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Biomedical subjects

I M James

Publications and source records attributed to I M James.

At least 55 records · Page 3Linked to original sources
PubMed1977

Effect of oxprenolol on stage-fright in musicians.

The effect of 40 mg oxprenolol on stage-fright was assessed in 24 musicians in a double-blind crossover trial. Musical performance judged by two professional assessors was found to improve. Greatest improvement was seen on the first performance and in those most affected by nervousness.

Administration, Oral↗
PubMed1975

The role of baroreceptors and chemoreceptors in the regulation of the cerebral circulation.

1. Ten experiments, each using two dogs, were performed to evaluate the effect of chemoreceptor and baroreceptor activity on the cerebral circulation. 2. The carotid bifurcation areas were vascularly isolated bilaterally and perfused with arterial blood from a second animal. 3. Bilateral vagotomy interrupted stimuli from the aortic group of receptors. 4. Administration of 5% carbon dioxide to the donor animal resulted in an increase in cerebral (cortical) blood flow in the recipient. 5. A change in the arterial perfusion pressure from the donor resulted in a reciprocal change in the cerebral blood flow of the recipient. These changes were abolished by sectioning the sinus nerves.

Animals↗
PubMed1975

Factors affecting the cerebrovascular response to noradrenaline in the dog.

1 Noradrenaline infused into the internal carotid artery of the dog (0.01-1 mug kg(-1) min(-1)) constricts the blood vessels of the cortex. This constriction is mediated by the action of noradrenaline on alpha-adrenoceptors of the cerebral arteries.2 Intravenous (1 mug kg(-1) min(-1)) or intra common carotid arterial (0.01-1 mug kg(-1) min(-1)) infusions of noradrenaline cause an increase in cortical blood flow that can be dissociated from changes in blood pressure.3 The effect of intravenous noradrenaline on the cortical blood vessels and metabolism is blocked by high PaCO(2) levels, or by the prior administration of (+/-)-propranolol. (+)-Propranolol is without such effect.4 Following section of both vagi and both sinus nerves, intravenous noradrenaline fails to cause an increase in cortical blood flow.5 In another series of animals the area of the carotid bifurcation was vascularly isolated and perfused with blood from a second dog. Chemoreceptor and baroreceptor activity was shown to be intact.6 Administration of 5% CO(2) to the donor dog caused an increase in cerebral blood flow in the recipient dog.7 Administration of intravenous noradrenaline (1.0 mug kg(-1) min(-1)) to the donor animal caused an increase in cerebral blood flow, cerebral O(2) and glucose utilization of the recipient.8 Administration of 5% CO(2) and intravenous (-)-noradrenaline (1.0 mug kg(-1) min(-1)) caused a further increase in flow and metabolism.9 This evidence suggests that the cerebrovasodilatation observed following intravenous noradrenaline is reflex and is triggered by chemoreceptor activity.10 The evidence also suggests that the antagonism of the cortical dilatory effects of intravenous noradrenaline by raised PaCO(2) in the intact animal must be at a site different from the peripheral chemoreceptors.

Animals↗
PubMed1974

Treatment of chronic hepatic encephalopathy with levodopa.

Three of six patients with chronic hepatic encephalopathy treated with levodopa showed a significant improvement. One patient was probably improved whilst the remaining two patients failed to show any benefit. Serial electroencephalography did not demonstrate significant changes. Treatment with levodopa was associated with an improvement in ;speed-based' tasks as assessed by computerized psychometry. A significant rise in cerebral oxygen consumption was found during levodopa therapy. Gastrointestinal side effects were dose limiting. It is concluded that a therapeutic trial of levodopa in patients with chronic hepatic encephalopathy is indicated when the response to conventional therapy has been poor.

Adult↗
PubMed1974

Effect of ammonium salts on brain metabolism.

Ammonium acetate (13 m-mol), ammonium bicarbonate (13 m-mol), and ammonium hydroxide (30 m-mol) were administered intravenously to three separate groups of five dogs. Ammonium acetate and bicarbonate were given over a period of 15 minutes, ammonium hydroxide was given for 30 minutes. In all dogs, after 15 minutes' infusion, the blood ammonia concentration was similar to that found in patients with hepatic coma. When the ammonium hydroxide had been given for 30 minutes, lightening of anaesthesia was noted in all dogs studied. At this time blood ammonia values were over 1,000 μg/100 ml in two animals. Subsequent deepening of anaesthesia was observed after termination of the infusion. In all animals studied there was an increase in cerebral glucose consumption with little change in oxygen utilization. Arterial lactic acid was studied in the group given ammonium bicarbonate and found to increase at the same time as the increase in glucose utilization. Hyperventilation was precipitated by both acid and alkalilne ammonium salts. Lactic acidosis appeared to be the cause rather than the result of the hyperventilation. The protective effect of hyperventilation on brain metabolism is discussed.

Acetates↗