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Biomedical subjects

M Dixon

Publications and source records attributed to M Dixon.

At least 145 records · Page 8Linked to original sources
PubMed1982

The action of barbiturates on contractile responses of canine and feline bronchial smooth muscle.

Pentobarbitone, thiopentone and phenobarbitone in concentrations ranging from 10(-4) M to 10(-3) M reduced the contractile responses of isolated canine and feline trachealis muscle to electrical field stimulation without affecting contractile responses to acetylcholine. The order of potency was thiopentone, pentobarbitone and phenobarbitone. Experiments using carbachol and neostigmine or physostigmine suggested that the barbiturates act by preventing the release of acetylcholine from nerve endings. In vivo, pentobarbitone (2.5-20 mg/kg i.v.) produced dose-related reductions in the increase in total lung resistance induced by vagal stimulation in chloralose-anaesthetised cats.

Acetylcholine↗
PubMed1981

Leukotrienes C and D induce bronchoconstriction in man.

Pulmonary responses to aerosols of synthetic leukotrienes C and D were examined in two normal volunteers. The leukotrienes were equipotent and equieffective in producing moderate bronchoconstriction accompanied by coughing. Changes in FEV1 were slight, but changes in expiratory flow at low lung volumes were more notable. FPL 55712 abolished the cough response and partially inhibited the bronchoconstriction.

Adult↗
PubMed1980

The action of sodium cromoglycate on 'C' fibre endings in the dog lung.

The effect has been studied of sodium cromoglycate (SCG) on the activity of 'C' fibre sensory nerve endings in the canine lung. Pretreatment with SCG (100 microgram/kg i.v.) reduced the excitation of these endings by capsaicin (10 microgram/kg i.v.) for approximately 45 min. This property of SCG may explain its ability to suppress certain types of bronchoconstrictor responses in man.

Airway Resistance↗
PubMed1980

The effects of 5-hydroxytryptamine, histamine and acetylcholine on the reactivity of the lung of the anaesthetized dog.

1. Anaesthetized dogs were given aerosols of 5-hydroxytryptamine (5-HT), histamine and acetylcholine; the effects on the changes in total lung resistance (RL) and dynamic lung compliance (Cdyn) produced by electrical stimulation of the peripheral cervical vagi, and I.V. histamine and acetylcholine were studied. 2. Pretreatment with 5-HT significantly potentiated the increases in RL caused by vagal stimulation, histamine or acetylcholine. Pretreatment with histamine significantly potentiated the increases in RL caused by vagal stimulation but the potentiation of the increases in RL produced by histamine and acetylcholine were not significant. Pretreatment with acetylcholine did not potentiate the increases in RL due to vagal stimulation, histamine or acetylcholine. The falls in Cdyn produced by vagal stimulation, histamine or acetylcholine were not potentiated by pretreatment with aerosols of 5-HT, histamine or acetylcholine. 3. The effects of I.V. histamine, 5-HT and acetylcholine on RL and Cdyn were studied when given alone and when combined with vagal stimulation. 4. Vagal stimulation significantly potentiated the increases in RL due to 5-HT and histamine, but did not affect the increases in RL caused by acetylcholine or the falls in Cdyn produced by any of the three agonists. 5. By comparing these results with those from a previous study, it is concluded that, for the three agents studied, in order for increased irritant receptor discharge to reflexly increase RL, the agent has to increase the reactivity of the airway to vagal stimulation. It is also concluded that the degree of vagally mediated broncho-constriction can be varied by changing either the afferent limb through a change in irritant receptor discharge, or the efferent limb, by a change in airway reactivity.

Acetylcholine↗
PubMed1980

A study of the afferent and efferent nerve distribution to the lungs of dogs.

The distribution of afferent and efferent nerves to the lung has been studied using dogs anaesthetised with chloralose in which the lungs had been separated, enabling independent inflation and measurement of lung mechanics. Reflex bronchoconstriction produced by giving an aerosol of 5-hydroxytryptamine (5HT) or histamine to either the right or left lung failed to elicit a change in resistance (RL) of the contralateral lung. In vagotomised dogs, electrical stimulation of the peripheral end of the left or right cervical vagus produced frequency-dependent increases in RL of the ipsilateral lung. Stimulation of the left vagus also produced significant changes in RL of the right lung.

Afferent Pathways↗
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

A model role of occupational therapy in back education.

This paper presents a description of the Canadian Back Education Units (CBEU) which was formed in 1974. It presently has three programmes; hospital, community and industry. The authors describe the basic philosophy and objectives of the CBEU with specific emphasis on the role of occupational therapy. The paper illustrates how occupational therapy is particularly essential in the community and industrial settings. The authors mention recommendations for expansion of the role of occupational therapy in community and industrial settings.

Back Pain↗
PubMed1978

Lung reflexes in rabbits during pulmonary stretch receptor block by sulphur dioxide.

Anaesthetized rabbits were given 200 ppm sulphur dioxide to breathe for 10 min. This abolished activity in 23 of 26 pulmonary stretch receptors, while leaving that of lung irritant receptors unimpaired. The Breuer-Hering reflex was abolished and breathing became deeper and slower. Inspiratory time (tI) was increased and expiratory time (tE) decreased. Subsequent vagotomy increased tidal volume (VT), tI and tE. In animals with stretch receptors blocked, injections of phenyl diguanide and histamine still increased breathing frequency and decreased VT, indicating that reflexes from lung irritant and J-receptors were intact. Inhalation of 8% CO2 caused a bigger increase in frequency and tidal volume in rabbits with stretch receptor block compared with controls or those after vagotomy. Induction of pneumothorax with stretch receptor block transiently prolonged tI and shortened tE; removal of the pneumothorax also transiently shortened tE and usually also decreased tI. The results suggest that lung irritant receptors reflexly shorten tE in all our experimental conditions, but have various effects on tI which may depend on the timing of the irritant receptor discharge and refractoriness of the inspiratory response.

Animals↗