Respiratory ventilation.
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Biomedical subjects
Publications and source records attributed to A Guz.
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The medically qualified academic research worker under university aegis but within the National Health Service has recently been subjected to frightening forces. His traditional role of being allowed and financed to do what he wants is questioned in an age of economic crisis and of concern about how to spend limited resources. The call for 'relevance' in academic research makes sense when looked at from society's viewpoint but nonsense when looked at from the research worker's viewpoint. Recent personal experience has generated a proposal for the resolution, in part, of these conflicting claims; namely, the university hospital. Unless academic research continues to flourish within our present framework, the quality of the practitioners of medicine and paramedical subjects will drop slowly over the next 20 years as the spirit of enquiry dies!
1. The effect of breathing an anaesthetic aerosol of 5% bupivacaine hydrochloride has been assessed in dog and man. 2. In the dog, the cough reflex was abolished and the Hering-Breuer inflation reflex severely impaired or abolished; breathing became slower and deeper; no pathological changes were found in the lungs of these dogs. 3. In man, no untoward effects resulted from a 10 min period of aerosol inhalation; there were no systematic effects on airway resistance or lung volumes and the cough reflex in response to either tactile or chemical (citric acid aerosol) stimulation was invariably abolished. The Hering-Breuer inflation reflex was impaired, but this was not associated with any change in resting ventilation. The Ve/CO2 response was enhanced after aerosol anaesthesia; subjects felt an exaggerated dyspnoea. The aerosol anaesthesia abolished the afferent pathway of a reflexly elicited bronchoconstriction in one subject. There was no effect on the ability to hold the breath, or on the quality of the associated sensation. 4. Control aerosols of sodium chloride solution or phosphate buffer produced no effects. Control experiments with intravenous infusions of bupivacaine proved that none of the effects could have been produced by systemic effects of the absorbed anaesthetic. 5. Plasma concentrations of bupivacaine in man did not exceed a recognized toxic level. The experiments demonstrate a safe reversible anaesthesia of the airways in man lasting for a period of 10-20 min.
1. A rapid method for the analysis of CO in expired air has been developed, which is suitable for use in studies of smoking. 2. The Bohr equation has been used to calculate the mean alveolar CO partial pressure (PA,CO). 3. The values of PA,CO obtained are highly correlated with direct measurements of venous carboxyhaemoglobin (r = 0-96). 4. The method will distinguish between populations of smokers and non-smokers, and can allow the changes of CO in a smoker throughout a 12 h period to be followed. It provides a measure of the dose of cigarette smoke (vapour phase) that results from smoking a single cigarette.
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Two groups of dogs were anaesthetised, paralysed and artificially ventilated using a respirator driven by the phrenic motoneurone output, electrically processed to resemble transpulmonary pressure. In one group, blood gases were maintained constant with closed-chest cardiopulmonary bypass; the second group were studied without "bypass". Therefore it was possible to determine the relative contributions of vagal and chemial feedback to the effect of altering the depth of an inspiration on the associated phrenic motoneurone output. Mono-exponential regressions between change of respirator gain and changes in both inspiratory time and peak amplitude of the processed phrenic signal were found for all dogs. The rate of rise of the processed phrenic signal usually changed in the direction of the change in respirator gain, suggesting the presence of vagal positive feedback during eupnoeic breathing. After vagotomy, all responses were absent in the "bypass" group and small in the "non-bypass" group. These experiments quantitate the role of pulmonary vagal afferent discharge, in phase with inspiration, in the regulation of phrenic motoneurone output in a closed-loop situation.
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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).
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1. Breuer's hypothesis that the vagus nerves exert a tonic control of respiratory rhythm, in addition to the phasic control, was examined.2. Closed-chest cardiopulmonary bypass was instituted in dogs weighing 20-30 kg anaesthetized with chloralose. Respiratory rhythm was recorded from a phrenic electroneurogram.3. Complete muscular paralysis induced with gallamine triethiodide produced an increase in the duration of inspiration and an increase in the amplitude of the integrated phrenic electroneurogram. There was no consistent effect on expiratory duration. Gallamine produced no effect when given after vagotomy.4. In the paralysed state, an increase in lung volume of 25-100 ml. for 30-60 sec produced a sustained increase in the duration of expiration and a decrease of respiratory rate: there was little effect on inspiratory duration, or the amplitude of the integrated phrenic electroneurogram.5. A decrease in lung volume of the same order of magnitude for the same period produced a sustained decrease in the duration of expiration and an increase of respiratory rate: there was little effect on inspiratory duration or the amplitude of the integrated phrenic electroneurogram.6. The phenomena described in (5) and (6) constitute a high gain respiratory frequency controller. They did not occur after bilateral cervical vagotomy.7. Bilateral cervical vagotomy during complete muscular paralysis produced a further increase in the duration of inspiration and in the amplitude of the integrated phrenic electroneurogram; there was no consistent effect on expiratory duration.8. The results confirmed Breuer's hypothesis and showed that inspiratory duration and expiratory duration are controlled independently.
The type J receptors are stimulated during pulmonary congestion produced by occluding the aorta or left a-v junction which causes the left atrial pressure to rise with consequent rise in pulmonary artery pressure. Such acute congestion can be maintained only for brief periods (1-2 min). Longer lasting congestion leading eventually to pulmonary oedema is produced by injecting alloxan into the right atrium or right ventricle. A marked rise in pulmonary artery pressure follows the injection and after a lag there follows intense excitation of the type J receptors. It was concluded that this excitation was due to a rise in pulmonary capillary pressure and increase in permeability of the capillary membrane. Recent experiments have revealed that a considerable increase in activity can also be produced by injecting plastic microemboli (diameter 50 minus-plus 10 micrometers, i.v.). This increase occurs a few minutes after the rise in pulmonary artery pressure and is not due to a direct action of the microemboli on the endings nor can it be due to increased capillary permeability. Here, there can be no doubt that the increase in activity is a consequence of the rise in pulmonary artery pressure leading to a rise in pulmonary capillary pressure. This causes increase in interstitial volume leading to excitation of the endings. It was postulated that the endings were located in collagen tissue which acts like a sponge. Recently electronmicroscopic evidence has been obtained showing the presence of non-medullated sensory fibres in this collagen tissue but the precise structure of the endings (presumably type J) and their physical relation to the collagen tissue still remains to be established.
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