Propranolol, exercise, and arterial plasma potassium.
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Biomedical subjects
Publications and source records attributed to D M Band.
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We have monitored oscillations in arterial pH (of respiratory frequency) in normal man at rest and during exercise. The pH oscillations are known to reflect respiratory oscillations in arterial carbon dioxide tension generated at the lungs. We have found that the pH oscillations increase in their upslope and downslope during exercise. This means that oscillations in arterial carbon dioxide tension can be considered as a control signal.
Various preparations of calcium are recommended for use in treatment of cardiac arrest and advantages are claimed for one preparation over another because of increased availability of the calcium to the heart. Ionised calcium levels in human blood have been assayed following the addition of calcium increments by use of the calcium electrode. The results showed no difference between calcium chloride and calcium gluconate.
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1. The discharge of chemoreceptor afferents in preparations of the sinus nerve in spontaneously breathing anaesthetized cats has been subjected to an averaging procedure in records obtained when the animals breathed (a) air and (b) a hypoxic gas mixture. 2. The mean discharge frequency was higher in hypoxia than at normal oxygen tension. 3. Oscillations in chemoreceptor discharge frequency with the same period as respiration were obtained by the averaging procedure both at normal arterial oxygen tensions and in hypoxia, but there was no significant increase in oscillation amplitude with hypoxia. 4. The carotid body response to arterial PCO2 oscillations does not therefore appear to be amplified by hypoxia. This finding is discussed in relation to the reported dependence upon hypoxia of the ventilatory effects of tube breathing in man.
Respiration, sinus nerve chemoreceptor discharge, and carotid arterial pH were monitored in cats. Chemoreceptor discharge frequency showed oscillations that had a respiratory period when averaged over many respiratory cycles. These oscillations disappeared when pH oscillations of respiratory period were eliminated from the carotid arterial blood. The maximum sinus nerve discharge was associated with the most acid point of the recorded pH oscillation. Briefly increasing PCO2 by giving CO2-rich saline into the aortic root resulted in brief reduction in carotid arterial pH, and when this reduction occurred during inspiration tidal volume increased, even with a pH change no larger than the pH oscillations. However, increased chemoreceptor discharge could only be demonstrated when each pH change had twice the amplitude of the pH oscillations. Injections of fixed acid mixed with free carbonic anhydrase transiently increased chemoreceptor frequency, whereas injections of fixed acid alone had no effect. The carotid body is therefore sensitive to small rapid changes in arterial PCO2, and the pH electrode record indicates the size of the stimulus except when fixed acid changes are produced too closely upstream.
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We have previously shorn that the respiratory control system in the cat has the requisite sensitivity and speed to respond to changes in arterial pH which are equal to, or smaller than, the normal fluctuations in pH with respiration. A respiratory response was only observed when the changes in pH were produced by alterations in PCO2 and not when they were induced by non-gaseous acids. We describe now the respiratory effect produced by various procedures which modify or abolish the naturally occurring arterial pH oscillations before they reach the peripheral chemoreceptors. The pH oscillations were abolished by a mixing chamber, whilst their phase relationship to respiration was altered by delay coils; by presenting a moving plastic surface to the arterial blood stream it was possible to distort the shape of the oscillations without increasing the transport lag between lung and peripheral chemoreceptors. All manoeuvres produced a brief period of respiratory stimulation which was greater than could occur by chance. We were particularly concerned in these experiments with the possibility of artefacts in our experimental design. We feel that we have excluded respiratory effects due to changes in arterial pressure, blood temperature and mean pH. We are less confident that we have excluded changes in ventilation resulting from the release of a substance (or substances) from the contact of blood with plastic or glass surfaces. This problem is discussed in relation to experiments on the control of breathing where blood, which is perfusing the chemoreceptors, has been in contact with artificial surfaces.