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Biomedical subjects

G Cumming

Publications and source records attributed to G Cumming.

At least 55 records · Page 3Linked to original sources
PubMed1984

Assessment of smoking behaviour and ventilation with cigarettes of differing nicotine yields.

Nine established cigarette smokers were each studied four times, smoking two identical cigarettes on each occasion. After an acclimatization study, they smoked one of three types of cigarettes, either their usual brand or one of two types of special low tar cigarettes. These latter both had tar yields of about 8 mg with nicotine yields of 0.55 (LN) and 0.90 (MN) mg respectively. The test order was randomized between individuals and before using the special cigarettes the subjects were given a pack to accustomize themselves. While smoking each cigarette, magnetic tape recordings were made of puff rate, ventilation measured by respiratory inductive plethysmography (RIP) and nasal airflow measured with a modified oxygen cannula. The data were then processed digitally off-line. Salivary nicotine and alveolar carbon monoxide levels were measured before and after smoking each cigarette, and the cigarette butt was analysed for nicotine. While smoking behaviour varied considerably between the various subjects only small differences were seen between the different cigarette types in puff volume and duration and shape of the puff profile. Some changes in smoking behaviour occurred during the course of smoking a single cigarette. Ventilatory patterns showed consistent inter-subject differences but there were no apparent variations due to the various cigarettes. Most subjects puffed during an expiration with the buccal cavity closed off, and then took a slower, deeper inspiration breathing through the mouth. Others, however, took puffs at any point in the respiratory cycle. The different nicotine yields of the cigarettes produced marked changes in the butt and salivary nicotine measurements, but neither these, nor the changes in alveolar carbon monoxide, were closely related to ventilatory measurements. Possible explanations for these discrepancies are discussed.

Adult↗
PubMed1983

The assessment of nocturnal oxygen saturation.

Existing methods of assessing nocturnal episodic hypoxaemia are either insensitive or ignore the majority of the available data. We describe a method of analysis using off-line digital processing. A distribution of oxygen saturation (SaO2) with time is produced from all the available data, and subjected to moment analysis to produce a simple index which describes an entire night's SaO2. Our results suggest that the mean and the coefficient of skew fully described a night's SaO2. However, in subjects with chronic air-flow obstruction, the third moment about 100% oxygen saturation (M3100), a single figure, has the same descriptive power as mean and skew. In 17 subjects with chronic air-flow obstruction a significant correlation was found between both daytime SaO2 and PaCO2 when plotted against either the M3100 or the skew. Measurements made on two occasions in seven subjects showed good reproducibility for the skew and M3100 indices.

Adult↗
PubMed1983

Breathing near to residual volume with positive expiratory pressure.

Breathing near to residual volume produces arterial desaturation demonstrable by ear oximetry. This paper describes the effect on arterial saturation measured by an ear oximeter of expiring to residual volume, taking a normal inspired volume of air from ambient pressure, and then expiring to residual volume against a pressure of 10-15 cm of water. This breathing pattern was continued for several minutes. Carbon dioxide output and oxygen consumption were measured during the study and the closing volume at ambient pressure was compared with that at increased expiratory pressure. Arterial desaturation was actually increased by the increased airways pressure, the increase being modified both by minute volume and tidal volume. Closing volume was only slightly increased, but residual volume was considerably increased, by the raised pressure. The desaturation is only partially explicable on a ventilatory basis, and there is probably a component concerned with perfusion, and the absence of perfusion adaptation from hypoxic areas does not appear to accord with current hypotheses.

Adult↗
PubMed1982

Effect of atropine on alveolar gas mixing in man.

1. Atropine is known to diminish bronchomotor tone. In order to investigate the acute effect of atropine on respiration and alveolar gas mixing, a dose of 2.4 mg was given intravenously. 2. Ten normal male volunteers were each studied three times with a nitrogen washout method, once before administration of atropine and then 20 min and 60 min thereafter. 3. After the administration of atropine there was a reduction in tidal volume, a slight increase in frequency of respiration and an increase in series dead space. The tidal mixing volume showed a fall of 25%. In spite of the reduced alveolar dead space the effective mixing volume fell by 29%. Multi-breath alveolar mixing efficiency fell by 3.5%. 4. Multi-breath alveolar mixing efficiency was found to be less with smaller tidal mixing volumes, a fall of 518 ml in the latter causing a reduction of 17.2% in mixing efficiency. 5. A reduction of 100 ml in tidal volume in normal subjects was associated with a decrease of 6.9% in alveolar mixing efficiency. In the subjects receiving atropine tidal volume reduced by 96 ml, but the observed fall in alveolar mixing efficiency was only 3.5%, This suggests an improvement in alveolar mixing of 3.4% due to the administration of atropine. Despite this small improvement, the mixing efficiency is still only 66%. The residual inefficiency of 34% cannot therefore be explained on the basis of bronchomotor tone.

Adult↗
PubMed1982

Gas mixing in a model of the pulmonary acinus with asymmetrical alveolar ducts.

An asymmetrical model of the human pulmonary acinus is described, in which elements of volume are represented by nodes joined by conductors permitting convective flow and molecular diffusion. The method of analysis permits simultaneous convection, diffusion, and dimensional change in any direction and requires only simple boundary conditions. Inspiration of O2 into a resident gas of 79% N2 followed by expiration was simulated at two flows. On expiration the slope of the alveolar plateau was 1.7%, and the alveolar N2 mixing efficiency was 97.0%. A symmetrical but otherwise similar model gave a slope of zero and a mixing efficiency of 99.9%. The patterns of gas concentration within the asymmetrical acinus during the respiratory cycle confirm and extend previous observations on the interactions between simultaneous convection and diffusion in asymmetrical structures (16, 21, 22). Even though these in combination within alveolar duct asymmetry can account for the slope of the alveolar plateau, they are insufficient to account for the failure of complete gas mixing found in normal subjects.

Humans↗
PubMed1982

Effect of heart rate and stroke volume on gas mixing in dog lung.

In nine anesthetized and ventilated dogs heart block was induced at thoracotomy, a pacemaker was inserted, and an electromagnetic flow transducer was placed round the main pulmonary artery. The chest was then closed. Stroke volume (SV) was varied by changing central blood volume. Ventilatory dead space (VDS) and alveolar nitrogen mixing efficiency (ANME) were measured at three levels of heart rate (HR) and three levels of SV independently varied during life and also after cessation of heartbeat. Neither VDS nor ANME showed a significant change with HR or SV during life, but mean VDS increased by 43 ml (22%) and mean ANME decreased by 4.4% postmortem. We conclude that cardiac action increases gas mixing at the interface between inspired and resident gas but has only a small effect on gas mixing distal to the interface during respiration without breath holding.

Animals↗
PubMed1982

Acute oxygen toxicity in a saturation diver working in the North Sea.

A commercial diver taking part in a saturation dive (O2-He) was exposed intermittently to 1.4 b of oxygen for a total of 55 h. He developed the syndrome associated with oxygen pulmonary toxicity. Detailed pulmonary function spirometry tests before and after the incident showed that a significant decrease in the forced vital capacity and forced expired volume in 1 s occurred and full recovery was at this time not present 12 weeks after the incident, although by this time he demonstrated a high state of cardiopulmonary fitness. These findings indicate that the lung damage caused by acute oxygen toxicity take more than 12 weeks to disappear, but the condition does seem to be reversible.

Adult↗
PubMed1981

Comparison of ventilation/perfusion lung-imaging and dead-space measurements in airway disease.

1. Nineteen patients (three normal subjects, at 16 patients with chronic airway disease) were investigated with radionuclide lung-imaging and pulmonary function tests. 2. There was a statistically significant correlation between the ratio of residual volume to total lung capacity and alveolar dead-space ventilation for nitrogen as a percentage of alveolar ventilation (an index of gas mixing inefficiency); rs = 0.54, P less than 0.05. 3. There were statistically significant associations between an abnormal ventilation or perfusion radionuclide lung image and (a) the ratio of residual volume to total lung capacity and (b) the alveolar dead-space ventilation for nitrogen as a percentage of alveolar ventilation. 4. The radionuclide counts from the posterior images were normalized for lung size and injected dose; perfusion counts were then subtracted from ventilation counts at locations from the top to the bottom of the lungs. 5. There was a statistically significant association between low ventilation minus perfusion areas and arterial hypoxia. 6. There was a statistically significant association between high ventilation minus perfusion areas and an increased alveolar dead-space ventilation for carbon dioxide as a percentage of alveolar ventilation.

Adult↗
PubMed1981

The concept of deadspace with special reference to the single breath test for carbon dioxide.

We present a review and a theoretical analysis of factors determining airway deadspace (VDaw) and alveolar deadspace (VDalv), the two constituents of physiological deadspace (VDphys). VDaw if the volume of gas between the lips and the alveolar/fresh gas interface, the location of which is determined by inspiratory flow pattern and airway geometry. VDalv can be caused by incomplete alveolar gas mixing and associated V/Q mismatching within the terminal respiratory units, temporal V/Q mismatching within units, spatial V/Q mismatching between units, and venous admixture. Most causes of VDphys are influenced by inspiratory flow pattern and the time available for gas diffusion and distribution. Analysis can be made from the single breath test for carbon dioxide (SBT--CO2) which is the plot of fraction of carbon dioxide in expired gas against expired volume. The common causes of VDalv are associated with a sloping SBT-CO2 phase III. Combination of SBT-CO2 with PaCO2 yields VDphys and VDalv. A sloping phase III with a negative arterial-end-tidal PCO2 gradient implies compensation by perfusion for early emptying, overventilated alveoli.

Breath Tests↗
PubMed1981

Boundary-layer oxygen depletion in blood gas analysis.

When O2 is withdrawn from blood by diffusion through a membrane and an O2-depleted boundary layer is formed, it is suggested that the depletion can cause significant dissociation of oxyhemoglobin (HbO2) in this layer. The resulting nonlinear relation between net diffusive flux of O2 through the membrane and the blood PO2 should be observable with membrane systems having a sufficiently high permeability to O2. Evidence for this suggestion is presented from in vitro experiments using a mass spectrometer to analyze the O2 flux through membrane systems. A theoretical model of HbO2 dissociation in the depleted boundary layer of blood that explains these results qualitatively is developed to yield quantitative predictions found to be in reasonable agreement with the experimental observations. The effect was seen to be of significance for membrane systems with O2-sampling rates of about 2 X 10(-9) ml. s-1. Torr-1 and over; so if such systems are to be used for the analysis of blood PO2, the phenomenon must be taken into account.

Blood Gas Analysis↗
PubMed1981

Can carbon monoxide be absorbed from the upper respiratory tract in man?

To investigate the possible absorption of carbon monoxide into the blood from tobacco smoke confined to the mouth and upper airways, an indirect study was made on 12 normal subjects of the recovery of CO from a bolus administered at various levels during a preceding inspiration. No measurable CO uptake was observed unless the bolus was inhaled early enough in inspiration to reach the alveolar region of the lung. Some movement of a tracer gas, argon, was however seen from the upper airways during breath-holding so that some CO might escape into the lungs this way. No detectable CO uptake occurred in one subject who inspired the bolus into his nasal cavities. We conclude that the elevated carboxyhaemoglobin levels seen in smokers, can only occur when smoke is inhaled into the lung, since no appreciable uptake can occur in the upper airways.

Absorption↗
PubMed1980

Perception at the blind spot and tilt aftereffect.

Black and white stripes were used to induce a tilt aftereffect near the blind spot. Stripe fragments on either side of the blind spot were seen as being completed across the blind spot, but the magnitude of the tilt aftereffect they induced suggested that the perceptually "filled-in" portions of the stripes did not contribute to the aftereffect. So perceptually filled-in lines seem not to be fully potent percepts.

Adult↗
PubMed1979

Estimation of lung volumes from chest radiographs using shape information.

The cross-sectional shapes of the chest and its contained structures have been assessed in post-mortem anatomical sections and from computerised tomographic scans in living subjects. These shapes are described by simple equations that can be used to increase the accuracy of measuring lung volumes from chest radiographs. Radiographic estimates of total lung capacity, using the equations, were compared with plethysmographic and single-breath helium dilution measurements in 35 normal subjects. The postures commonly used for taking chest radiographs were found, on average, to decrease total lung capacity (TLC) and to increase residual volume by about 200 ml when compared with the sitting positions used for the other two measurements (studies made in 18 of the subjects). After correction for this effect, the radiographic estimates of TLC, which measure the displacement volume of the lung, exceeded the plethysmographic estimates of contained gas volume by a mean of 720 ml, which was taken as the volume of tissue, blood, and water in the lungs. The single-breath dilution estimates of TLC fell short of the plethysmographic values by a mean of 480 ml, taken as the volume of contained gas that was inaccessible to helium in 10 seconds. The tomographic studies suggested that the radiographic technique of measuring lung displacement volumes has an accuracy of +/- 210 ml. The method is rapid and simple to use and has intra- and inter-observer variabilities of less than 1% and less than 5% respectively.

Helium↗
PubMed1978

The isolation and partial characterization of the major bronchial glycoproteins.

Partial characterization of glycoprotein obtained from mucous secretion of the bronchi and stomach has been attempted. The isolated glycoproteins and the glycoproteins from gastric aspirates showed similar carbohydrate and amino-acid composition. They consist of a protein core to which are attached carbohydrate side chains of galactose, N-acetylglucosamine and N-acetylgalactosamine in the ratio of 4 : 3 : 1. Superimposed on this structure were additional sugar residues, the blood group determinants. The carbohydrate side chains are linked by an alkali-labile O-glycosidic linkage to the threonine and serine residues of the protein core, with N-acetylgalactosamine forming the link.

Acetylgalactosamine↗