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Biomedical subjects

D M Jackson

Publications and source records attributed to D M Jackson.

At least 217 records · Page 12Linked to original sources

A new blood warmer.

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Blood Transfusion↗

Interaction of cannabis and general anaesthetic agents in mice.

1 A cannabis extract (I) (in a concentration equivalent to 10 mg Delta(9)-tetrahydro-cannabinol(THC)/kg) prolonged pentobarbitone anaesthesia in mice maximally 20 min to 2 h after medication. The effect was still significant after 8 h, but less than at 2 hours.2 The cannabis extract (I) (equivalent to 10 mg Delta(9)-THC/kg) prolonged both pentobarbitone and ether anaesthesia in mice when administered 20 min before the anaesthetic. After eight consecutive daily doses of cannabis, the pentobarbitone anaesthesia was still significantly longer than a control group, while ether anaesthesia was not significantly prolonged.3 A second cannabis extract (II) with a different ratio of cannabinoids (also administered in dosage equivalent to 10 mg Delta(9)-THC/kg) failed to affect pentobarbitone anaesthesia in mice. This extract presented about 4% the dose of cannabidiol as extract I.4 Delta(8)-THC, Delta(9)-THC and cannabidiol prolonged pentobarbitone anaesthesia with cannabidiol being generally more active than Delta(9)-THC. Cannabinol (10 mg/kg) was inactive.5 The effects of cannabidiol and Delta(9)-THC were found to be additive, and there was a consistent trend for cannabinol to reduce the effectiveness of Delta(9)-THC and cannabidiol when given in combination.6 Premedication with phenoxybenzamine, phentolamine, propranolol, iproniazid, protriptyline, desipramine, reserpine, alpha-methyl tyrosine or parachlorophenylalanine did not affect the extract I-induced prolongation of pentobarbitone anaesthesia.7 It is concluded that cannabis may affect pentobarbitone and ether anaesthesia in mice at least partially by a direct depressant effect, and that the cannabis-induced prolongation of anaesthesia is probably unrelated to any effect on central 5-hydroxytryptamine or catecholamine neurones.

Anesthesia, General↗

Prostaglandin 15 (R) 15-methyl-E2 methyl ester for suppression of gastric acidity in gravida at term.

During the second hour after giving 100 mug of orally administered prostaglandin 15 (R) 15-methyl-E(2) methyl ester in the pregnant patient at term a noticeable reduction in basal gastric acid secretion took place. At this dose no excessive uterine stimulation was observed. Prostaglandin 15 (R) 15-methyl-E(2) methyl ester could prove of value in the preoperative preparation of the pregnant patient before anaesthesia for reducing the incidence of acid regurgitation.

Esters↗

The effect of cannabinoids on intestinal motility and their antinociceptive effect in mice.

1. After oral administration to mice, pethidine, Delta(8)-tetrahydrocannabinol (THC), Delta(9)-THC, a cannabis extract and cannabinol had a dose-dependent antinociceptive effect when measured by the hot-plate method. Cannabidiol was inactive at 30 mg/kg. Delta(8)-THC, Delta(9)-THC and pethidine did not differ significantly in potency, but Delta(9)-THC was 6.5 times more active than cannabinol.2. After oral administration, three different cannabis extracts, Delta(8)-THC, Delta(9)-THC and morphine produced dose-dependent depressions of the passage of a charcoal meal in mice. Delta(8)-THC and Delta(9)-THC were equipotent and were about five times less potent than morphine. Cannabidiol was inactive up to 30 mg/kg. The effect of the three cannabis extracts on intestinal motility could be accounted for by their Delta(9)-THC content.3. The antinociceptive effect of pethidine and the effect of morphine on intestinal motility were antagonized by nalorphine whilst the effects of the cannabis extracts and the pure cannabinoids were not.4. From these results it is concluded that although cannabis and the narcotics share several common pharmacological properties, the mode of action of each is pharmacologically distinct.

Administration, Oral↗

The pharmacology of the rat ureter in vivo.

1. A method of recording the peristaltic frequency and the rate of transport of fluid (perfusion rate) in the rat ureter in vivo is described.2. Acetylcholine and atropine did not alter ureteral activity. Histamine increased the rate of peristalsis by up to 15% and the rate of perfusion by up to 10%. Low doses of 5-hydroxytryptamine increased peristaltic frequency whereas high doses decreased peristaltic frequency; all doses reduced the rate of perfusion.3. Morphine reduced the rate of perfusion by 5-10% at all dose levels, but only the highest dose used reduced the frequency of ureteral peristalsis.4. (-)-Adrenaline, (-)-noradrenaline and (+/-)-isoprenaline reduced the frequency of peristalsis. The order of potency was isoprenaline>noradrenaline>adrenaline. The response was dose-related and blocked by propranolol, which itself did not affect ureteral activity.

Acetylcholine↗