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Biomedical subjects

G Ross

Publications and source records attributed to G Ross.

At least 253 records · Page 14Linked to original sources
PubMed1975

Inhibition of in vivo Neural Vasoconstriction by exogenous catecholamines.

Intaarterial infusions of norepinephrine and dopamine markedly attenuated the mesenteric vasoconstrictor response to periarterial nerve stimulation in anesthetized cats, but did not attenuate the response to intravenous norepinephrine. The degree of attenuation was independent of stimulation voltage, but inversely related to frequency. The results are compatible with previous in vitro evidence that NE and DA decrease adrenergic transmitter release during nerve stimulation.

Animals↗
PubMed1975

Experiences with 16 cases of pararenal pseudocyst.

Pararenal pseudocysts developed after an operation, after blunt and penetrating trauma or after contiguous disease processes in 16 patients. Nephrectomy was necessary in 8 cases. Although the duration of the pseudocyst and the extent of conduit injury did to an extent determine the fate of the kidney, the location of the encapsulated extravasate and its propensity for curtailment of urine formation appeared to be more significant factors. The cases were reviewed in light of the individualization in management required for the complex problems they present.

Drainage↗
PubMed1973

Duston ward.

Explore the source record for details and available documents.

Child↗
PubMed1973

Effects of intracoronary infusions of acetylcholine and nicotine on the dog heart in vivo.

1. In anaesthetized dogs intracoronary infusions of high doses of nicotine and acetylcholine increased myocardial contractile force and this could be prevented by pre-treatment with desmethylimipramine or phenoxybenzamine.2. The inotropic effect of nicotine was brief and subsided during the continuing infusion of the drug. The infusion of nicotine did not reduce the inotropic effects of cardiac sympathetic nerve stimulation.3. The motropic effect of intracoronary acetylcholine often fluctuated during prolonged infusions and was not altered by pretreatment with atropine. Acetylcholine infusions reduced the inotropic responses produced by cardiac sympathetic nerve stimulation and led to a substantial transient reduction in the associated pressor responses. Intracoronary acetylcholine also reduced the pressor and inotropic effect of intravenous noradrenaline. The attenuation of these adrenergic cardiovascular responses by acetylcholine was prevented by atropine.

Acetylcholine↗