1. In view of the importance of 5-hydroxytryptamine in coronary thrombosis, we wanted to know whether a potentially protective decrease in platelet 5-hydroxytryptamine could be achieved by treatment with an inhibitor of 5-hydroxytryptamine uptake, fluoxetine. 2. We studied 15 patients treated for psychiatric indications with fluoxetine, and compared the findings with those obtained with blood from 18 patients treated with amitriptyline and 13 controls previously treated for affective disorders. 3. Platelet-rich plasma 5-hydroxytryptamine levels were significantly decreased in the fluoxetine group ( P > 0.005) but not in the amitriptyline group compared with the control group. 4. Collagen-induced aggregation in whole blood anti-coagulated with hirudin was measured by sequential single platelet counting. The contribution of 5-hydroxytryptamine was assessed from the effect of adding the 5-hydroxytryptamine specific antagonist ICI 170809. This contribution was significantly decreased in the fluoxetine group but not in the amitriptyline group compared with the control group. 5. It is concluded that platelet 5-hydroxytryptamine is indeed decreased by fluoxetine, and we would predict a protective effect of fluoxetine against coronary thrombosis.

1. The potential value of right vagotomy for the relief of breathlessness has been explored in five patients with emphysema. Two patients had symptomatic improvement, two had minor symptomatic improvement, and one was unchanged. 2. Exercise ventilation was not noticeably depressed by unilateral right vagotomy in the two patients investigated fully, but the pattern of breathing was altered. After vagotomy, breathing was deeper, and the rise in the frequency of breathing with exercise was depressed. 3. After right vagotomy the response to rebreathing carbon dioxide also consisted of slower deeper breaths. 4. Right vagotomy sometimes appears to remove an influence preventing slow deep breathing and exacerbating dyspnoea. 5. Results of bilateral pulmonary denervation, attempted in one patient, were complicated by the need for left thoracotomy, which removed any possible beneficial effects.

1. Nineteen patients (three normal subjects, and 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); r S = 0.54, P < 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.

1. Maximum acceleration of blood has been measured in the aorta using a catheter tip velocity transducer in twelve patients undergoing diagnostic coronary angiography. Signals were obtained with the catheter tip transducer 5–6 cm above the aortic valve. From these signals, the values for peak velocity were measured, and acceleration was derived by continuous differentiation of the velocity signal. 2. The values obtained for maximum acceleration and peak velocity were inversely related to the severity of coronary artery disease as indicated by coronary angiography. 3. There was a close relationship between peak velocity, maximum acceleration and ejection fraction calculated from the left-ventricular angiogram. 4. Three patients with chest pain and no cardiac abnormality detectable by cardiac catheterization had maximum acceleration values above 1500 cm/s 2 and peak velocity above 60 cm/s. 5. Four patients with definite coronary artery disease had normal intracardiac pressures and cardiac indices, but decreased ejection fractions. The values for maximum acceleration were between 750 and 1100 cm/s 2 and for peak velocity between 32.0 and 58.0 cm/s. 6. Five patients had severe coronary disease with abnormal intracardiac pressures, cardiac indices and decreased ejection fraction. Values for maximum accelerations were below 850 cm/s 2 and for peak velocity, below 41.0 cm/s.

1. The effect of breathing anaesthetic aerosols (lignocaine 20% and bupivacaine 5%) on respiratory reflexes was studied in rabbits. 2. The cough reflex was blocked in every experiment. 3. The inflation reflex was abolished in eleven out of twenty-six rabbits given lignocaine aerosol and in fourteen out of fifteen rabbits given bupivacaine aerosol. 4. The deflation reflex was blocked pari passu with the inflation reflex. 5. The ventilatory response to histamine was sometimes blocked; more commonly it was partially preserved. 6. The ventilatory response to phenyldiguanide was never impaired and often enhanced. 7. Bronchoconstriction produced by electrical stimulation of the peripheral cut ends of the cervical vagus nerves was unaffected. 8. Block of the above respiratory reflexes was associated with slower, deeper breathing. 9. Bupivacaine has produced more consistent and reliable results than lignocaine; the effects were reversible in both cases usually within 30 min. 10. Plasma concentrations of both anaesthetics were usually below the generally accepted toxic concentrations in man. 11. Control experiments using intravenous infusions of the anaesthetics proved that none of the effects could have been produced by systemic effects of the absorbed anaesthetic. 12. No pathological changes were found in the airways on both macroscopic and microscopic examination. 13. The experiments show that it is possible to block respiratory reflexes whose afferents arise from the airways, and to preserve a reflex arising at alveolar level.

1. Block of the phrenic nerves in three normal subjects, produced by injection of lignocaine in the neck, caused alleviation of the thoracic sensation during breath holding and prolonged breath-holding time. 2. Injection of lignocaine in the neck without nerve block had no effect on breath holding sensation or breath-holding time. 3. A patient with a spinal-cord transection at the third cervical segment with paralysed diaphragm and chest wall, had no sensation in the chest or abdomen during breath holding. 4. This patient maintained normal ventilation by using hypertrophied sternomastoid muscles. During breath holding he experienced no sensation in the neck despite the presence of sternomastoid contraction. 5. There is previous evidence that complete muscular paralysis abolishes breath-holding sensation but that paralysis of all muscles innervated from spinal segments below the eighth cervical has no effect.

1. Resistive loads were added to the airways of patients with tracheostomies; the patients were blindfolded and the loads introduced without their knowledge. 2. The ability to detect the loads was the same in a patient with C3 transection (chest wall and diaphragm disconnected from the brain) as in a control group of patients with no neurological lesion. 3. It is concluded that receptors in the chest wall and diaphragm are not involved in the genesis of the sensation by which added resistive loads are detected.

1. The effect of lung deflation was studied during treatment of patients for spontaneous pneumothorax: (a) in four patients acute lung deflation was produced by opening the chest drain to the atmosphere and the immediate effect on breathing was observed and (b) breath-holding time and the ventilatory response to CO 2 were determined on admission to hospital and after recovery in a further four patients. 2. Allowing one lung to deflate suddenly produced an immediate increase in respiratory rate and electrical activity in inspiratory muscles. 3. Maximum breath-holding times were always decreased by pneumothorax. 4. In the presence of pneumothorax, the ventilatory response to rebreathing CO 2 was increased at the break point, the respiratory rate was increased and the P co 2 at the breakpoint decreased in three out of four patients. 5. These results are consistent with the hypothesis that lung deflation has a reflex excitatory effect on breathing (Hering—Breuer deflation reflex). If this hypothesis is correct, it would appear that the threshold for the reflex is higher than for other mammalian species.