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Biomedical subjects

G S Allen

Publications and source records attributed to G S Allen.

At least 73 records · Page 4Linked to original sources
PubMed1974

Effects of the muscarinic agonist McN-A-343 on the release by sympathetic nerve stimulation of (3H)-noradrenaline from rabbit isolated ear arteries and guinea-pig atria.

1 McN-A-343 (4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride) in concentrations of 10(-5) and 10(-4)M inhibits the stimulation-induced efflux of radioactivity from segments of rabbit ear artery that have previously been incubated with (-)-[(3)H]-noradrenaline, and also decreases the contractile response.2 The inhibitory effects of McN-A-343 (10(-5)M) on the efflux of radioactivity and the contractions induced by low frequencies of stimulation (2 and 5 Hz) are reversed by atropine, but atropine does not modify these effects with high frequencies of stimulation (20 and 50 Hz).3 McN-A-343 (10(-4)M) enhances the stimulation-induced efflux of radioactivity from guinea-pig atria that have previously been incubated with (-)-[(3)H]-noradrenaline, and prolongs the positive inotropic response. These effects are not modified by atropine.4 It is concluded that McN-A-343 has different effects on adrenergic transmitter release in the two tissues. In the artery, it acts as an agonist on muscarinic receptors of adrenergic terminals to inhibit transmitter release at low frequencies of stimulation. In the atria it enhances transmitter efflux from the tissue, largely by inhibiting re-uptake.

Alkynes↗
PubMed1973

Comparison of effects of six cholinomimetic drugs on inhibition of uptake of 3 H-( )-noradrenaline by guinea-pig atria.

The effects of N,N-dimethyl-N'-phenyl-piperazinium (DMPP), 4-(m-chlorophenyl-carbamoyloxy) - 2 - butynyltrimethylammonium chloride (McN-A-343), pilocarpine, acetylcholine, methacholi-ne and nicotine in inhibiting the uptake of (3)H-(+/-)-noradrenaline by guinea-pig atria were compared. In concentrations of 1 x 10(-4)M, the percentage inhibitions were as follows: DMPP, 89.1%; McN-A-343, 78.7%; pilocarpine 43.5%; acetylcholine, 35.7%; methacholine, 32.9%; nicotine, 21.6%.

Acetylcholine↗
PubMed1972

Effects of McN-A-343 and DMPP on the uptake and release of 3 H-noradrenaline by guinea-pig atria.

1. McN-A-343 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride and DMPP (N,N-dimethyl-N'-phenylpiperazinium iodide) inhibit the uptake of (+/-)-(3)H-noradrenaline by guinea-pig atria, being approximately as potent as cocaine in this respect.2. The inhibition of uptake produced by McN-A-343 or DMPP was not affected by atropine or hexamethonium in concentrations which antagonized actions on muscarinic and nicotinic receptors respectively.3. McN-A-343 in the presence of atropine had a positive inotropic action on atria, but this was not accompanied by efflux of radioactivity from atria previously incubated with (-)-(3)H-noradrenaline.4. In the presence of McN-A-343, responses of atria to noradrenaline were increased and those to tyramine were decreased.5. DMPP had positive inotropic and chronotropic actions on atria, and these effects were accompanied by an increase in efflux of radioactivity from atria previously incubated with (-)-(3)H-noradrenaline.

Animals↗
PubMedDate not supplied

Control of the artificial heart.

The artificial heart (AH) is devoid of physiologic connections to the recipient's native feedback control loops. Control of an AH can be either passive or dynamic. Passive intrinsic control provides limited AH response to physiologic demands. Dynamic control requires the sensing of metabolic and hemodynamic signals and their incorporation into self-adjusting AH function. A single metabolic or hemodynamic parameter cannot provide sufficient data accurately to adjust AH pumping in response to varying blood flow demands. A combination of input control signals is required for reliable and flexible AH function. The selection of appropriate input control parameters and their incorporation into AH controller designs remains a critical step in the achievement of a permanent, totally implantable AH.

Heart Failure↗
PubMedDate not supplied

Cerebral arterial spasm: A discussion of present and future research.

The author presents a discussion of research on cerebral arterial spasm. Arterial smooth muscle contraction, receptor and relaxation mechanisms are presented in the context of what is known about cerebral arterial spasm and the biochemistry of vascular smooth muscle. Several new experimental approaches are suggested and a theoretical biochemical basis for the idea that damage to the artery alone could cause cerebral arterial spasm is postulated. Methods of determining cerebral arterial spasm and the need for a quantitative, in vivo method are discussed and the question of an irreversible stage of cerebral arterial spasm is considered. Finally, the problems associated with the delivery of a potentially successful treatment to the cerebral arterial smooth muscle cells are examined.

Actins↗