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Pressure-diameter relationships of segments of human finger arteries, aged 57-85 years, were measured in vitro. The arteries, obtained at autopsy within 48 h after death, were stored in glucose-free Tyrode at 4 degrees C. Experiments began within 40 h after autopsy. The diameter responses to various transmural pressure changes, with and without the addition of noradrenaline to the Tyrode solution in the specimen chamber, were compared with the responses of freshly excised rat tail arteries. In general, pressure-diameter relations of human finger artery segments were similar to those of rat tail artery segments, with a steep slope in the collapse region near zero pressure. Also, spontaneous rhythmic contractions and myogenic activity induced by high transmural pressures were similar to those observed in the fresh rat tail arteries. Human finger arteries, however, could contract to complete closure both spontaneously and after addition of noradrenaline, while rat tail arteries did not. The diameter changes of the arterial segments during forced 1 Hz oscillations of 20-50 mm Hg (2.7-6.7 kPa) amplitude superimposed on a mean transmural pressure were substantially smaller than those during quasi-steady inflation-deflation ramps over the same pressure range, indicating the presence of a strong viscous wall component.

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To study the significance of damage to the nasal mucosa for the induction of nasal tumours by formaldehyde in rats, a long-term inhalation study was conducted in which male rats with severely damaged or undamaged nose were exposed 6 h/day for 5 days/week to 0, 0.1, 1.0 or 10 ppm formaldehyde vapour for 28 months, or for 3 months followed by a 25-month observation period. The damage to the nasal mucosa was induced by bilateral intranasal electrocoagulation. The total number of rats used was 720, 480 with damaged and 240 with intact nose. Compound-related degenerative, inflammatory and hyperplastic changes of the nasal respiratory and olfactory mucosa were invariably observed when rats with intact nose were exposed to 10 ppm but not when exposed to 1.0 or 0.1 ppm formaldehyde. Nasal electrocoagulation increased the incidences of formaldehyde-induced rhinitis, hyper- and metaplasia of the respiratory epithelium, and degeneration and hyper- and metaplasia of the olfactory epithelium. In addition, exposure to 10 ppm formaldehyde for 28 months produced nasal squamous cell carcinomas in rats with damaged nose (15/58) but not in rats with intact nose. Three months of exposure to 10 ppm formaldehyde or exposure to 0.1 or 1.0 ppm formaldehyde for 28 months had no such effect. It was concluded that severe damage to the nasal mucosa may contribute to the induction of nasal tumours by formaldehyde.

The influence of inspiratory and expiratory flow magnitude, lung volume, and lung volume history on respiratory system properties was studied by measuring transfer impedances (4-30 Hz) in seven normal subjects during various constant flow maneuvers. The measured impedances were analyzed with a six-coefficient model including airway resistance (Raw) and inertance (Iaw), tissue resistance (Rti), inertance (Iti), and compliance (Cti), and alveolar gas compressibility. Increasing respiratory flow from 0.1 to 0.4 1/s was found to increase inspiratory and expiratory Raw by 63% and 32%, respectively, and to decrease Iaw, but did not change tissue properties. Raw, Iti, and Cti were larger and Rti was lower during expiration than during inspiration. Decreasing lung volume from 70 to 30% of vital capacity increased Raw by 80%. Cti was larger at functional residual capacity than at the volume extremes. Preceding the measurement by a full expiration rather than by a full inspiration increased Iaw by 15%. The data suggest that the determinants of Raw and Iaw are not identical, that airway hysteresis is larger than lung hysteresis, and that respiratory muscle activity influences tissue properties.

Short duration washin and washout experiments were carried out with the gases ether (diethyl ether), ethyl acetate and acetone in order to study the excretion behaviour in the lung of gases highly soluble in blood and tissues. Carbon dioxide (CO2) was analyzed as a reference gas during the washout. The excretion values for acetone were generally the lowest, those for ether the highest, and intermediate ones were obtained for ethyl acetate. These results are in accord with the experimental data of others. Analysis of the washout curves shows that for acetone the volume of gas expired before the beginning of phase II is considerably smaller than found for CO2 and ether. During washout, the slope of the alveolar plateau for acetone is negative for the first few breaths and becomes positive thereafter; however, it remains lower than the slopes for CO2 and ether, which are always positive. These two phenomena occurring during washout clearly demonstrate that the acetone in the expired air must originate from the epithelial tissue lining the conducting airways. We conclude, therefore, that, in terms of gas transport, the conducting airways behave differently for poorly and highly soluble gases and this provides a physiological basis for the deviating excretion behaviour of highly soluble gases.

Results of animal experiments using sinusoidal changes in inspired halothane concentration showed that the ratio of variation in end-expired concentration to the variation in inspired concentration reached a plateau in the Bode diagram. With the help of an uptake and distribution model, the interpretation of the results showed that the level of the plateau is determined by the overall ventilation-perfusion ratio. With a good selection of input frequency, tracer agent, and known ventilation, the ventilation-perfusion ratio and the lung perfusion can be consequently obtained noninvasively. Mean ventilation-perfusion ratio was determined with 20 human voluteers. At rest a mean ratio was found of 0.87 +/- 0.28 (SD). At a work load of 90 W a mean ratio was found of 1.19 +/- 0.19 (SD). In two individuals reproducibility and influence of CO2 was studied. At rest without additional CO2 the ventilation-perfusion ratio was 0.71 +/- 0.06 (SD) obtained with a constant breathing rate of 10/min. At an end-expired CO2 level of 6% the ventilation-perfusion ratio was increased almost 2.5 times. The calculated perfusion with and without increased end-expired CO2 levels under the same work load were well reproducible.

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