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Biomedical subjects

G H Hall

Publications and source records attributed to G H Hall.

At least 73 records · Page 4Linked to original sources
PubMed1972

Changes in body temperature produced by cholinomimetic substances injected into the cerebral ventricles of unanaesthetized cats.

1. The effects on body temperature of a number of substances injected into a lateral cerebral ventricle were examined in the unanaesthetized cat.2. Nicotine (50 and 100 mug) caused a fall in body temperature ranging from 0.95-2.1 degrees C associated with skin vasodilatation, tachypnoea and panting. These responses were prevented by the intraventricular injection of hexamethonium or mecamylamine, but not of atropine or phentolamine.3. Carbachol (5 mug) caused a rise in temperature associated with skin vasoconstriction, piloerection and severe shivering. These effects were prevented by the intraventricular injection of atropine, but not of hexamethonium or mecamylamine.4. An acetylcholine/eserine mixture (10 mug of each) had no reproducible effect on body temperature. Because of the variability in the response, interaction studies with antagonist drugs were not performed.5. Hexamethonium (100 mug) or mecamylamine (100 mug) caused a prolonged rise in temperature, together with skin vasoconstriction, piloerection and intense shivering. Atropine (200 mug) was without effect on body temperature.6. Noradrenaline (100 mug) caused a fall in temperature with skin vasodilatation. The fall was converted to a rise with skin vasoconstriction, piloerection and vigorous shivering following an intraventricular injection of phentolamine (100 mug).7. These observations suggest the existence of cholinergic heat loss and heat gain mechanisms in the hypothalamic thermoregulatory pathways of the cat and the interaction studies with hexamethonium, mecamylamine and atropine, support the involvement of ;nicotinic' and ;muscarinic' receptors within the cholinergic thermoregulatory system.

Acetylcholine↗
PubMed1970

Anticoagulation by ancrod for haemodialysis.

The defibrinating agent ancrod (Arvin) was used instead of heparin for intermittent haemodialysis. It was an effective, and apparently safe, anticoagulant and reduced the deposition of fibrin and leucocytes on the Cellophane membrane. Administration was more complicated and urea dialysance was less with ancrod than with heparin.

Adult↗
PubMed1970

Effects of nicotine and tobacco smoke on the electrical activity of the cerebral cortex and olfactory bulb.

1. Effects of nicotine, cigarette smoke and carbon monoxide have been compared in the cat encéphale isolé preparation, exhibiting a synchronized electrocorticogram (ECoG) and behavioural sleep.2. 2 ml samples of smoke, containing approximately 7 mug nicotine (approximately 2 mug nicotine/kg for a 3 kg cat), introduced into the lungs at 30 s intervals from a smoking simulator, caused desynchronization of the ECoG and behavioural arousal.3. Effects of smoke were matched in the same experiments by intravenous injections of nicotine, 2 mug/kg every 30 s.4. The use of specific nicotine antagonists, for example mecamylamine, and filters for removing nicotine, indicated the presence in smoke of other agents capable of exerting a pharmacological response.5. Cigarette smoke contains approximately 5.0% carbon monoxide. Introduced into the lungs of cats pretreated with mecamylamine (2 mg/kg), 2 ml samples of 5% carbon monoxide caused changes in the ECoG similar to those caused by smoke.6. Effects of nicotine or smoke were not modified by pretreatment with chlorpromazine (2.0-4.0 mg/kg). Atropine (0.3 mg/kg), however, prevented the cortical activation, but not the behavioural arousal.7. 2 ml samples of smoke applied to the nostrils caused the occurrence in the olfactory bulb of a discharge or burst of "induced" waves. This discharge was sometimes accompanied by a transient period of cortical activation.8. These studies demonstrate that in cats, nicotine is the principal pharmacological constituent of tobacco smoke as far as effects on the central nervous system are concerned, although other constituents of smoke may play a contributory role.

Animals↗
PubMed1969

Effects of nicotine on electrocortical activity and acetylcholine release from the cat cerebral cortex.

1. The effects of small amounts of nicotine on electrocortical activity and central acetylcholine (ACh) release have been studied on anaesthetized cats.2. The most common effect of nicotine given intravenously in a dose of 2 mug/kg every 30 sec for 20 min was to cause desynchronization of the electrocorticogram, indicating cortical activation, and an increase in the release of cortical ACh.3. A larger dose given less frequently (4 mug/kg every min for 20 min) caused, in some experiments, an increase and in others a decrease in cortical activity. Such changes were accompanied respectively by an increase or decrease in cortical ACh output.4. The amounts of nicotine that affected the electrocorticogram and ACh release are probably similar to those absorbed by the cigarette smoker who inhales.5. The effects of nicotine on the electrocorticogram were transient, but the effects on ACh were prolonged. This suggests that at least two pathways are involved in the nicotine response.

Acetylcholine↗