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Biomedical subjects

D M Jackson

Publications and source records attributed to D M Jackson.

At least 163 records · Page 9Linked to original sources
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Mice withdrawn for 7 days from a 35-day treatment period with haloperidol (3 mg/kg/day) displayed significantly greater spontaneous locomotor activity (hyperkinesia) than animals withdrawn from the vehicle.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suggest that noradrenergic systems are of importance for the manifestation of the hyperkinetic syndrome seen in mice withdrawn from long-term haloperidol treatment.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↗
PubMed1978

Further evidence for a change in central alpha-adrenergic receptor sensitivity after withdrawal from long-term haloperidol treatment.

Phenoxybenzamine, FLA-63 and alpha-MT produced less locomotor depression in mice withdrawn for 4 days from a 21 day treatment with haloperidol than that produced in vehicle-treated animals. There were no differences between the two groups when challenged with yohimbine or phentolamine. The data support the hypothesis that central alpha-adrenergic receptors had become supersensitive and suggest that the sensitivity changes are restricted to post-synaptic receptors.

Animals↗
PubMed1978

Prophylaxis against tetanus in non-immune patients with wounds: the role of antibiotics and of human antitetanus globulin.

The potential value of oral erythromycin for antitetanus prophylaxis in non-immune patients with open wounds was assessed. Serum obtained by venepuncture from health persons 2 h after an oral dose of an erythromycin preparation was used as a culture medium rendered anaerobic by addition of cooked meat. Strains of Clostridium tetani inoculated into these sera failed to multiply when the donor had taken 500 mg of erythromycin estolate before a meal; other erythromycin preparations and the estolate at a dosage of 250 mg were ineffective or inconsistent in their inhibition of the growth of Cl. tetani. Human antitetanus globulin (ATG) was given to 12 patients, 9 with severe injuries and 3 with extensive burns, all of whom were judged, from their history, to be non-immune (or with expired immunity); all except one had received large intravenous infusions of blood and/or other fluids. Serum antitoxin assays by a mouse protection technique on days 0, 1--2, 3--5, 6--10 and 14+ showed no detectable antitoxin (less than 0.01) unit/ml) in the initial (pre-ATG) sample from three patients with severe injuries and in one with extensive burns. All the patients in the severely injured group showed an early appearance or increase in tetanus antitoxin to protective titres. Two of the three severely burned patients showed, respectively, a delayed appearance or an increase in antitoxin; the other burned patients showed a reduction from the initial pre-ATG titre, followed by a return to that titre after day 5.

Blood Transfusion↗
PubMed1978

The binding of adjuvant-active mycobacterial peptidoglycolipids and glycopeptides to mammalian membranes and their effect on artificial lipid bilayers.

The nature of the binding of adjuvant-active amphiphilic mycobacterial peptidoglycolipids and glycopeptides to mammalian plasma membranes was investigated together with their effect on the stability of artificial lipid bilayers. The importance of these interactions between mycobacterial components and membranes is discussed in relation to immunopotentiation, mitogenicity and tuberculous infection.

Adjuvants, Immunologic↗