigating fluid during transurethral resection of the prostate performed under inhaled anesthesia. A breath-alcohol analyzer (Alcolmeter SD-2) was placed between the endotracheal tube and the Bains' circuit. The concentration of ethanol in the breath, serum sodium concentration, and volumetric fluid balance were measured at 10-min intervals during 38 operations when the irrigating fluid contained 1.5% glycine and 1% ethanol. Ethanol monitoring detected absorption rates that exceeded 14 +/- 8 mL/min (mean +/- SD). In 17 patients in whom hyponatremia developed immediately in connection with absorption, the volume of irrigating fluid absorbed (up to 1950 mL) could be predicted from a single expired-breath test with a standard error of 325 mL. When the alcohol measurements were corrected for absorption time, the standard error was 215 mL. Seven other patients received 2.2% wt/vol glycine as irrigating fluid, and ethanol (0.35 g/kg) was administered by intravenous infusion. The direct and indirect measurements of the blood-alcohol concentration agreed well. These results confirm that ethanol monitoring is a viable technique during inhaled anesthesia for transurethral resection of the prostate.

Absorption↗
PubMed1992

Oligodendroglioma of the fourth ventricle with intracranial and spinal oligodendrogliomatosis: a case report.

We report a case of oligodendroglioma of the fourth ventricle complicated by disseminated intracranial and spinal oligodendrogliomatosis. This is further evidence that primary oligodendrogliomas arising in close proximity to the cerebrospinal pathway have a predilection for spontaneous dissemination. This condition should be considered in the differential diagnosis of hydrocephalus and myelopathy.

Adolescent↗
PubMed1992

Kinetics of ethanol and methanol in alcoholics during detoxification.

We investigated the kinetics of ethanol and methanol in 20 dependent alcoholics (16 men and four women) during the first 24 hr after admission to hospital for detoxification. The blood-ethanol concentration (BEC) on admission ranged from 238 to 489 mg/dl (mean 386 mg/dl). The mean rate of ethanol disappearance from the blood was 23 mg/dl/hr with a spread from 13 to 36 mg/dl/hr. The concentrations of methanol in blood at the start of detoxification ranged from 0.16 to 2.8 mg/dl (mean 1.15 mg/dl) and these levels remained more or less unchanged until the BEC had dropped below 30 mg/dl. The concentrations of ethanol and methanol in blood at the start of detoxification were not correlated (r = 0.032, P > 0.05). The results of this study do not support the notion that the metabolism of methanol in chronic alcoholics proceeds independently of the prevailing BEC. We found a three-fold difference in the rate of disappearance of ethanol from blood in alcohol-dependent subjects.

Adult↗
PubMed1992

Ethanol distribution ratios between urine and capillary blood in controlled experiments and in apprehended drinking drivers.

Healthy men drank 0.51, 0.68, and 0.85 g of ethanol per kilogram of body weight as neat whisky in the morning after an overnight fast. During 6 to 8 h after the whisky was consumed, nearly simultaneous specimens of fingertip blood and pooled bladder urine were obtained for analysis of ethanol using an enzymatic method. The mean ratios of ethanol concentration [urine alcohol concentration (UAC)/blood alcohol concentration (BAC)] were mostly less than unity during the absorption phase. The UAC exceeded the BAC in the postpeak phase. The mean UAC/BAC ratios varied between 1.4 and 1.7 when the BAC exceeded 0.50 mg/mL. When the BAC decreased below 0.40 mg/mL, the UAC/BAC ratios increased appreciably. The mean UAC/BAC ratios of ethanol were not dependent on the person's age between the ages of 20 and 60 years old, but there were large variations within the age groups. In apprehended drinking drivers (N = 654) with a mean BAC of 1.55 mg/mL, the UAC/BAC ratio of ethanol varied widely, with a mean value of 1.49. In 12 subjects (3.2%), the ratio was less than or equal to unity. In a second specimen of urine obtained approximately 60 min after an initial void (N = 135), the mean UAC/BAC ratio was 1.35 (standard deviation = 0.17). The magnitude of the UAC/BAC ratio of ethanol can help to establish whether the BAC curve was rising or falling at or near the time of voiding. The status of alcohol absorption needs to be documented if drinking drivers claim ingestion of alcohol after the offence or when back-estimation of the BAC from the time of sampling to the time of driving is required by statute.

Absorption↗
PubMed1992

Measuring ethanol in blood and breath for legal purposes: variability between laboratories and between breath-test instruments.

We determined the concentrations of ethanol in nearly simultaneous specimens of venous blood (BAC) and end-expired breath (BrAC) after healthy volunteers drank moderate amounts of alcohol. BAC was measured at two laboratories and BrAC was analyzed with two instruments (Intoxilyzer 5000) from the same manufacturer. The mean difference in BAC between laboratories was 0.0105 mg/g (SD 0.0219); 95% of the differences ranged from -0.0333 to 0.0543 mg/g. The mean difference in BrAC between instruments was 0.0153 mg/L (SD 0.0136), and 95% of the differences ranged from -0.0119 to 0.0425 mg/L. The coefficient of variation (CV) between laboratories was 2.9% compared with 4.5% between breath-test instruments. Venous BAC (y) and BrAC (x) were highly correlated (r = 0.978). However, when the Intoxilyzer instruments indicated that BrAC had reached zero, the actual BAC was 0.135 mg/g, according to the average forensic laboratory reports. The Intoxilyzer 5000 breath analyzers used in this study seem to have a constant analytical bias.

Adult↗
PubMed1991

Altered phospholipase activities related to alpha 1-adrenergic receptor supersensitivity of aortas from aldosterone-salt hypertensive rats.

Many of the concepts presented in this paper are summarized in Fig. 7. Some aspects are well supported while others are speculative. The operation of PLC in VSM is well established, and in some hypertensive models (AHR, SHRSP) PLC assays exhibited altered activation. Currently this pathway leading to the production of IP3 and DAG is considered to be the major regulator of Ca release from sarcoplasmic reticulum (SR) and Ca entry by channels (CaC). Regulation of PKC by [Ca]i and DAG is thought to play a major role in controlling Ca entry. PKC has also been proposed to regulate PLA2 as well as PLD in conjunction with elevated [Ca]i. An important issue to be resolved is whether receptor regulation of other lipases occurs independently of the PLC-[Ca]i-PKC axis. Currently information supporting receptor regulation is lacking for VSM, but few studies have been conducted. Our observation that NE stimulation of PLD activity occurs in VSM indicates that the control of VSM by biochemical messengers is much more complicated than previously proposed. This seemingly redundant pathway may allow VSM to use alternate substrates for producing PA and DAG than are readily available to PLC. It also allows PA to be produced directly without phosphorylation of DAG. Although the role of PA in the regulation of Ca entry was proposed earlier, definitive studies establishing this linkage are still required. Any PLD activity on PIP2 would produce biochemical messengers (PA, DAG) which could stimulate Ca entry without producing the messenger, IP3, associated with Ca release (inactive IP2 would be produced). If PLC and PLD were independently regulated by receptor-guanine nucleotide-regulatory protein (G-protein) complexes, this would offer the potential for some agonists to excite VSM by Ca release and Ca entry mechanisms while others may excite by Ca entry alone. This system would also circumvent the problem of limited substrate for cellular regulation of [Ca]i if PIP2 were the primary substrate. This limitation does not exist with other phospholipids such as phosphatidylcholine which is a preferred substrate for PLD. The presence of multiple phospholipases under separate receptor regulation allows for a wider range of tissue responses to various agonists, than a system which is linked only through the PLC-[Ca]i-PKC axis. The presence of a PLD pathway also reopens the interpretation of previous studies which demonstrated a resetting between receptor occupancy and production of second messengers by PLC.(ABSTRACT TRUNCATED AT 400 WORDS)

Aldosterone↗