856 has drawn attention to the study by Currie all which suggested that spironolactone, an aldosterone antagonist, prevents acute mountain sickness A.M.S.. The hypothesis upon which the use of spironolactone was based now seems vulnerable. Singh et al.3 suggested that people who got A.M.S. had fluid retention and, conversely, that a "Hohendiurese" on exposure to altitude augured well. I have suggested’ that aldosterone secretion increases at altitude in those who get A.M.S. and that this is causally related to the A.M.S. It seemed logical, therefore, to use an aldosterone antagonist to prevent A.M.s.’ There are difficulties with this hypothesis, however, because only one study has convincingly demonstrated an increase in aldosterone secretion at altitude." At least six others have demonstrated decreased aldosterone secretion.7-u In one study, when the severity of A.M.S. was assessed,13 plasma-aldosterone was significantly reduced, 12 and it was from this same location that the increased aldosterone secretion had previously been reported.6 Thus on balance it seems that aldosterone secretion decreases at altitude and that the hypothesis has been refuted. It would, therefore, seem unlikely that an aldosterone antagonist would be of use where plasma-aldosterone is already reduced. However, the study by Currie et al./ though largely anecdotal, does suggest that spironolactone can prevent A.M.S. If this effect is confirmed the mechanism might be by extrarenal mechanisms reducing cerebral acdema 14 and/or by spironolactone decreasing cerebrospinal-fluid secretion" via mechanisms unrelated to its aldosterone antagonism. Whatever new drugs become available to help the impatient climber to "bag his peak", they should always be combined with slow acclimatisa-

SIR,-Ramsay’

et

tion. University Medical Centre, Hamilton, Ontario, Canada L8S 4J9 McMaster

JOHN R. SUTTON



in this area, and this may well be true of man. The bronchi are, therefore, potential sites for hyperreactivity to stimuli and could produce excessive mucus and bronchoconstriction through the nervous mechanism. Such stimuli could, for example be air pollution, cigarette smoke, infections, cold air, or fog. Indeed, Widdicombe has lately discussed the1 hypothesis that allergic asthma might be nervously mediated.’ The investigation of apparently normal people to see if some of them have parasympathetic hyperreactivity and, if they have, the study of the relation of this to the subsequent incidence of disease might shed new light on chronic bronchitis. The Surgery, 18 Compton Avenue,

T. W. ASTIN

Luton, Bedfordshire LU4 9AZ

MULTIPURPOSE NEEDLE FOR GYNAECOLOGICAL SURGERY is not made easier by the wide variety of materials which the surgeon may use in a single operation. Trainees and theatre sisters are often confused about what has to be used to suture the various tissue

SIR,-Surgery

needles and

suture

layers. We have designed, in conjunction with a suture manufacturer, a multipurpose needle that can be used throughout most routine gynaecological operations. It has a 4 gauge U.S.P. halfcircle atraumatic needle with a diamond pointed clip attached to 0 ’Dexon’. The suture material is coloured green to make it easier to see. The simplification of having a single needle and suture material allows the operation to proceed more smoothly. Several gynaecologists at this hospital have found it satisfactory, and this approach may be of interest to general surgeons. The needle is available from Davis &

Geck Ltd., Fareham Road,

Gosport, Hampshire. BRONCHIAL HYPERREACTIVITY IN CHRONIC

Samaritan Hospital for Women, London NW1

R. W. BEARD

BRONCHITIS

SiR,—Iwould like to discuss one point arising from your excellent editorial on chronic bronchitis (Feb. 19, p. 403). I agree that the Dutch concept of bronchial hyperreactivity of an allergic type does not seem to be a factor in the causation of chronic bronchitis, but there is a danger that the concept of hyperreactivity might be lost altogether. There may well be a bronchial hyperreactivity of a non-allergic type. The bronchial tree is very sensitive, innervated by the parasympathetic system through the vagus nerve. Physiologists have shown that animals have many parasympathetic reflexes 1. 2. 3.

Ramsay, L. E. Lancet, 1977, i, 540 Currie, T. T., and others, Med. J. Aust. 1976, ii, 168. Singh, I., Khanna, P. K., Srivastava, M. C., Lal, M., Roy, S. B., Subramanyam, C. S. V. New Engl.

J. Med. 1969, 280,

175.

Sutton, J. R. Med. J. Aust. 1971, ii, 243. 5. Sutton, J. R., Lazarus, L. ibid. 1973, i, 545. 6. Frayser, R., Rennie, D. I., Gray, G. W., Houston, C. S. J. appl. Physiol. 1975, 38, 635. 7. Ayres, P. J., Hurter, R. C., Williams, E. S. Nature, 1961, 191, 78. 8. Slater, J. D. H., Williams, E. S., Edwards, R. H. T., Ekins, R. P., Sönksen, P. H., Beresford, C. A., McLaughlin, M. Clin. Sci. 1969, 37, 311. 9. Slater, J. D. H., Tuffley, R. E., Williams, E. S., Beresford, C. H., Sönksen, P. H., Edwards, R. H. T., Ekins, R. P., McLaughlin, M. ibid. p. 327. 10. Hogan, R. P., Kotchen, T. A., Boyd, A. E., Hartley, L. M.J. appl. Physiol. 1973, 35, 385. 11. Sutton, J. R., Viol, G. W., Gray, G. W., McFadden, M., Keane, P. M. ibid. (in the press). 12. Sutton, J. R., Rennie, D. I., Viol, G. W., Gray, G. W., Keane, P. M., Hous4.

ton, C. S. Unpublished. 13. Sutton, J. R., Bryan, A. C.,

Gray, G. W., Horton, E. S., Rebuck, A. S., Woodley, W., Rennie, D., Houston, C. S. Aviat. Space envir. Med. 1976, 47, 1032. 14. Schmiedek, P., Baethmann, A., Schneider, E., Brendel, W., Enzenbach, R., Marguth, F. Extrarenal Activity of Aldosterone and its Antagonists; p. 234. Amsterdam, 1972. 15. Davson, H., Segal, M. B.J. Physiol, Lond. 1970, 209, 131.

AMINOGLYCOSIDE RESISTANCE DUE TO MUTATION

SiR,-Dr Mawer and Dr Greenwood (April 2, p. 749) report isolates of a Providence strain and Pseudomonas ceruginosa. Although they did not test their isolates for the production of aminoglycoside-inactivating enzymes, we suggest that the development of resistance to gentamicin and other aminoglycosides was due to mutation. We agree with them that the Ps. aeruginosa isolated by Mr Amirak and his colleagues (March 5, p. 537) showed similar crossresistance to aminoglycosides (gentamicin, tobramycin, and amikacin); this resistance was probably due to mutation. Kanamycin acetyl-transferase is the only enzyme so far reported to inactivate amikacin, and it modifies, but does not significantly inactivate, gentamicin and tobramycin.2 The finding by Dr Mawer and Dr Greenwood of the development of resistance to gentamicin, tobramycin, and amikacin in a Providence strain exposed to gentamicin corresponds with our own. We colonised an in-vitro model ulcer with a sensitive strain of Ps. ceruginosa and then applied gentamicin cream to it; subsequent isolates showed resistance to gentamicin, tobramycin, and amikacin, in the absence of gentamicin acetylating or adenylating enzymes. Both tl.se experimental systems have selected mutants. We have studied3 gentamicin-resistant isolates of Ps. ceruginosa (13 from leg ulcers and 5 from ears affected by otius

aminoglycoside-resistant

1. 2. 3.

Widdicombe, J. G. Jl R. Coll. Physns, 1977, 11, 141. Benveniste, R., Davies, J. A. Rev. Biochem. 1973, 42, 471. Seal, D. V., Strangeways, J. E. M. Unpublished.

Bronchial hyperreactivity in chronic bronchitis.

856 has drawn attention to the study by Currie all which suggested that spironolactone, an aldosterone antagonist, prevents acute mountain sickness A...
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