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Biomedical subjects

D M Jackson

Publications and source records attributed to D M Jackson.

At least 19 recordsLinked to original sources
PubMed1979

The effect of cannabidiol, alone and in combination with ethanol, on human performance.

Fifteen volunteers received cannabidiol (CBD) (320 microgram/kg) or placebo (both orally, T0), and 60 min later they consumed an ethanolic beverage (0.54 g/kg) or placebo. The effects were measured at T1 (100 min after CBD ingestion), T2 (160 min) and T3 (220 min) using cognitive, perceptual and motor function tests. Factorial analysis indicated that test procedures could be adequately expressed by three rotated factors: A reaction speed factor (I), a standing steadiness factor (II) and a psychomotor coordination/cognitive factor (III). Ethanol produced a significant decrement in factor III. There was no demonstrable effect of CBD, either alone or in combination with ethanol. Neither CBD nor ethanol produced any significant effect on pulse rate. Prior administration of CBD did not significantly affect the blood ethanol levels. Whilst the subjects were able to identify correctly when they were given ethanol, they did not report any subjective effects of CBD.

Adolescent↗
PubMed1979

The effect of (-) trans-delta9-tetrahydrocannabinol, alone and in combination with ethanol, on human performance.

Twenty five volunteers received (-) trans-delta9-tetrahydrocannabinol (THC) (320 microgram/kg) or placebo (both orally, T0), and, 60 min later, they consumed an ethanolic beverage (0.54 g/kg) or placebo. The effects of this medication were measured at T1 (100 min after THC ingestion), T2 (160 min), T3 (220 min) and T4 (280 min) using a battery of cognitive, perceptual and motor function tests. Factorial analysis indicated that the test procedures could be adequately expressed by four rotated factors: a reaction speed factor (I'), a cognitive factor (II'), a standing steadiness factor (III') and a psychomotor coordination factor (IV'). The first principal component (I) was used as a measure of general performance across the whole test battery. Both THC and ethanol produced significant decrements in the general performance factor. Ethanol produced significant decrements in standing steadiness and psychomotor coordination, while THC caused a significant deterioration in performance on all the four rotated factors. In all cases the peak effect of ethanol occurred at T1 and by T4 the effect had worn off. The performance decrements induced by THC were slower in onset and lasted longer than those induced by ethanol. In general, the peak effect of THC occurred at T1 and T2. There was no evidence of any interaction between THC and ethanol, and the effects of a combination of THC and ethanol were no more than additive. THC (but not ethanol) produced a significant rise in pulse rate. Prior administration of THC did not significantly affect the blood ethanol levels obtained. The subjects were able to identify correctly which of the treatments they had received.

Adolescent↗
PubMed1979

Interactions among the cannabinoids in the antagonism of the abdominal constriction response in the mouse.

The ability of delta 9-tetrahydrocannabinol (THC), cannabinol (CBN), cannabidiol (CBD), 11-OH THC and 8 alpha, 11-diOH THC to antagonise the abdominal constriction response in the mouse induced by formic acid, phenylquinone, 5-hydroxytryptamine, prostaglandin E1 (PGE1) and bradykinin was tested. THC was an effective antagonist against all nociceptive agents with an ED50 in all cases between 1.0 and 2.6 mg/kg. CBN, while also effective against all nociceptive agents, was less potent than THC, with an ED50 range between 46.2 and 112.5 mg/kg. CBD in doses as high as 200 mg/kg was without effect. Using PGE1 as the nociceptive agent, 11-OH THC was equipotent to THC while 8 alpha, 11-diOH THC was inactive. Naloxone, while able to antagonise the antinociceptive effect of morphine against formic acid-induced writhing, did not reverse the antinociceptive effects of THC. There were no pharmacological interactions between THC, CBD and CBN.

Abdominal Muscles↗
PubMed1979

The attenuation of delta 9-tetrahydrocannabinol and morphine of the quasi-morphine withdrawal syndrome in rats.

The effect of delta 9-tetrahydrocannabinol (THC), morphine, haloperidol and chlordiazepoxide on the exhibition of the signs of the quasi-morphine withdrawal syndrome was studied in rats. In preliminary studies approximately equi-sedative doses of these drugs were chosen. Morphine and THC produced a very similar degree of suppression of the signs of the quasi-morphine withdrawal, but unlike morphine, the effects of THC were not reversed by the narcotic antagonist, naloxone. The dopamine receptor antagonist, haloperidol, produced a moderate suppression of the withdrawal syndrome and chlordiazepoxide was without significant effect. It is concluded that THC is of very similar potency to morphine in suppressing the quasi-morphine withdrawal syndrome, but its activity in this regard does not appear to be dependent upon the availability of opiate or dopamine receptors, nor is it due to sedation alone.

1-Methyl-3-isobutylxanthine↗
PubMed1979

The hyperkinetic syndrome following long-term haloperidol treatment: involvement of dopamine and noradrenaline.

Mice withdrawn for 7 days from a 35-day treatment period with haloperidol (3 mg/kg/day) displayed significantly greater spontaneous locomotor activity (hyperkinesia) than animals withdrawn from the vehicle. The hyperkinesia was antagonized by phenoxybenzamine (an alpha-adrenergic receptor antagonist) and by FLA-63 (a dopamine-beta-hydroxylase inhibitor) but not by haloperidol (a dopamine receptor antagonist). alpha-Methyl tyrosine (a tyrosine hydroxylase inhibitor) was effective in antagonizing the hyperkinesia and this blockade by alpha-methyl tyrosine could be completely reversed by the administration of a low dose of the catecholamine precursor, DOPA. The data suggest that noradrenergic systems are of importance for the manifestation of the hyperkinetic syndrome seen in mice withdrawn from long-term haloperidol treatment.

Animals↗
PubMed1979

Long-term haloperidol-treatment of mice: a change in beta-adrenergic receptor responsiveness.

Mice administered haloperidol 3 mg/kg/day in their drinking water for 21 days were tested for their locomotor responsiveness to saline or acid vehicle, dl-, l- or d-propranolol, metoprolol, butoxamine or practolol. Haloperidol-treated animals administered saline or acid-vehicle were, in five of six experiments, more active than animals withdrawn from vehicle-treatment. Haloperidol- and vehicle-treated animals responded differently to the non-selective beta-adrenoreceptor antagonists (dl-propranolol and l-propranolol) and selective beta1-adrenoreceptor antagonists (practolol and metoprolol), but not to a selective beta2-adrenoreceptor antagonist (butoxamine). With dl-propranolol (4 mg/kg) the locomotor activity of haloperidol-treated animals was significantly (0.01 less than P less than 0.02) greater than that of the vehicle-treated animals. Similar effects in the same direction were seen with l-propranolol (1 mg/kg, 0.005 less than P less than 0.01), practolol (10 and 100 mg/kg, 0.025 less than P less than 0.05 and 0.01 less than P less than 0.025 respectively) and metoprolol 8 mg/kg, 0.005 less than P less than 0.01). The d-isomer of propranolol which is about 50 times less active as a beta-adrenoreceptor antagonist than the l-isomer, although having equal membrane stabilizing effects, did not differentially affect haloperidol- or vehicle-treated groups. The results suggest that there has been a change in beta 1-adrenoreceptor responsiveness in animals withdrawn from long-term haloperidol treatment.

Adrenergic beta-Antagonists↗
PubMed1979

The effects of sodium cromoglycate on lung irritant receptors and left ventricular cardiac receptors in the anaesthetized dog.

1 The time from the injection of sodium cromoglycate 10 to 50 mug/kg into a saphenous vein, the cervical carotid arteries, the left ventricle and the aortic arch, to the onset of reflex hypotension has been measured in anaesthetized dogs. The shortest latency was 16.9 s on injection of sodium cromoglycate into the left ventricle.2 Instillation of 2% lignocaine into the pericardium of an anaesthetized dog blocked the reflex hypotensive response to sodium cromoglycate (10 to 50 mug/kg i.v.), and also prevented sodium cromoglycate (100 mug/kg) from reversing reflex bronchoconstriction induced by inhalation of an aerosol of histamine.3 The effect of sodium cromoglycate (100 mug/kg i.v.) on resting discharge and histamine-induced discharge (20 mug/kg i.v.) of five lung irritant receptors in five anaesthetized dogs has been studied. Sodium cromoglycate (100 mug/kg i.v.) did not affect the resting discharge of these receptors or their ability to respond to histamine.4 Sodium cromoglycate (100 mug/kg i.v.) increased the rate of discharge of three receptors found in the endocardium of the left ventricle of the canine heart. A solution of sodium cromoglycate (0.1%) was applied topically to one receptor and its rate of discharge was increased.5 It is suggested that in the dog, sodium cromoglycate produces reflex hypotension and reverses histamine-induced reflex bronchoconstriction by activating receptors in the left ventricle of the heart.

Action Potentials↗
PubMed1979

The effects of H1- and H2-receptor agonists and antagonists on total lung resistance, dynamic lung compliance and irritant receptor discharge in the anaesthetized dog.

1 The effects of histamine and 4 methylhistamine (i.v.) alone, and in the presence of chlorpheniramine or cimetidine, on total lung resistance (RL), dynamic lung compliance (Cdyn) and irritant receptor activity have been studied in dogs anaesthetized with chloralose. 2 Histamine produced dose-related increases in RL and irritant receptor activity with associated falls in Cdyn which were blocked by chlorpheniramine but unaffected by cimetidine. 3 4 Methylhistamine produced small insignificant changes in RL and Cdyn and small significant increases in irritant receptor activity which were reduced with chlorpheniramine but unaffected by cimetidine. 4 The results suggest that histamine increases irritant receptor activity, either directly or indirectly, via H1-receptors.

Animals↗
PubMed1979

The effects of histamine, acetylcholine and 5-hydroxytryptamine on lung mechanics and irritant receptors in the dog.

1. The ability of histamine, acetylcholine, acetylcholine (ACh) and 5-hydroxytryptamine (5-HT) given I.V. and by aerosol to induce reflex bronchoconstriction and to activate lung irritant receptors has been studied in dogs anaesthetized with chloralose. 2. Histamine (four breaths of an aerosol from 0.0625%, 0.125% and 0.25% solutions and 5, 10 and 20 microgram kg-1 I.V.), 5-HT (four breaths of an aerosol from 0.5% or 1.0% solutions and 10, 20 and 40 microgram kg-1 I.V.) produced significant relex changes in RL (total lung resistance). The changes in RL produced by ACh (four breaths of an aerosol from 0.25%, 0.5% and 1.0% solutions, of 5, 10, 20 and 40 microgram kg-1 I.V.) were unaffected by vagal cooling. 3. The falls in Cdyn (dynamic compliance) produced by ACh given by aerosol or I.V. were unaffected by vagal cooling. The falls in Cdyn produced by histamine (10 microgram kg-1 and 40 microgram kg-1 I.V.) and 5-HT (four breaths of an aerosol generated from a 0.5% solution and 20 microgram kg-1 and 40 microgram kg-1 I.V.) were significantly reduced by vagal cooling. 4. Histamine, 5-HT and ACh given by aerosol and I.V. increased lung irritant receptor discharge. Irrespective of the route of administration, for a given change in RL histamine produced a greater increase in irritant receptor discharge than did ACh or 5-HT, which produced similar increases. 5. For a given change in RL, histamine, ACh and 5-HT were more effective in activating lung irritant receptors when given I.V. than by aerosol. 6. The mechanisms of irritant receptor activation by histamine, ACh and 5-HT and the relationship between irritant receptor discharge and reflex bronchoconstriction are discussed.

Acetylcholine↗
PubMed1979

The effect of a respiratory tract infection on histamine-induced changes in lung mechanics and irritant receptor discharge in dogs.

The effects of intravenously administered histamine on total lung resistance (RL), dynamic lung compliance (Cdyn), and the discharge of lung irritant receptors have been measured in normal dogs and in dogs whose upper respiratory tract was naturally infected with the organism Bordetella bronchiseptica. The resting values for RL and irritant receptor discharge were similar for the infected and control dogs, but Cdyn was significantly lower in the infected group of dogs. Intravenous administration of 20 microgram of histamine/kg of body weight produced significantly greater direct and reflex changes in RL in the infected dogs than in the control animals. The changes in Cdyn in both groups of animals were similar. Intravenous administration of histamine (20 microgram/kg) produced a significantly greater increase in the rate of discharge of lung irritant receptors found in infected dogs than in control dogs. A possible mechanism responsible for the hyperreactivity to histamine is seen in the hypersensitivity of the irritant receptors introduced by the epithelial lesions observed in the infected dogs.

Action Potentials↗
PubMed1979

McIndoe lecture, 1978. Burns: McIndoe's contribution and subsequent advances.

My first aim is to present the state of burn care during the few years before the Battle of Britain in August-October 1940. This gives the climate of thought in which McIndoe and his collegues faced the challenge of burns. We are inclined to forget the helplessness of surgeons faced with extensive burns at that time. Some of the great changes in burn management in the past 40 years are then described and a claim is made that the results show a real improvement in treatment.

Adult↗
PubMed1978

The binding of lipopolysaccharide from Escherichia coli to mammalian cell membranes and its effect on liposomes.

The kinetics of the absorption of 32P- or 14C-labelled lipopolysaccharide from Escherichia coli NCTC 8623, serotype 0 125, chemotype XII, to erythrocytes, leukocytes, peritoneal macrophages and peritoneal lymphocytes was examined. Under variable conditions maximal levels of binding were found due to saturation of receptor sites on the cell membrane or steric hindrance by bound lipopolysaccharide. During adsorption slight leakage of haemoglobin was found but complete lysis of erythrocytes was ruled out after noting the effect of lipopolysaccharide on artificial lipid bilayers. The affinit of lipopolysaccharide to cell membranes revealed a consistent pattern of cyclic fluctuation between adsorption and desorption. A model was proposed to explain this cyclic fluctuation in binding based on membrane reorganization. It was significant that the cycle of lipopolysaccharide adsorption-desorption proceeded to completion even if the process was interrupted. The indication was that, once triggered, membrane reorganization occurred independently without influence from the test environment.

Animals↗