Search PubMed⌕ Search

Biomedical subjects

J D Graham

Publications and source records attributed to J D Graham.

At least 109 records · Page 6Linked to original sources
PubMed1973

Cardiovascular and respiratory effects of cannabis in cat and rat.

1. In anaesthetized rats, intravenous administration of cannabis extract (10 mg/kg), Delta(1)-tetrahydrocannabinol (THC) (0.5 mg/kg) and Delta(6)-THC (0.5 mg/kg) caused a reduction in systemic blood pressure, pulse rate and respiratory rate.2. Neither cannabinol (1 mg/kg, i.v.) nor cannabidiol (1 mg/kg, i.v.) had any observed effects on the cardiovascular and respiratory systems of the rat.3. Pretreatment of rats with atropine (1 mg/kg, i.v.) reduced the hypotension and bradycardia caused by Delta(1)-THC or the extract.4. In anaesthetized cats with autoperfused hindquarters, cannabis extract (10 mg/kg, i.v.) and Delta(1)-THC (0.2 mg/kg, i.v.) caused hypotension, bradycardia, depression of respiratory rate and reduction of hindlimb perfusion pressure.5. Both cannabis extract and Delta(1)-THC potentiated reflex vasodilation and direct vasoconstriction in the hindlimb induced by intravenous noradrenaline in the cat; they reduced reflex hindlimb vasoconstriction elicited by histamine, acetylcholine or bilateral carotid occlusion.6. Tolerance to these cardiovascular and respiratory effects of cannabis extract developed in rats which had been treated i.p. with the extract at (50 mg/kg) per day for 14 days.

Animals↗
PubMed1972

The actions of prostaglandins E 1 and F 2 on the on the perfused vessels of the isolated rabbit ear.

1. In the isolated rabbit ear vascular bed, perfused with Krebs solution, prostaglandins E(1) and F(2alpha) produce dose-dependent, phentolamine-sensitive constrictions.2. These are absent if the animal is pre-treated with reserpine or if the ear is denervated in advance.3. If noradrenaline or vasopressin is added to the Krebs solution, vascular resistance is high and PGE(1) and PGF(2alpha) produce vasodilatation which is unaffected by hyoscine or propranolol.4. Perfusion with theophylline, with added ATP, ADP or 3'5'-AMP, or pre-treatment of the animal with stilboestrol antagonizes the dilator response to PGE(1) in the presence of noradrenaline, which may be reversed. Most of the responses to PGF(2alpha) are reversed. These treatments elevate the level of 3'5'-AMP in tissues.5. It is postulated that prostaglandins exert a regulatory action on 3'5'-AMP levels through inhibition of adenyl cyclase and/or phosphodiesterase and that the resulting rising or falling level of 3'5'-AMP determines the nature of the response by the smooth muscle to the released noradrenaline.

Adenosine Monophosphate↗
PubMed1971

Binding of N-(2-bromo ethyl)-N-ethyl-N 1 -naphthylmethylamine HBr (SY28) to the proteins of guinea-pig vas deferens.

1. Vasa deferentia from guinea-pigs were exposed to (14)C-SY28 HBr (5.32 x 10(-6)M) washed, lipid extracted, and broken up.2. The tissue was digested with papain, hydrolyzed with 6 N HCl, and gel filtration performed.3. Aliquots at each stage were used for paper chromatography and autoradiography.4. Three labelled spots (in addition to unbound 2-halogenoalkylamine) were located from acid hydrolysate and a fourth from gel filtrate.5. Selected amino-acids were complexed with (14)C-SY28 and the procedure repeated. The R(F) values were compared with those of the same amino-acids with and without 6 N HCl.6. Histidine, aspartic acid, arginine and serine gave a significant degree of binding of (14)C-SY28.7. The theoretical implications are discussed.

Animals↗
PubMed1971

3 H-noradrenaline-accumulating ability of cholinergic nerve terminals in cat sympathetic ganglia.

1. After incubation of pieces of cat posterior mesenteric ganglion in [(3)H]-noradrenaline solution, the localization of the isotope was assessed by electron-autoradiography.2. Significantly higher concentrations of [(3)H]-noradrenaline were found over acetylcholinesterase-positive axons terminal on ganglion cells than in adjacent background areas.3. [(3)H]-Noradrenaline was not accumulated by ganglion cells under these circumstances.4. The significance of these findings in relation to previous physiological and pharmacological investigation is discussed.

Acetylcholinesterase↗
PubMed1971

In pursuit of the alpha-adrenoceptor: a fine-structural and electron autoradiographic study using 3H-phenoxybenzamine and smooth muscle from the cat and guinea-pig.

1. Electron microscopical evaluation of sets of serial fine sections of pancreatic arteriolar muscle of the cat showed no significant difference between the number of pinocytotic vesicles per unit length of smooth muscle cell membrane in ;synaptic' and ;non-synaptic' regions.2. With high resolution autoradiography, (3)H-phenoxybenzamine was found to be distributed over the cytoplasm and nuclei of smooth muscle cell profiles of guinea-pig vas deferens, although no localization in relation to discrete morphological organelles was evident.3. ;Specific protection' of alpha-adrenoceptors using 606 muM noradrenaline resulted in a significant diminution in the binding of (3)H-phenoxybenzamine as evidenced by a decrease in silver grain concentrations over smooth muscle cell profiles in autoradiographs.4. The significance of these findings in relation to the site and distribution of alpha-adrenoceptors is discussed.

Animals↗
PubMed1971

Response to acetylcholine and nicotine of the perfused vessels of the rabbit ear.

1. The vessels of the isolated rabbit ear were perfused at 23 mbar with Krebs solution with (tonic) and without (atonic) noradrenaline (5.9 x 10(-7)M) at selected temperatures of 20 degrees -38 degrees C. Peripheral resistance units (PRU) were calculated from the observed peak flow rates and alterations caused by drugs expressed as Delta% PRU.2. ACh is constrictor in the atonic vessel.3. ACh is a vasodilator of the tonic vessel perfused with NA. This effect is potentiated by anticholinesterase and by denervation, unaffected by botulinum toxin and antagonized by atropine. ACh also dilates the vessel perfused with vasopressin.4. Increasing the temperature reduces the responses to ACh but increases the effect of anticholinesterase.5. Nicotine causes a dose dependent dilatation of the tonic vessels, reduced but not abolished by C(6), by atropine, by botulinum toxin and by denervation.6. Nicotine causes a dose dependent constriction of the atonic vessels, abolished by C(6) and by phentolamine, reduced by denervation, but unaffected by botulinum toxin.

Acetylcholine↗