1. We assessed lung density, determined by computerized tomography, as a measure of emphysema and related this to lung function and measurement of the elastic recoil of the lung in normal subjects and patients with chronic obstructive lung disease. 2. We found a significant correlation between measurements of elastic recoil pressure at 90% of total lung capacity and both the forced expiratory volume in 1 s ( r = 0.80, P <0.001) and the transfer factor for carbon monoxide ( r = 0.70, P <0.001). Measurements of elastic recoil of the lung also correlated with lung density as measured by computerized tomography scanning ( P <0.001). 3. Multiple regression analysis demonstrated a correlation between the density of the lowest fifth percentile of the computerized tomography lung-density histogram, and both the natural logarithm of the shape parameter of the pressure-volume curve ( P <0.01), and the transfer factor for carbon monoxide ( P <0.01). However, the mean computerized tomography lung density correlated, in addition, with the elastic recoil pressure of the lungs at 90% of total lung capacity ( P <0.001). 4. Since the elastic recoil pressure correlates with computerized tomography lung density, and hence with emphysema, and since elastic recoil pressure also correlates with the forced expiratory volume in 1 s, these results suggest that loss of elastic recoil is one determinant of airflow limitation in patients with chronic obstructive lung disease.

1. Exponential analysis of lung pressure-volume curves is used to deal with the non-linearity of the pressure-volume relationship. A major problem of this procedure is to define the lower volume limit for exponential curve fitting. 2. In 12 healthy subjects and 24 patients with chronic airflow obstruction, a cubic function was fitted to the quasi-static pressure-volume curves to define an inflection point. 3. The exponential function of Colebatch et al . (Colebatch, H.J.H., Ng, C.K.Y. & Nikov, N. J. Applied Physiol. 1979; 46, 387–93) was then fitted to the data for volumes above the inflection point. 4. Exponential analysis with a cubic determination of an inflection point provides an objective way to describe the elastic properties of the human lungs in vivo .

1. To determine the mode of action of doxapram in man we have measured ventilation, oxygen uptake, CO 2 production, hypoxic and hypercapnic ventilatory responses in six healthy men before and during intravenous infusion to maintain a constant plasma level. 2. Doxapram changed neither resting oxygen uptake nor CO 2 production but produced a substantial increase in resting ventilation at both levels of end-tidal CO 2 studied. 3. Doxapram increased the ventilatory response to isocapnic hypoxia from − 0.8 ± 0.4 litre min −1 (% S a o 2 ) −1 to −1.63 ± 0.9 litres min −1 (% S a o 2 ) −1 . This was similar to the increase in hypoxic sensitivity which resulted from raising the end-tidal CO 2 by 0.5 kPa without adding doxapram. 4. The slope of the ventilatory response to rebreathing CO 2 rose from 11.6 ± 5.3 litres min −1 kPa −1 to 20,4 ± 9.8 litres min −1 kPa −1 during doxapram infusion. 5. The marked increase in the ventilatory response to CO 2 implies that doxapram has a central action, but the potentiation of the hypoxic drive also suggests that the drug acts on peripheral chemoreceptors, or upon their central connections, at therapeutic concentrations in normal unanaesthetized subjects.

1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia ( ) during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN−). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients ( in DAN+ patients = −0·9 ± 0·2 litre min −1 kPa −1 ; in DAN− patients = −1·2 ± 0·6 litres min −1 kPa −1 ) even allowing for differences in the level of exercise achieved (CO 2 production in DAN+ patients = 743 ± 103 ml/min; CO 2 production in DAN– patients = 800 ± 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly ( P < 0·05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients. 1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia ( ) during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN−). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients ( in DAN+ patients = −0·9 ± 0·2 litre min −1 kPa −1 ; in DAN− patients = −1·2 ± 0·6 litres min −1 kPa −1 ) even allowing for differences in the level of exercise achieved (CO 2 production in DAN+ patients = 743 ± 103 ml/min; CO 2 production in DAN– patients = 800 ± 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly ( P < 0·05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients. 1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia ( ) during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN−). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients ( in DAN+ patients = −0·9 ± 0·2 litre min −1 kPa −1 ; in DAN− patients = −1·2 ± 0·6 litres min −1 kPa −1 ) even allowing for differences in the level of exercise achieved (CO 2 production in DAN+ patients = 743 ± 103 ml/min; CO 2 production in DAN– patients = 800 ± 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly ( P < 0·05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients.

1. The purpose of this study was to determine whether events early in systole, a period which may be more descriptive of ventricular performance than the average of events in systole, can be determined by multiple gated radionuclide cardiac blood pool imaging. 2. We examined 16 ventricular volume curves, using a digital filtering method in the frequency domain to smooth statistical noise. Ejection fraction was unchanged by such filtering but the peak rate of change of volume during systole was greatly affected by different bandwidths. Therefore we derived an index, the mean ejection time, which is influenced by changes in the shape of the systolic portion of the volume curve but is unchanged when measured from curves treated by different filter bandwidths. 3. We infused isoprenaline (2 μg/min; eight patients), atropine (1.2 mg; eight patients) or dobutamine (360 μg/min; six patients). 4. Isoprenaline and atropine caused a similar increase in heart rate (isoprenaline + 27 beats/min; atropine + 20 beats/min) but after dobutamine there was little change in heart rate (+4 beats/min). After isoprenaline and dobutamine ejection fraction increased (0.51 ± sem 0.04 control; 0.73 ± 0.04 after isoprenaline; 0.53 ± 0.03 control; 0.65 ± 0.06 after dobutamine) but was unchanged by atropine (0.46 ± 0.07 control; 0.48 ± 0.07 after atropine). 5. The mean ejection time decreased by 55 ms after isoprenaline, by 49 ms after dobutamine but by only 14 ms after atropine. Changes in peak rate of change of volume in systole were more variable. 6. Radionuclide gated blood pool studies can be used to study the effects of pharmacological intervention on events in early systole and the variable ‘mean ejection time’ is independent of curve-fitting techniques.