1. Acute bronchitis secondary to viral infection is associated with an influx of neutrophils. We hypothesized that bronchial epithelial cells are capable of releasing neutrophil chemotactic activity in response to viral infection. 2. To test this hypothesis, primary cultures of bovine bronchial epithelial cells were inoculated with a bovine respiratory pathogen, bovine herpes virus-1. 3. Supernatants collected from inoculated cells, before signs of toxicity, demonstrated significant neutrophil chemotactic activity using a blind well chamber neutrophil chemotaxis assay. Lipoxygenase inhibitors markedly reduced the amount of neutrophil chemotactic activity released after bovine herpes virus-1 inoculation. Analysis of arachidonic acid metabolites in cell supernatants by reverse-phase h.p.l.c. confirmed that leukotriene B 4 , a potent neutrophil chemoattractant, was released. 4. We also confirmed that adhesion of neutrophils to bovine herpes virus-1-inoculated bronchial epithelial cells was increased and mediated in part by the neutrophil integrin, LFA-1. 5. Thus, virally infected airway epithelial cells release leucocyte chemoattractants and hence adhesive interactions, functions that are likely to be important in the inflammatory acute response to viral infection.

1. Nicotine is of interest as a major constituent of cigarette smoke and as an additive to chewing gum used to help patients to stop smoking. 2. Specific pathogen-free rats were given an aerosol or injections of nicotine hydrogen (+) tartrate ( l -isomer) for 2 or 3 weeks at three doses and the number of secretory cells in the surface epithelium of airways was determined. 3. By aerosol, a dose giving 10 ng of nicotine/ml of plasma had no effect on secretory cell number. 4. By injection, nicotine had a ‘bi-phasic’ effect depending on dose: it reduced secretory cell number at plasma concentrations of 650 ng/ml of plasma or increased it at 2360 ng/ml of plasma. 5. Thus nicotine alone, given to rats at doses similar to those found in cigarette smokers and those who chew nicotine gum, does not cause secretory cell hyperplasia in the conducting airways of the rat.

1. Arterial pH oscillations have been monitored in vivo in patients with well defined chronic obstructive bronchitis, asthma and clinical emphysema. 2. the patients with clinical emphysema were shown to differ from those with chronic obstructive bronchitis on the basis of a number of clinical and physiological criteria. 3. Patients with asthma showed least attenuation of their pH oscillations as a group, in contrast to emphysematous patients who showed most attenuation. in patients with clinical emphysema the attenuation was relatively homogeneous. the patients with chronic obstructive bronchitis showed the full range from normal oscillations (zero attenuation) to zero (complete attenuation). 4. the amplitude and approximate rate of change of upslope of the P aco 2 oscillations in vivo were calculated, from measured pH oscillation amplitudes, using buffer slope values in vitro from Siggaard Anderson [(1962, 1963) Scandinavian Journal of Clinical and Laboratory Investigation , 14 , 598–604; 15 , 211–217], then dividing the P aco 2 amplitude by half the respiratory period. 5. Mean arterial P co 2 in vitro showed a very strong correlation with the downslope of the pH oscillation in vivo (calculated as for P aco 2 upslope) in patients without clinical emphysema. This correlation would be expected to some extent, owing to the logarithmic relationship of P aco 2 oscillations to pH oscillations. However, the mean arterial P co 2 also showed a very strong correlation with the upslope of the calculated Paco 2 oscillations, again excluding patients with clinical emphysema.

1. Pulmonary blood volume was measured in 39 patients with severe chronic bronchitis, of whom 29 had recently recovered from an acute exacerbation. P a,o 2 was below 10·3 kPa in all but five patients, P a,co 2 was above 5·6 kPa in 26 cases, and pulmonary artery mean pressure was above 20 mmHg in 29 cases. Pulmonary blood volume was measured with the double-injection—single-sampling technique using Indocyanine Green and pulmonary wedge injection. 2. Pulmonary blood volume in the 39 patients was significantly lower (343 ± 95 ml) than in a group of 16 normal subjects (469 ± 117 ml) studied previously by the same method. There was no correlation between pulmonary blood volume and driving pressure across the pulmonary circulation, or between pulmonary blood volume and P a,o 2 . 3. Breathing 26–29% oxygen in 19 patients caused no significant changes in either pulmonary blood volume or pulmonary vascular resistance. Therefore the reduced pulmonary blood volume could not be attributed to hypoxic pulmonary vasoconstriction. 4. The finding of a diminished pulmonary blood volume in chronic bronchitis is best explained by a loss of pulmonary vessels. Pulmonary blood volume was not correlated with total lung capacity nor with the residual volume/total lung capacity ratio, nor was it significantly higher in the 16 patients with normal total lung capacity (352 ± 73 ml) than in the 23 patients with a total lung capacity greater than 110% of normal (331 ± 110 ml). There was therefore no correlation between the amount of emphysema and the reduction in pulmonary blood volume.

1. The time-courses of the respiratory changes at the start of exercise were assesse in twenty middle-aged normal men and in twenty patients with chronic obstructive bronchitis with a moderate reduction in forced expiratory volume in 1 s (FEV 1 ) (group M: mean 1.451; range 1.0–2.2 1) and in twenty patients with a more severe reduction in FEV 1 (group S: mean 0.62 1; range 0.2–0.9 1). All subjects exercised at a constant work rate for 6 min, starting abruptly from a steady resting state. Cardiac frequency (fH), ventilation (V̇E), oxygen uptake (V̇o 2 ) and carbon dioxide output (Vco 2 ) were measured at the end of each minute and the rates of adaptation of these variables determined. 2. When the normal middle-aged men exercised at a low work rate [mean V̇o 2 = 44.7 mmol (1.0 1 STPD) min −1 ] the increases by the end of the first minute were in the order: f H > V̇E > V̇o 2 > V̇co 2 . At a work rate of 50% of their working capacity [V̇o 2 = 67.1 mmol (1.5 1 STPD) min −1 ] the pattern of adaptation in the normal subjects was fH > V̇o 2 > V̇E > V̇co 2 . In the patients working at 50% of their working capacity [V̇o 2 approximately 44.6 mmol (1.01 STPD) min −1 ], the rates of adaptation were in the order: fH > V̇o 2 >V̇E > V̇co 2 , but all adapted significantly more slowly than in the normal subjects exercising at the same work rate. 3. A reduced ventilatory capacity does not appear to be associated with any special influence on the time-course of the ventilatory adaptation at the start of exercise. The rate of adaptation of V̇E at the start of exercise is (in common with that of fH, V̇o 2 and V̇co 2 ) reduced in proportion to the overall reduction in working capacity.

1. The incorporation of tritiated glucose into bronchial gland cells enables their glycoprotein secretion to be followed by radioautography. The number of cells from which secretion is observed after 4 h of cell culture is the secretory index. 2. Large variations in secretory index were observed between the bronchi of different subjects, but the secretory index was proportional to gland size. 3. The secretory index was increased by parasympathomimetic drugs and diminished by parasympatholytic drugs, the magnitude of the effect being proportional to gland size in the former and inversely proportional in the latter case. 4. Sympathomimetic drugs, bradykinin and mucolytic drugs had no effect on the secretory index. 5. In cystic fibrosis, bronchitis and bronchiectasis gland size and not the disease process was the main determinant of the secretory index.