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Biomedical subjects

J R Sneyd

Publications and source records attributed to J R Sneyd.

At least 55 records · Page 3Linked to original sources
PubMed1994

Electrophysiologic effects of propofol sedation.

The scalp electroencephalogram (EEG), the long latency cognitive P300 auditory evoked response (AER), and reaction times were recorded in 10 volunteers sedated with a computer-controlled infusion of propofol to target plasma concentrations of 0.3, 0.6, 0.9, and 1.2 micrograms/mL. The observed mean +/- SE venous plasma concentrations were 0.152 +/- 0.042, 0.372 +/- 0.078, 0.679 +/- 0.104, and 1.065 +/- 0.112 micrograms/mL, respectively. Scalp EEG topographic mapping revealed that beta 1 activation was primarily frontal and central with relative sparing of the temporal lobes. The P300 response was dramatically reduced by propofol in a concentration-dependent manner, even though the subjects were conscious but clearly sedated. Mean +/- SE reaction times were increased by propofol sedation from 347 +/- 35 ms (control) to 391 +/- 48, 460 +/- 70, 549 +/- 64, and 622 +/- 120 ms at increasing mean venous plasma propofol concentrations. The mean percentage +/- SE of correct responses decreased from 98.1 +/- 2.0 (control) to 99.1 +/- 1.7, 87.4 +/- 9.2, 82.8 +/- 12.9, and 69.8 +/- 20.9 at increasing propofol concentrations. Dramatic alterations in the EEG, P300 response, and reaction times were observed, especially with the higher plasma concentrations which produced conscious sedation.

Adult↗
PubMed1994

Use of proton nmr spectroscopy to measure propofol metabolites in the urine of the female Caucasian patient.

1. Six female Caucasian patients received i.v. doses of propofol (2.7 +/- 0.3 (SE) mg/kg) for induction of anaesthesia. Anaesthesia was maintained with nitrous oxide, oxygen and enflurane for periods up to 3 h. A total urine collection was made from each subject for 24 h after administration of propofol; samples were concentrated and analysed for propofol metabolites by nmr spectroscopy. 2. By 24 h, 50.9 +/- 4.0% of the dose of propofol was recovered as metabolites. The proportions of propofol metabolites, 1-quinol glucuronide (1-QG), 4-quinol glucuronide (4-QG), propofol glucuronide (PG) and 4-quinol sulphate (4-QS) recovered in urine (0-24 h) of the patients were 12 +/- 1, 8 +/- 2, 76 +/- 4 and 4 +/- 1% respectively. However, one patient showed a metabolite profile in which PG comprised 93% and 1-QG 7% of the total metabolites. 3. Nmr spectroscopy has been shown to be a satisfactory method for the quantification of propofol metabolites in urine without the necessity for reference samples.

Adult↗
PubMed1993

Determination of plasma propofol levels using gas chromatography-mass spectrometry with selected-ion monitoring.

Propofol (2,6-diisopropylphenol, I.C.I. 35,868) is a rapid-acting, intravenous anesthetic agent recently introduced for the induction and maintenance of general anesthesia. This paper describes a gas chromatographic-mass spectrometric procedure using selected-ion monitoring for the determination of plasma propofol levels. The drug and the internal standard (thymol) were extracted from plasma into diethyl ether-pentane, and derivatized to their trimethylsilyl derivatives before analysis. The reproducibility of the daily standard curves had coefficients of variation ranging from 2.7% to 10.2%. The precision of the assay yielded a coefficient of variation ranging from 4.5% to 5.6%, and the concentration means for the seeded control samples were found to be within -1.6% to +0.6% of the theoretical values for propofol. No interfering peaks have been observed in application of this procedure to either normal volunteer or patient samples. The minimum detectable level under the conditions described was 0.20 ng propofol/ml plasma. This assay and a high-performance liquid chromatographic assay with fluorescence detection were both used to measure plasma propofol concentrations in 89 human plasma samples, and the correlation between the two methods was excellent.

Chromatography, High Pressure Liquid↗
PubMed1992

Intrathecal diamorphine (heroin) for obstetric analgesia.

Intrathecal diamorphine (heroin, diacetyl morphine) 2.5 mg in isotonic saline 2.5 ml was given to 13 patients in labour through a 26 gauge Quincke needle. Three patients were given epidural bupivacaine at a mean of 295 min after injection of diamorphine and a further 2 used 50% nitrous oxide during the second stage of labour. Eight patients needed no additional analgesia for labour although 1 received a pudendal nerve block for forceps delivery. No neonatal complications attributable to diamorphine were observed. There was a high incidence of post partum headache (6/13 cases). The use of a Sprotte needle and a fine spinal catheter might overcome the limitations of spinal headache and limited duration of action respectively.

Journal Article↗
PubMed1992

Effect of physiotherapy on the auditory evoked response of paralysed, sedated patients in the intensive care unit.

Auditory evoked response (AER) was recorded before, during and after physiotherapy in 11 paralysed (atracurium 0.56 (SD) 0.13 mg kg-1 h-1), sedated (propofol 2.2 (1.0) mg kg-1 h-1; fentanyl 4.4 (2.3) micrograms kg-1 h-1) and critically ill patients undergoing ventilation in the intensive care unit (ICU). The latency of the negative wave, NB, was reduced by physiotherapy (mean 44.8 (SD) 7.9 ms before, 41.0 (6.8) ms during (P less than 0.01, non-parametric Friedman test) and 45.6 (6.3) ms after physiotherapy); NB amplitude showed no consistent change (-0.81 (1.4) microV, -0.81 (1.5) microV and -0.71 (1.3) microV, respectively). NB latency responded to patient arousal at constant levels of sedation and this requires further evaluation as a means of monitoring sedation in paralysed patients in the ICU.

Adult↗
PubMed1992

The effect of pre-induction glycopyrronium on the haemodynamic response of elderly patients to anaesthesia with propofol.

This study investigated whether pretreatment with glycopyrronium can attenuate the hypotension caused by anaesthesia of the elderly with propofol. Twenty elderly patients (77.1 +/- 2.44 years, mean +/- SEM) of ASA physical status 2 or 3 scheduled for elective urological procedures were given glycopyrronium 0 (n = 10) or 5 micrograms.kg-1 (n = 10) in a randomised, double-blind manner, 5 min before induction of anaesthesia with propofol infused at 600 ml.h-1 (average induction dose 1.7 +/- 0.06 mg.kg-1, mean +/- SEM) followed by maintenance with a propofol infusion at 10 mg.kg-1.h-1. Although glycopyrronium significantly increased heart rate (p less than 0.01, ANOVA), the decrease in blood pressure 2 and 5 min after induction was similar in both groups. The study had a power of 80% to detect a 20 mmHg difference in systolic arterial pressure between treatment groups with p less than 0.05.

Aged↗
PubMed1990

Potassium as a respiratory signal in humans.

Six renal transplant recipients underwent a series of incremental exercise experiments. Minute ventilation (VE), carbon dioxide production rate (VCO2), and arterial blood chemistry were measured at rest and while subjects exercised on a stationary bicycle. Four of the subjects performed a similar experiment while exercising on a static rowing machine. Within each subject, arterial potassium concentration ([K+]a) was linearly related to VCO2 and VE during exercise. The slope of the relationship between [K+]a and VCO2 was similar in the cycling and rowing experiments. This implies that the absorption of potassium by resting muscle does not significantly limit the arterial hyperkalemia seen during exercise. When VE, VCO2, and [K+]a were measured 1 and 5 min after the end of cycling there was no correlation, whereas VE continued to be closely correlated with VCO2. The relationship demonstrated between change in [K+]a and VCO2 in these experiments is compatible with change of [K+]a acting as a respiratory signal during exercise but not during recovery from exercise in humans.

Adult↗
PubMed1988

Ventilatory effects of potassium during hyperoxia, normoxia and hypoxia in anaesthetized cats.

Anaesthetized cats breathing 100% O2, air or 14% O2 received intravenous infusions of KCl (0.075 mmol/kg body weight per 30 sec). Ventilation increased significantly during the infusion and returned to control values within 10 sec of its completion. The ventilatory response to acute changes in arterial plasma potassium concentration is not abolished by hyperoxia. Some of these findings have already been briefly communicated (Band et al., in press).

Anesthesia↗
PubMed1986

A simple atracurium infusion regimen for intra-abdominal surgery.

Atracurium was used to provide relaxation for intra-abdominal surgery in 15 patients. The regimen comprised an initial bolus (0.4 mg kg-1) followed by an infusion (0.3 mg kg-1 h-1) from 10 min after induction until closure of the peritoneum. Average duration of infusion was 80 min (range 48-166 min). This regimen provided satisfactory relaxation in 13 patients; two patients required one additional bolus of atracurium. Fourteen patients showed a sustained tetanic response to 50-Hz stimulation at the end of surgery and in these neuromuscular blockade was not antagonized. One patient required antagonism following very rapid closure of the abdomen.

Abdomen↗
PubMedDate not supplied

Oxidative metabolism in platelets, platelet aggregation, and hematology in patients undergoing multiple hyperbaric oxygen exposures.

Repeated hyperbaric oxygen (HBO2) treatments at 2.2 ATA for 90 minutes each are used to treat chronically ill patients with problem wounds, but there are concerns about the cytotoxicity of oxygen to blood cells and platelet function during prolonged HBO2 therapy. We recruited 31 consenting patients scheduled for multiple HBO2 treatments to evaluate oxidative metabolism in platelets, platelet aggregation, and hematology (mean age +/- standard error, 61 +/- 2.6 years, 20 males, 11 females). Venous blood was collected before and after the 1st and 20th HBO2 treatments. No effect of HBO2 was observed on red cell counts, hematocrit, hemoglobin, mean red cell volume (MCV), platelet counts, basal levels of lactate production by platelets, ferric reducing ability of plasma (FRAP), or plasma protein. The capacity for oxidative metabolism (lactate ratio) in platelets was not affected by HBO2, except in smokers where it increased by the 20th HBO2 treatment. Mean lymphocyte count was increased by 38% after the 20th treatment. There was also a 23% increase in platelet protein content, and a 24% increase in arachidonic acid-dependent platelet activation. Collagen-dependent platelet aggregation was unaffected. Blood glucose showed HBO2-dependent variability, but remained in the normal range. Plasma lactate levels decreased significantly from 3.2 to 2.5 mmol/l by the end of the study. Overall, we found no evidence that 20 HBO2 sessions caused adverse effects on platelet aggregation or oxidative metabolism in platelets, red or white cell counts, or total antioxidant status of the plasma.

Acetaminophen↗