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BACKGROUND: Salbutamol is the most widely prescribed short acting beta 2 agonist and salmeterol is the first long acting inhaled beta 2 agonist. The dose equivalence of salmeterol and salbutamol is disputed. Estimates of weight-for-weight dose ratio have ranged from 1:2 to 1:16. A study was undertaken to clarify the true dose ratio. METHODS: The bronchoprotection afforded against repeated methacholine challenge by inhaled salmeterol 25 micrograms and 100 micrograms and salbutamol 100 micrograms and 400 micrograms was compared in a randomised, double blind, placebo controlled, crossover trial. Subjects were 16 stable asthmatics with a baseline forced expiratory volume in one second (FEV1) of > or = 65% predicted, screening concentration provoking a fall in FEV1 of 20% (PC20FEV1) of < or = 8mg/ml, and a shift in PC20FEV1 of more than two doubling concentration steps following inhalation of salbutamol 400 micrograms. On five separate occasions subjects underwent methacholine challenge before and 30 and 120 minutes after drug administration. PD20FEV1 was calculated for each challenge. FEV1 at 90 minutes after drug administration was also recorded. RESULTS: Bronchoprotection afforded by salmeterol was increased at 120 minutes compared with 30 minutes and protection by salbutamol was decreased. Protection by both doses of salmeterol was similar to salbutamol 100 micrograms at 30 minutes but significantly greater at 120 minutes. FEV1 at 90 minutes was significantly greater after salmeterol 100 micrograms than after placebo, but there were no other significant differences between treatments. Maximal observed protection was equivalent for salmeterol 100 micrograms and salbutamol 400 micrograms. CONCLUSIONS: The data are compatible with a weight-for- weight dose ratio for salmeterol:salbutamol of < or = 1:4.

Background With increasing cannabis use, physicians need to know more about its respiratory effects. However, there are few long term studies of cannabis smoking, due to legality issues and confounding effects of tobacco. Aims We reviewed effect of chronic cannabis use on respiratory symptoms and lung function, particularly FEV1, FVC and FEV1/FVC ratio. Methods 19 out of 256 English-language publications, prior to June 2015, from MEDLINE, Scopus, and Web of Science databases, reporting lung function in chronic cannabis users, were examined. Results 11 cross-sectional studies and 8 observational cohort studies were included. All 9 studies (n = 11,848) examining respiratory symptoms reported an increase with cannabis smoking (odds ratio up to 3.0). 2 studies (n = 1,336) reported that quitting cannabis with/without tobacco reduced chronic bronchitis symptoms to those of never cannabis smokers. 8 studies (n = 9,939) reported no significant changes in FEV1/FVC; 6 (n = 3,722) found a significant decrease (0.5%−1.9%) in chronic marijuana only smokers compared to controls. While most reports omitted absolute FVC results, 3 large studies (n = 13,858) demonstrated increased FVC with marijuana smoking. 4 studies (n = 13, 674) found dose-related reductions in FEV1/FVC. 7 studies associated chronic cannabis smoking with other evidence of airflow obstruction [increased airway resistance in 3; (0.03 to 0.38 cm H 2 O/L/s), reduced specific airway conductance in 4; (0.007 to 0.07 mL/s/cm H 2 O/L)]. The larger studies (n = 13,858) suggested increased FVC may cause reduced FEV1/FVC chronically. 1 This contrasts with airflow obstruction in tobacco smoking. Anti-inflammatory or acute bronchodilator effects of cannabis, on top of chronic effects, may partly explain these results. Conclusions Cannabis, like tobacco, smoking causes chronic bronchitis but increased FVC is more consistently found than reduced FEV1. No studies in marijuana smokers have found a linear decline in FEV1 with time. More work is needed to explain the differing effects on lung function and to examine effects on small airways, imaging and histology. Reference Hancox RJ, et al . Effect of cannabis smoking on lung function: a population-based cohort study. Eur Respir J 2010; 35 :42–7.

Background With increasing cannabis use, physicians need to know more about its respiratory effects. However, there are few long term studies of cannabis smoking, mostly due to legality issues and the confounding effects of tobacco. Aims We reviewed the effect of chronic cannabis use on bullous lung disease. Methods 18 out of 69 English-language publications, prior to April 2016, from MEDLINE, Scopus, and Web of Science databases, which reported bullous lung disease in cannabis users, were examined. Case reports and case series were included. Results The only cross-sectional study reported an increase in the rates of macroscopic emphysema in tobacco only (17 of 92) and tobacco + cannabis smokers (15 of 91), but not in cannabis only smokers (1 of 75) compared to non-smokers.1 The remaining case series and case reports described a total of 56 marijuana smokers presenting with bullous lung disease, often with pneumothorax and predominantly upper lobe involvement (Table 1). Concurrent tobacco smoking was present in all but 3 cases. The majority of cases reported heavy cannabis use, though direct comparison was difficult due to variation in usage measurements. All 4 case series that measured lung function reported normal findings. Conclusions While the clinical association of cannabis smoking and peripheral lung bullae is well recognised (and consequently often not reported) there is scant documentation in the literature correlating marijuana smoking with bullous lung disease. Reference Aldington S, et al . Effect of cannabis on pulmonary structure, function and symptoms. Thorax . 2007; 62 (12):1058–63.

BACKGROUND: Platelet activating factor (PAF) is a potent mediator of inflammation. Inhalation of PAF causes acute bronchoconstriction and a transient fall in white blood cell count in humans. Salmeterol inhibits pulmonary inflammation induced by PAF in guinea pigs. METHODS: The effect of salmeterol on effects induced by PAF was investigated in eight normal subjects who inhaled salmeterol (50 micrograms) twice daily or a matched placebo for one week before challenge with PAF. Blood samples were taken from a forearm catheter for total white cell and neutrophil counts before and for 30 minutes after administration of PAF (48 micrograms) through a Mefar dosimeter. Blood films were stained for unsegmented neutrophils before and after treatment with PAF on a placebo day. RESULTS: Mean baseline total white cell counts and neutrophil counts did not differ on the two days. Mean baseline sGaw was significantly higher after inhaled salmeterol (1.84 (95% C1 1.45-2.23) s-1kPa-1) than after placebo (1.53 (1.24-1.82)). After placebo mean total white cell counts, neutrophil counts, and sGaw were reduced to 60 (43-78)%, 39 (14-64)%, and 82 (71-93)% of baseline respectively five minutes after inhaled PAF. After salmeterol treatment mean reductions five minutes after inhaled PAF were 59 (45-73)%, 40 (19-61)%, and 82 (71-93)% of baseline respectively. At 30 minutes after treatment with PAF the neutrophil count rebounded to 143 (82-204)% of baseline after placebo and to 127 (93-161)% after inhaled salmeterol. There was no significant difference in the percentage of immature neutrophils before and after treatment with PAF (2.0 (0.5-2.6)% compared with 3.9 (2.2-5.6)%. CONCLUSIONS: Treatment with salmeterol did not inhibit reduction in total white cell count or neutrophil count, rebound neutrophilia, acute bronchoconstriction, or transient flushing after inhalation of PAF. These results conflict with the inhibitory effect of salmeterol on lung inflammation in guinea pigs but are consistent with the lack of effect of salbutamol in humans. Salmeterol does not have an anti-PAF effect in vivo in humans.

A large mediastinal bronchogenic cyst presented acutely with paroxysmal atrial fibrillation and severe airflow obstruction. The patient had experienced identical symptoms on two other occasions over the previous 24 years. These had been previously misdiagnosed as due to a mediastinal lymphoma. Percutaneous extrapleural aspiration successfully decompressed the cyst with substantial improvement in lung function. Recurrent swelling of the cyst occurred that could not be relieved surgically. After repeat aspiration percutaneous instillation of bleomycin and alcohol has been used to prevent further increase in the size of the cyst.

“Crack lung” is an acute pulmonary syndrome with a spectrum of clinical and histopathological findings. Smoking crack, a potent and highly addictive crystalline form of cocaine, usually involves deep inspiration followed by the valsalva manoeuvre and coughing. A 30 year old man presented 8 hours after smoking crack with severe chest pain and coughing. His chest radiograph showed …

Non-adrenergic inhibitory nerves may have an important role in regulating airway calibre. A recently discovered peptide, peptide histidine valine, is a potent relaxer of airway smooth muscle in vitro and has been proposed as a possible neurotransmitter in this tissue. The cardiovascular and respiratory effects of graded infusions of this peptide (2.5-10 pmol kg-1 min-1) have been examined in six normal subjects in a placebo controlled, randomised double blind study. The mean (SEM) peak plasma concentration of peptide histidine valine during the highest infusion rate was 2392 (170) pmol/l, representing a 29 fold increase above the basal concentration. This was accompanied by flushing, a significant increase in heart rate of 28 (3.7) beats/min and skin temperature of 1.8 degrees (0.16 degrees) C, but no effect on systolic or diastolic blood pressure. Despite these high plasma concentrations of the peptide and the substantial tachycardia and increase in skin blood flow, there was no change in partial expiratory flow at 40% of vital capacity (Vp40) or in the airway response to inhaled histamine (geometric PD40 9.37 and 9.73 mumol during saline and peptide histidine valine infusion respectively). Although these findings provide no support for a physiological role of peptide histidine valine in controlling airway function in healthy subjects, important effects of locally released peptides in the vasoactive intestinal peptide family cannot be excluded.