297 which enhance their removal are thus beneficial. Lorin and DenningS measured the volume and consistency of expectorated sputum samples from patients with cystic fibrosis after periods of postural drainage and cough. They found that postural drainage produced over twice the volume of sputum as an equal period of cough alone. Although this study demùnstrated a beneficial effect, no information was gained about the movement of bronchial secretions from peripheral to central lung regions. Chopra et al. 13 determined tracheal transport velocity in anaesthetised dogs and found that both postural drainage and percussion significantly increased its velocity but that the combination was not significantly greater than either alone. The movement of secretions present in the trachea was directly observed, but not in the more peripheral airways. In normal subjects clearance of bronchial secretions is primarily achieved by the action of the mucociliary escalator,22 with cough acting as a reserve mechanism.23 In this way bronchial toilet extends as far as the sixteenth airway generation. Cough is said to be ineffective beyond the sixth generation,24 but it becomes an important adjunct for the removal of excessive secretions in patients with chronic obstructive lung disease.25 Observations on the effectiveness of cough have been based upon normal lung architecture and thus may not be applicable in the pathological state. Further studies are thus required to determine the precise role of cough alone in clearing secretions from peripheral lung regions, where small airways predominate. Our aim in this study was to demonstrate the value of chest physiotherapy, consisting of postural drainage, vibration, percussion, shaking, and cough, in accelerating the removal of excessive bronchial secretions from central, intermediate, and peripheral lung regions. The results have confirmed the effectiveness of this treatment and the method used will enable determination of the relative value of each component. manceuvres

for reprints should be addressed to J. R. M. B., Departof Thoracic Medicine, Royal Free Hospital, Pond Street, London

Requests ment

NW32QG.

REFERENCES 1. Palmer, K. N. V., Sellick, B. A. Lancet, 1953, i, 164. 2. Opie, L. H., Spalding, J. M. K. ibid. 1958, ii, 671. 3. Anthonisen, P., Riis, P., Søgaard-Anderson, T. Acta med. scand. 1964, 175, 715 4. Laws, A. K., McIntyre, R. W. Can. Anœsth. Soc. J. 1969, 16, 487. 5. Lorin, M. I., Denning, C. R. Am. J. phys. Med. 1971, 50, 215. 6. March, H. Archs phys. Med. Rehabil. 1971, 52, 528. 7. Lefcoe, N.M., Paterson, N. A. M. Am. J. Med. 1973, 54, 343. 8. Clarke, S. W., Cochrane, G. M., Webber, B. Thorax, 1973, 28, 262. 9. Pham, Q. T., Peslin, R., Puchelle, E., Salmon, D., Caraux, G., Benis, A. M. Bull. physio-path.Resp. 1973, 9, 293. 10. Jones, N. L. Am.Rev. resp. Dis. 1974, 110, 132. 11. Campbell, A. H., O’Connell, J. M., Wilson, F. Med. J. Aust, 1975, i, 33. 12. Cochrane, G. M., Webber, B. A., Clarke, S. W. Br. med. J. 1977, ii, 1181. 13. Chopra, S. K., Taplin, G. V., Simmons, D. H., Robinson, G. D., Elam, D., Coulson, A. Am. Rev. resp. Dis. 1977, 115, 1009. 14. Newton, D. A. G , Stephenson, A. Lancet, 1978, ii, 228. 15. Newton, D. A G., Bevans, H. G. Br. med J. 1978, ii, 1525. 16. Graham, W. G. B., Bradley, D. A. New Engl. J. Med. 1978, 299, 624. 17. Thomson, M. L., Short, M. D. J. appl. Physiol. 1969, 26, 535. 18 Thomson, M. L., Pavia, D. Archs envir. Hlth, 1973, 26, 86. 19 Thomson, M. L., Pavia, D., McNicol, M. W. Thorax, 1973, 28, 742. 20. Snedecor, G. W., Cochran, W. G. Statistical Methods; p. 128. Ames, Iowa, 1968. 21 MacMahon, C. Lancet, 1915, ii, 769. 22 Kilburn., K H. Archs envir. Hlth, 1967, 14, 77. 23 Newhouse, M., Sanchis, J., Bienstock, J. New Engl. J. Med. 1976, 295, 990. 24 Leith, D. E. Phys. Ther. 1968, 48, 439. 25 Newhouse, M. T. Thorax, 1973, 28, 262.

ACTIVITY OF ARYL HYDROCARBON HYDROXYLASE IN PSORIATIC SKIN P. H. CHAPMAN

M. D. RAWLINS

S. SHUSTER

Departments of Pharmacological Sciences (Clinical Pharmacology) and Dermatology, University of Newcastle upon

Tyne

activity of aryl hydrocarbon hydroxylase (A.H.H.), a microsomal monooxygenase, was reduced in epidermis from both the psoriatic lesions and clinically normal lesion-free skin from psoriatic patients. Induction of epidermal A.H.H. activity by benzanthracene was also significantly less than normal in both psoriatic lesions and in clinically normal skin from patients with psoriasis. The enzyme defect may be related to the primary genetic abnormality of the

Summary

The

disease. Introduction a chronic disorder of increased epidermal cause of which is unknown.’ Aryl hythe proliferation, drocarbon hydroxylase (A.H.H., EC 1.14.14.2), a microsomal mono-oxygenase, has been identified in most human tissues,2 including skin,3where we have found it to be located almost exclusively within the epidermis.4 Since A.H.H. may play an important part in determining the efficacy and toxicity of drugs within the skin, we have examined its activity in biopsy specimens of epidermis from psoriatic patients. In the course of this study we have found an abnormality which may be of

PSORIASIS is

astiological importance.5 Patients and Methods 20 patients with chronic discoid psoriasis agreed to participate in the study. All had lesions covering more than 10% of their body-surface area and had received no topical drug ther- . apy in the 3 weeks preceding the study. The patients’ ages ranged from 20-73 years (mean 41±s.E.M. 4 years). For comparison 13 normal subjects without evidence of skin disease were also studied (age range 18-37, mean 26±s.E.mt. 2 years). Epidermal blisters were raised with a suction pump on forearm skin of both patients and healthy volunteers.6 The blister tops, consisting of separated viable epidermis, were removed with sterile forceps and immediately placed in ice-cold isolation medium (20 mmol/1 "tris"- [hydroxymethyl] methylamide in 0.3 mol/1 mannitol, pH 7-4). The epidermis was divided into two parts, and each was weighed and transferred to a tissue-culture systeM8 with or without benzanthracene

(100 µmo1/1). After preincubation for 18 h at 37 °C in an atmosphere of 95% O2 :5% CO2 the activity of A.H.H. in epidermal microsomes was determined as previously described.4 Benz(a)pyrene was used as substrate, and the activity of A.H.H. was expressed as pmol 3-hydroxybenz(&agr;)pyrene formed/mg microsomal protein/h (pmol 3-OH-B.p./mgprotein/h). Results In the absence of benzanthracene the activity of very low in epidermis from the psoriatic lesions (1-84±0-37 pmol 3-OH-B.p./mg protein/h, n=17). This was just below (P