Impedance pneumography, electrical impedance measurements of the lung, is a technique which has been widely used to monitor respiration non-invasively and more recently, the onset of pulmonary oedema. Attempts have been made to try to localise the changes in impedance using electrode arrays and electrode guarding. These techniques allow localisation to a particular hemithorax, but the resolution of the majority of the systems remains poor. To assess the performance and possible clinical applications of APT, measurements have been made following increases in lung volume and pulmonary blood volume. During inspiration an increase in both the area and the magnitude of the impedance changes over the area of the lungs was observed. Numerical analysis of the impedance changes in normal subjects reveals a consistently high correlation between the volume of air inspired and the magnitude of the impedance changes. The resolution of the system is sufficient to monitor differences in ventilation in the right and left lung and to measure variations in these levels with posture. Preliminary clinical work suggests that APT may be used to detect ventilatory defects in certain types of lung disease. APT measurements show a decrease in resistivity over the area of the lungs when the pulmonary blood volume is increased by the intravenous infusion of 1.5 litres of isotonic saline. Similar changes in the volume of fluid in the lungs are known to occur in pulmonary oedema. APT measurements of lung impedance may detect the onset of pulmonary oedema in high risk patients.

(1978). Thorax, 33,[468][469][470][471][472][473]. Resolution of pulmonary hypertension and other features induced by chronic hypoxia in rats during complete and intermittent normoxia. Rats subjected to 10% 02 (hypoxic rats) for various periods and recovery regimens were compared with control animals with respect to pulmonary artery pressure (Ppa), right ventricular hypertrophy (RVH), and muscularisation of small pulmonary vessels. Mean Ppa was measured in anaesthetised animals spontaneously breathing air and rose from 16 mmHg in controls to 36 mmHg in rats exposed to hypoxia for three weeks. Ppa had returned to normal after 20 weeks' recovery in air. RVH regressed a little more quickly, but muscularisation of small pulmonary vessels was still apparent after 20 weeks. Some hypoxic rats were subjected to an intermittent normoxic recovery regimen for either 40 or 80 hours a week in air, the remainder in 10% 02. Some reduction in RVH probably occurred after six weeks on the 80-hour regimen, but there was no reduction in Ppa or muscularisation of small pulmonary vessels. These results suggest that the pulmonary hypertension of chronic alveolar hypoxia resolves very slowly and is probably related to structural changes in the pulmonary vessels. Their relevance to human cor pulmonale and intermittent long-term oxygen treatment for these patients is discussed.We have shown that rats kept in a hypobaric or a normobaric hypoxic chamber develop many of the features found in human hypoxic disease and in man at high altitude (Hunter et al, 1974;Leach et al, 1977a). In an attempt to simulate the situation in patients with hypoxic cor pulmonale on long-term°2 treatment, we subjected the hypoxic rats to periods in air (intermittent normoxic regimen) and showed that resolution of right ventricular hypertrophy (RVH) and muscularisation of small pulmonary vessels was very slow (Leach et al, 1977a). In the present study we have measured pulmonary artery pressure (Ppa) in similar rats and have further examined RVH and muscularisation of small pulmonary vessels. A preliminary account has been published (Leach et al, 1977b). 'Present address:

Applied potential tomography (APT) images can be collected at a rate of 24 per second and data collection can be synchronised with the ECG. Images thus obtained from a thoracic plane allow the spatial separation of impedance changes originating in the heart, aorta and lungs and have raised the possibility of detecting pulmonary perfusion abnormalities from the cardiac-related impedance changes in the lungs. We have recently started a study to compare isotope perfusion scans with APT images and present here a few initial examples which suggest that further investigation of this field may prove rewarding.

The mammalian respiratory tract contains innervated groups of endocrine cells which are believed to respond to hypoxia. We have demonstrated the involvement of a specific regulatory peptide produced by the cells, calcitonin gene-related peptide (CGRP), in this response. Cells immunoreactive for CGRP or for protein gene product 9.5 (PGP 9.5), a general marker of nerves and endocrine cells, were quantified in sections of lungs from hypoxic (21 days, 10 per cent O2) and normoxic rats. An immunostaining method employing supra-optimal dilutions of primary antiserum was used. This detects variations in antigen concentration which may be masked if the routine, optimal dilution is used. The number of CGRP-immunoreactive endocrine cells was significantly (P less than 0.001) greater in the lungs of hypoxic rats (76.9 +/- 10.1 cells/cm2, mean +/- SEM) compared with controls (19.7 +/- 2.4). However, the numbers of PGP 9.5-immunoreactive cells were the same in both groups (81.3 +/- 12.2, hypoxic; 79.5 +/- 9.8 control), suggesting that the total number of endocrine cells did not change. It is concluded therefore that the apparent increase in CGRP-immunoreactive endocrine cells in hypoxic rat lungs is due to increased intracellular levels of the peptide. Since CGRP is a vasodilator, this could have important implications in the vasoconstrictor response to hypoxia.