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Biomedical subjects

B A Cross

Publications and source records attributed to B A Cross.

At least 55 records · Page 3Linked to original sources
PubMed1974

The effect of carbon dioxide in the airways and alveoli on ventilation; a vagal reflex studied in the dog.

1. The inhalation of CO(2) produces a tachypnoea only in the presence of intact vagus nerves; the present study was designed to examine the mechanism of this phenomenon in the dog.2. Closed-chest cardiopulmonary bypass was established in dogs weighing 16-24 kg, anaesthetized with chloralose. When the ;bypass' was established pulmonary blood flow ceased, P(A, CO2) was reduced and the respiratory rate slowed. 3-10% CO(2) in O(2) could then be inhaled without change in the level of P(a, CO2) set at the oxygenator.3. The addition of CO(2) in these concentrations to the inspired oxygen resulted in an increase in respiratory frequency, maximal at the first breath and sustained for the 1 min period of exposure. The increase in respiratory frequency was due to a shortening of expiratory duration. Inspiratory duration did not change. The response was absent after vagotomy.4. Inert gases in O(2), given as a control, had no effect on breathing.5. The effect of raising P(a, CO2) (by increasing the concentration of CO(2) in the gas equilibrating the blood in the oxygenator), was primarily to increase tidal volume.6. The ventilatory effect of inspiring CO(2)/O(2) mixtures was shown to be additive to the effect of raising P(a, CO2).7. These experiments show that an afferent vagal reflex originating from the lungs causes tachypnoea, when a dog, on ;bypass', inhales low concentrations of CO(2) in O(2).

Animals↗
PubMed1971

Unit activity in rat diencephalic islands--the effect of anaesthetics.

1. Unit activity was recorded with steel micro-electrodes from 486 hypothalamic neurones in rat diencephalic island preparations.2. The histograms of firing frequencies for populations of hypothalamic units from unanaesthetized preparations and from those under urethane anaesthesia were not significantly different. The firing rates of both were significantly faster than those observed in intact brains under urethane.3. The mean distance between stable units in unanaesthetized island preparations did not differ significantly from that in preparations anaesthetized with urethane.4. The response of individual neurones to intravenous injections of urethane was variable, and apparently not associated with the onset or maintenance of anaesthesia. Some showed transient acceleration, some deceleration and some no change in rate or pattern of discharge.5. All neurones tested were slowed or stopped by intravenous injections of subanaesthetic doses of sodium methohexitone (Brietal). The responses were highly reproducible and dose-dependent.6. Brietal also produced a fall in arterial pressure and depressed respiration. Inhalation of amyl nitrite evoked larger hypotensive responses but did not affect unit activity; nor did inhalation of CO(2) (hypercapnia) or N(2)O (hypoxia).7. It is concluded that urethane anaesthesia is not associated with any direct action on hypothalamic neurones. The depression of firing rate in hypothalamic neurones induced by Brietal may represent an important forebrain mechanism in anaesthesia by this agent.

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