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Biomedical subjects

Y Okuda

Publications and source records attributed to Y Okuda.

At least 415 records · Page 23Linked to original sources
PubMed1978

Control of cerebral vascular smooth muscle during general anaesthesia.

The effects of some general anaesthetics, for example thiopentone, Althesin (alphaxalone + alphadolone) and ketamine, on cerebral vascular smooth muscle are those which would be expected from their metabolic actions. With other anaesthetics, mainly those administered by inhalation, and especially the volatile agents, cerebral blood flow increases in excess of the metabolic activity, which is usually depressed to varying degrees. During general anaesthesia with any of these agents, responses to changes in arterial Pco2 or blood pressure are maintained. Furthermore, when seizure activity occurs during enflurane administration, there is a flow response to the associated metabolic stimulation. The time course of the flow response to the metabolically depressant drug Althesin has been measured in baboons and shown to be very rapid. Wtih this drug cerebrovascular resistance begins to increase within 2 s of its arrival in the brain. This rapid flow change occurs also after sympathetic denervation. Extracellular fluid pH of the cortex does not alter until after the initiation of the vascular smooth muscle response.

Alfaxalone Alfadolone Mixture↗
PubMed1978

Time course of the cerebral circulatory response to metabolic depression.

Baboons anesthetized with halothane and N2O/O2 were given an intravenous steroid anesthetic (Althesin; Glaxo Laboratories Ltd., U.K.). The drug bolus was labeled with 99mTc, and the time from central venous injection to peak radioactivity in the brain was designated drug brain arrival (DBA-peak). The electroencephalogram slowed 1.2 +/- 0.9 s after DBA-peak (P greater than 0.2), and approximately 2 s after DBA-peak, internal carotid blood flow (ICarBF) decreased and calculated internal carotid vascular resistance (ICarVR) rose. During this 2-s delay in the cerebrovascular response to the arrival of a cerebral metabolic depressant in the brain, the decrease in mean cortical Pco2 was calculated to be less than 0.26 mmHg from cortical CO2 solubility, and less than 0.32 mmHg from cortical CO2 diffusivity, which indicated that mean cortical Pco2 changes do not control cerebral blood flow (CBF). The unaltered time course of the changes in EEG, ICarBF, and ICarVR after acute cervical sympathectomy and alpha-adrenergic receptor blockade excluded the involvement of the sympathetic nervous system in the vasoconstrictor response. Intracarotid Althesin showed that the cerebral vasoconstriction was not a direct effect of the drug. The postulated link between the effects of Althesin on CBF and cerebral metabolism remains to be elucidated but is probably indirect, involving the brainstem.

Adrenergic alpha-Antagonists↗
PubMed1976

The effect of althesin (CT 1341) on the oxyhaemoglobin dissociation curve in vitro.

Blood from non-smoking donors was incubated with Althesin and the PO2 for half-saturation of haemoglobin at standard pH, PCO2 and temperature (P 50) was measured. The mean P 50 values of blood with blood concentrations of Althesin of 0.14 ml/dl and 0.42 ml/dl were greater (1.14 +/- 0.31 (SEM) mm Hg (P less than 0.005) and 2.22 +/- 0.35 (SEM) mm Hg (P less than 0.001), respectively) than that of control blood. These increases were dose-dependent (P less than 0.05). Erythrocyte 2,3-diphosphoglycerate (2,3-DPG) concentrations were not significantly different between the Althesin-treated and the control blood. Although a decrease in the affinity of haemoglobin for oxygen in vitro in the presence of Althesin was statistically significant, this would have no clinical significance if the drug was being used for the induction of anaesthesia only.

Adult↗
PubMed1976

Effects of Althesin on cerebral blood flow and oxygen consumption in man.

Cerebral circulation and metabolism during Althesin anaesthesia were studied in seven healthy patients. Althesin was given in a single dose of 0.1 ml/kg and thereafter infused at a constant rate of 0.3 ml/kg/h. During Althesin infusion, the cerebral blood flow (CBF), the cerebral metabolic rate for oxygen (CMRo2) were 29 +/- 10 ml/100 g/min and 1.7 +/- 0.4 ml/133 g/min, respectively. These values were significantly different from those obtained in awake subjects in our laboratory (CBF: 46 +/- 7 ml/100 g/min; CMRo2: 3.1 +/- 0.6 ml/100 g/min). During CBF measurement, the mean cerebral perfusion pressure, cerebral vascular resistance (CVR) and arterial carbon dioxide tension (PaCO2) were 89 +/- 16 mm Hg, 3.4 +/- 1.3 mm Hg/ml/100 g/min, and 36 +/- 9 mm Hg, respectively. The relationship between CBF and PaCO2 were studied and it was found that during Althesin anaesthesia reactivity of cerebral vessels to the alteration of PaCO2 was maintained. It is concluded that Althesin caused cerebral metabolic depression which was accompaned by a decrease in CBF and an increase in CVR.

Adult↗
PubMed1976

Changes in CO2 responsiveness and in autoregulation of the cerebral circulation during and after halothane-induced hypotension.

CO2 responsiveness of the cerebral circulation has been measured in baboons before, during, and after halothane-induced hypotension. At a systolic blood pressure (BP) of 60 mmHg, C02 responsiveness was abolished, but was maintained at higher levels of BP. After hypotension, CO2 responsiveness returned to control values. Autoregulation to BP increases induced by intravenous noradrenaline was impaired when cerebral perfusion pressure during the hypotensive period had been below 30-40 mmHg. It is concluded that at levels of halothane-induced hypotension commonly employed clinically, CO2 responsiveness of the cerebral circulation may be absent. The return of CO2 responsiveness in the post-hypotensive phase argues in favour of controlled hyperventilation after neurosurgery which has involved induced hypotension.

Animals↗