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Biomedical subjects

G Henderson

Publications and source records attributed to G Henderson.

At least 127 records · Page 7Linked to original sources
PubMed1984

Physician burnout.

Explore the source record for details and available documents.

Burnout, Professional↗
PubMed1983

Substance P excitation of rat locus coeruleus neurones.

We have made extracellular recordings from locus coeruleus neurones contained in a pontine slice preparation. The in vitro technique permits application of known concentrations of drugs in the perfusion medium. Substance P excites locus coeruleus neurones in a concentration-dependent manner. The activity of substance P was found to reside in the C terminal region of the molecule. The relative potency of substance P and related peptides suggests that the substance P receptors present within the locus coeruleus are predominately of the substance P-P type. The synthetic analogue [D-Pro2,D-Trp7.9]substance P was not found to antagonise the action of substance P on locus coeruleus neurones.

Animals↗
PubMed1983

Noradrenaline-mediated synaptic inhibition in rat locus coeruleus neurones.

Intracellular recordings were made from neurones in the nucleus locus coeruleus (l.c.) in slices of rat pons maintained in vitro. Focal electrical stimulation to the slice surface within the region of the l.c. evoked a synaptic depolarization followed by a hyperpolarization. These potentials were graded with stimulus intensity and were abolished in calcium-free and/or high-magnesium solutions. The nature of the hyperpolarizing synaptic potential (i.p.s.p.) was investigated. The i.p.s.p. amplitude decreased as the membrane was artificially made more negative and reversed at -114 mV. This reversal potential shifted to less negative potentials in solutions of elevated potassium ion content as predicted by the Nernst equation. The i.p.s.p. was potentiated in amplitude and its time course was prolonged by desmethylimipramine (DMI). Yohimbine (100 nM) and phentolamine (100 nM) reversibly abolished the i.p.s.p. and did not change the synaptic depolarization. Noradrenaline hyperpolarized all l.c. neurones tested, whether applied by perfusion (1-30 microM) or by pressure ejection from a micropipette placed in the solution near the recording site. The noradrenaline-induced hyperpolarization was accompanied by an increase in conductance and it reversed in polarity at -104 mV. The reversal potential of the noradrenaline hyperpolarization became less negative when the potassium ion content was increased. The noradrenaline-induced hyperpolarization was potentiated by DMI and was antagonized by yohimbine and phentolamine in the same concentrations which blocked the i.p.s.p. The results support the notion that l.c. neurones can release noradrenaline onto the somadendritic membrane of other l.c. neurones and thereby provide local feed-back inhibition.

Action Potentials↗
PubMed1982

Electrophysiological properties of neurons contained in the locus coeruleus and mesencephalic nucleus of the trigeminal nerve in vitro.

Intracellular recordings were made from neurones contained in the locus coeruleus and mesencephalic nucleus of the trigeminal nerve (MNV), in tissue slices cut from guinea-pig pons and maintained in vitro. Locus coeruleus neurones were of -52.7 +/- 2.7 mV resting membrane potential; had an input resistance of 58.0 +/- 7.6 M omega and a membrane time constant of 7.3 +/- 1.0 ms. These neurones fired action potentials in response to depolarizing current pulses. Depolarizing synaptic potentials (DSPs) were recorded in locus coeruleus neurones in response to focal stimulation of the surface of the slice. MNV neurones were of -51.9 +/- 3.6 mV resting membrane potential; had an input resistance of 15.0 +/- 1.8 M omega and a membrane time constant of 1.35 +/- 0.16 ms. These neurones were also excitable but differed from locus coeruleus neurones in that they showed accommodation to depolarizing current pulses and time-dependent anomalous rectification with hyperpolarizing current pulses. In MNV neurones focal stimulation did not give rise to DSPs. Intracellular injection of Lucifer yellow revealed that the cell bodies of locus coeruleus neurones were small and multipolar whereas MNV neurones had larger, monopolar cell bodies.

Animals↗
PubMed1982

Increased incidence and clinical correlation of persistently abnormal technetium pyrophosphate myocardial scintigrams following acute myocardial infarction in patients with diabetes mellitus.

"Persistently abnormal" technetium-99m stannous pyrophosphate myocardial scintigrams (PPi+) appear to be associated with a relatively poor prognosis after acute myocardial infarction (AMI). To assess the incidence and implications of PPi+, we performed a retrospective analysis in 29 patients with and 25 patients without diabetes mellitus who had abnormal myocardial scintigrams within 4 days of AMI and who had follow-up scintigrams at least 3 months after hospital discharge. There were no significant differences between patients with and without diabetes as regards age, incidence of transmural or nontransmural AMI, or degree of left ventricular dysfunction after AMI. Persistently abnormal PPi+ occurred more commonly in patients with diabetes than in nondiabetic patients (18 of 29, 62%, compared to 3 of 25, 12%; p less than 0.001). Patients with chronic PPi+ had more frequent cardiac complications following hospital discharge (p less than 0.005) including death, recurrent AMI, unstable angina, and intractable congestive heart failure. Postmortem analysis in two patients with diabetes and chronic PPi+ revealed marked myocytolysis. Thus, patients with diabetes mellitus have an increased incidence of post-AMI "persistently abnormal" technetium (PPi+) scintigrams and relatively poor prognosis following myocardial infarction.

Aged↗
PubMed1981

The effect of extracellular sodium ion concentration on the action of opiates to inhibit potassium-evoked release of [3H]noradrenaline from the mouse vas deferens.

Opiates depress the potassium-induced efflux of [3H]noradrenaline from the mouse vas deferens in a concentration-dependent (the IC50 for normorphine was 1.5 microM), stereospecific and naloxone-reversible manner. As the concentration of sodium in the extracellular fluid was reduced, the inhibitory action of opiates was also reduced. This attenuation of opiate action is the converse of that predicted by the 'sodium-shift' observed in opiate binding studies in which lowering the sodium concentration potentiates opiate agonist binding. The relevance of sodium to the pharmacological actions of opiates is discussed.

Adrenergic Fibers↗
PubMed1981

Intestinal function in infant rats: effect of maternal chronic ethanol ingestion.

Postnatal growth retardation is one of the principle features of fetal alcohol syndrome. The cause of this growth retardation is not known. Therefore the intestinal transport of an amino acid marker, L-valine-14C, was studied in vivo in small intestinal segments of 2-week-old infant rats born to mothers fed chronically ethanol during pregnancy. Control infant rats were born to mothers isocalorically pair fed throughout pregnancy. Transport rates of L-valine expressed on the basis of unit weight or unit length were similar in both groups of rats. We concluded that this neutral amino acid transport pathway was unaltered in infants of mothers fed chronic ethanol during pregnancy. Thus, the growth retardation seen in fetal alcohol syndrome is unlikely to be secondary to intestinal protein malabsorption.

Alcoholism↗
PubMed1980

Di-isopropyl phosphofluoridate-induced antinociception: possible role of endogenous opioids.

Di-isopropyl phosphofluoridate (DFP, 0.1--1.5 mg/kg, s.c.) produced antinociception in rats as measured by the hot plate test. Naloxone reduced DFP-induced antinociception but did not affect the attenuated locomotor activity or hypothermia produced by DFP. Animals rendered tolerant to the antinociceptive action of morphine failed to exhibit cross tolerance to the antinociceptive action of DFP. Morphine- and DFP-induced antinociceptive states were antagonized by MR 2266 and GPA 1843, the (-)-isomers of 5,9 alpha-Diethyl-2-(3-furylmethyl)-2'-hydroxy-6, 7-benzomorphan and -2-allyl-2'-hydroxy-9 beta-methyl-5-phenyl-6, 7-benzomorphan hydrochloride, respectively; the corresponding (+)-isomers, MR 2267 and GPA 1847, did not antagonize the antinociceptive state produced by DFP or morphine. These results suggest that DFP-induced antinociception may be mediated via the release of endogenous opioids; however, this could occur at sites different from those concerned with morphine tolerance.

Analgesics↗
PubMed1980

Cell counts in human cerebral cortex in normal adults throughout life using an image analysing computer.

Cortical cells have been counted in 11 areas of brain from each of 64 normal subjects from 18 to 95 years of age, all cases studied being selected after careful consideration of their clinical records and detailed histological examination of the brain. Cells (features) in cresyl fast violet stained 20 micrometer paraffin sections were initially divided into 8 groups according to size in multiple columns of cortical tissue; statistical evaluation of the results showed that there were 3 populations of cortical cells, based on size discrimination, which behaved in significantly different ways. The smallest cells have been designated "glial celons were initially divided into 8 groups according to size in multiple columns of cortical tissue; statistical evaluation of the results showed that there were 3 populations of cortical cells, based on size discrimination, which behaved in significantly different ways. The smallest cells have been designated "glial cells" and the other two groups "small" and "large" neurons. The number of cells in all three groups decreased from youth to old age, the least loss being in the "glial cells" and the greatest (up to 60%) in "large neurons". The variation and statistical significance of cell loss in each cell group in the different areas examined is described, and the findings in this investigation discussed in relation to previous studies using manual methods.

Adolescent↗
PubMed1978

Pharmacokinetics of fentanyl as determined by radioimmunoassay.

The pharmacokinetics of fentanyl were determined in human surgical patients using radioimmunoassay. Fentanyl was measured in the serum, cerebrospinal fluid (CSF), and urine of patients receiving 0.1, 0.5, or 1.0 mg/m2 of fentanyl intravenously. The kinetics of the disappearance of fentanyl from the serum were very similar at the three administered doses. At all doses, levels fell rapidly in the first five minutes to approximately 20% of the peak value. Thereafter, serum levels fell more slowly with an observed half-life (t 1/2) of approximately 10 to 20 min. depending on dose. By 2 hr serum levels had stabilized at low values (1, 5, and 8 ng/ml) and continued to decrease very slowly thereafter, with an observed t 1/2 of 1 to 2 hr at the low dose (0.1 mg/m2) and greater than 4 hr at 0.5 and 1.0 mg/m2. The serum elimination curves were dissected and described mathematically in terms of a three-compartment model. Urinary excretion of fentanyl accounted for 15% to 20% of the administered dose. Urinary excretion was very low during the first 2 hr, suggesting that this route of elimination is not important in terminating the actions of fentanyl in man. Fentanyl levels in the CSF of patients given terminating the actions of fentanyl in man. Fentanyl levels in the CSF of patients given the high dose (1 mg/m2) were low, and never exceeded 4 ng/ml. Peak levels of fentanyl in the CSF were not seen until at least 15 min after administration.

Adult↗
PubMed1977

In vitro pharmacology of the opioid peptides, enkephalins and endorphins.

In the guinea-pig ileum methionine-enkephalin, normorphine and morphine are equipotent in depressing electrically evoked contractions; leucine-enkephalin has about 25% of the activity. The mouse vas deferens is more sensitive to the enkephalins which are 30 to 60 times more potent than morphine. Fragments of beta-lipotropin61-91 (beta-endorphin) having sequences up to LPH76 are more potent in the mouse vas deferens than in the guinea-pig ileum but beta-endorphin is about equipotent in the two preparations. None of the peptides has antagonist activity. Methionine-enkephalin and normorphine are equipotent in inhibiting [3H]-naloxone binding by homogenate of guinea-pig brain in the absence of Na+ while leucine-enkephalin has only 25% of this activity. In the guinea-pig ileum, naloxone antagonises normorhine and the enkephalins equally well whereas in the mouse vas deferens about ten times more naloxone is required for the enkophalins that for normorphine. Methionine-enkephalin depresses output of acetylcholine in the guinea-pig ileum and of noradrenaline in the mouse vas deferens.

Animals↗
PubMed1976

Effect of normorphine and enkephalin on spontaneous potentials in the vas deferens.

Spontaneous excitatory junction potentials were recorded intracellularly from the smooth muscle of the mouse vas deferens. Exposure of the vas deferens to either normorphine (1 muM) or methionine-enkephalin (0.5 muM) did not alter the frequency or amplitude distribution of the spontaneous potentials. The possible mechanisms by which the narcotic agonists depress the release of noradrenaline on nerve stimulation without inhibiting the spontaneous release of noradrenaline are discussed.

Animals↗