I n h a l a t i o n o f , u l t r a s o n i c a l l y nebulized aqueous s o l u t i o n s r e s u l t s i n cough and bronchoconstrict i o n . The usual explanation f o r t h i s response ,is an a l t e r a t i o n i n t o n i c i t y of airway surface f l u i d (Elwood e t a l , Am Rev Respir D i s 1982; 125: 61). Recently an apnoeic laryngeal r e f l e x has been described i n anaesthetized neonatal animals following i n s t i l l a t i o n of aqueous solut i o n s i n t o the larynx which is dependent not on t o n i c i t y but t h e c h l o r i d e ion content (Boggs and B a r t l e t t . J Appl Physiol 1982; 53: 455). W e have t e s t e d whether i n man a s i m i l a r mechanism, dependent on chloride ion content, i s responsi b l e f o r t h e cough following i n h a l a t i o n of u l t r a s o n i c a l l y nebulized aqueous s o l u t i o n s . Ten non-smoking and non-asthmatic volunteers were studied. On s e p a r a t e days s u b j e c t s inhaled, double blind, 6 d i f f e r e n t s o l u t i o n s from an u l t r a s o n i c nebulizer (Devilbiss 65). Each subj e c t t e s t e d each s o l u t i o n twice i n random order. Normal s a l i n e was compared with d i s t i l l e d water, i s o t o n i c s o l u t i o n s of dextrose, urea, sodium a c e t a t e and bicarbonate.Coughing was determined using a pneuwtachograph on t h e expiratory p o r t of a 2 way-valve through which the mists were inhaled. Cough frequency, cough volume and peak cough flow r a t e were recorded w h i l s t t h e mists were inhaled. Solution quency (/min) Flow (I/m) Volume (mls) Urea 8.0 171. I 2 70 Dextrose 8.5 207.7 340 Water 11.3 195.4 320 S a l i n e 0 0 0 Ace tat e 9.4Cough is a common manifestation of r e s p i r a t o r y d i s e a s e , but is d i f f i c u l t t o q u a n t i t a t e . We have s t u d i e d cough during nocturnal s l e e p i n 3 men and 3 women (41-69yrs) s u f f e r i n g from chronic b r o n c h i t i s and emphysema (FEV1 0.91+0.3L fVC 2.59+1.16L; Pa0 kPa when-breathing Zir when awake). Coughs were recorded throughout t h e night by a d i r e c t i o n a l microphone and tape recorder, t r i g g e r e d t o run 9.25+0.00; PaC02 4.8320.44 f o r t h e duration of each cough. An i n t e r n a l delay loop recorded t h e whole of each cough, clock time a l s o being recorded d i g i t a l l y . Subsequent o f f -l i n e a n a l y s i s using a PET microcomputer yielded t h e time and duration o f coughs (as recognised by t h e l i s t e n e r ' s e a r s ) and were then c o r r e l a t e d with other s l e e p d a t a , including oro-nasal a i r flow, chest wall movement, e a r oxygen s a t u r a t i o n (SaO 1 and EEG s l e e p stage. The mean t o t a l s l e e p t h e was 284+25mins(+SEEl? and t o t a l coughs ranged from 0-447night, 42% o f a l l coughs occurring i n EEG s l e e p s t a g e s 0 & 1 (wakefulness and drowsiness). I n c o n t r a s t only 3% of coughs occurred i n REf4 sleep, although t h i s accounted f o r 198 of t h e t o t a l s l e e p time. These methods allow a c c u r i t e re...

SYNOPSISThe secretion of prolactin and growth hormone (GH), together with subjective ratings of sedation and hunger, were determined in 13 in-patients with anorexia nervosa and 15 controls during the intravenous infusion of L-tryptophan (100 mg/kg). Prolactin responses were not different between groups but GH responses were markedly blunted in patients. In addition sedation responses in patients were attenuated compared with controls. Hunger ratings were reduced by the infusion in controls but were too variable to be interpreted in the patients. Plasma amino acid levels were also determined before and after infusion of L-tryptophan. Tryptophan levels were comparable in the two groups as were the levels of tyrosine, phenyl alanine, valine, leucine and iso-leucine. The results suggest that some aspects of 5-hydroxytryptamine function may be attenuated in anorexia nervosa. However, they undoubtedly contrast with the finding of enhanced hormonal responses in acute dieting and may be relevant to the interpretation of similar experiments in depressive illness.

Nine poor sleepers of mean age 61 years were studied while they took loprazolam 0.5 mg, loprazolam 1 mg and triazolam 0.5 mg for 3-week periods. Loprazolam 1 mg and triazolam 0.5 mg increased sleep duration, but there was some tolerance to both, particularly triazolam, by the 3rd week. Withdrawal of either drug led to sleep significantly shorter than baseline. This rebound effect was significant greater than withdrawing triazolam. After withdrawing loprazolam 1 mg, the rebound was maximal on the 3rd night and after withdrawing triazolam it was maximal and severe on the 1st night. In the third week of use neither drug was associated with late-night wakefulness. Total overnight urinary cortisol was lower during drug intake and there were significant withdrawal rebounds to above baseline levels, immediately so after triazolam.

Withdrawal from hypnotics can produce a variety of problems, especially sleep difficulties, some of which may arise from the multiple actions of most hypnotics, thus producing a range of rebound effects. This study examined whether switching patients to a hypnotic with a narrower range of action and of a different class would reduce these problems. One hundred and thirty-four patients participated; they were randomly allocated to one of three methods of switching from "previous hypnotic" to zopiclone (a cyclopyrrolone). The methods were gap (an interval between taking the two drugs); abuttal (taking zopiclone immediately on stopping previous drug); and overlap (gradually reducing previous drug after starting zopiclone). The main findings were that zopiclone was associated with better sleep and increased alertness; the abuttal method was the best method of switching; and no serious side effects from zopiclone were reported. It was concluded that zopiclone has a useful role in benzodiazepine withdrawal, and that immediate substitution is the best method.