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Kent-Olov Jonsson when injected alone at a dose of 200 g, although the pattern was the same as in the initial experiment Fig. 10B ; . Concerning the effects of SR144528, the results are hard to interpret in terms of antagonising the effects of JWH133, since the SR144528 itself seemed to decrease the response of compound 48 80 Fig. 10B ; . Although this is at first sight somewhat an unexpected finding, it is in line with data by Iwamura and co-workers, who found that SR144528 decreased carrageenan-induced paw oedema in mice Iwamura et al., 2001 ; . Similar results were also found in a recent study, were topical application of SR144528 reduced TPA tetradecanoylphorbol acetate ; -induced ear swelling as well as leukotriene B4 production and neutrophil infiltration in the mouse ear Sugiura et al., 2004 ; . Smith et al 2001 ; also reported that SR144528 reduced neutrophil migration in a mouse peritonitis model, and cited preliminary data that this was also seen in a CB1 CB2 double knockout, indicating a CB1 and CB2 receptor independent effect. In the case of PIA, as well as PEA data not shown ; , initially no effects were seen on plasma extravasation when the compounds were administered in an ethanol vehicle Fig. 10C ; . Given the fact that these compounds are highly lipophilic, and that PEA has proven effective in other mast cell models, we wanted to test if the lack of effect in this model was due to the choice of carrier. As a consequence, PIA and PEA were dissolved in a preparation of ethanol: Cremophor: saline 1: 18 ; instead. In this case, both treatments seemed to decrease the compound 48 80-induced plasma extravasation, although this was not found to be statistically significant due to one animal in each PIA treated group which did not respond to the treatment Fig. 10D ; . One explanation could be that the injection of PIA in these animals did not result in a systemic administration of the drug, although there is no proof for this concept. If this is a plausible explanation, the present data are in line with the finding by Mazzari et al. 1996 ; that PEA is effective in reducing mast cell dependent inflammation in vivo, and that PIA and JWH133 produces similar effects. As a complement to the effects of the compounds in vivo, we wanted to evaluate if any effects could be seen using an in vitro system. Instead of using mast cell lines or isolated mast cells, in which the cells ability to respond is altered Robinson et al., 1989; Sweiter et al., 1993; Hamawy et al., 1994; Ra et al., 1994 ; , we chose to establish a skin tissue model where the cells are surrounded by a natural environment. When the mouse paw skin tissue was stimulated by compound and tobradex.

Reason for posting: Long-acting 2agonist LABA ; medications are bronchodilators used in the treatment of asthma and chronic obstructive pulmonary disease. More than a decade ago questions were raised about an excess of asthma-related events, including death, in a study of salmeterol.1 Randomized trials were completed in recent years of either salmeterol or formoterol to resolve these safety concerns, but serious questions remain. As reported previously in CMAJ , 2 the Salmeterol Multi-center Asthma Research Trial SMART ; , a 28-week randomized controlled trial that enrolled more than 26 000 patients, was stopped early because of salmeterolrelated safety concerns. The trial data have not been published and instead were submitted to the US Food and Drug Administration FDA ; . The FDA recently convened its PulmonaryAllergy Drugs Advisory Committee to review these and other LABA safety data; the committee decided that the potential risks seen in this salmeterol trial might be shared by other LABA medications. Safety warnings have now been issued by all manufacturers of LABAs in Canada hc-sc. gc dhp-mps medeff advisories-avis prof index e ; . The drugs: LABAs sold in Canada include salmeterol as Sereevent and, in combination with fluticasone, as Advair ; and formoterol fumarate as Oxeze and Foradil and, in combination with budesonide, as Symbicort ; . They drugs have been shown to improve measures of lung function, disease control and quality of life for people with asthma.3 However, safety concerns exist. SMART participants in the salmeterol group experienced an absolute increase in risk of the study's primary end point respiratory-related death or lifethreatening experience ; of 0.106% over that seen in the placebo group Table 1 ; . This gives a number needed to harm NNH ; of 943 95% confidence interval [CI] 410 to infinity ; . The NNH for the secondary end point asthma-related death or life-threatening experience ; was similar. However, a post hoc analysis showed that black patients had much higher relative and absolute risks than non-black patients: the NNH among black salmeterol users was only 159 95% CI 96468 ; for respiratoryrelated death or life-threatening experience and 158 95% CI 97433 ; for asthma-related death or life-threatening experience. After 3 small phase III studies of formoterol suggested that the risk of asthma exacerbations increased with higher drug doses, 4 a 16-week phase IV study was conducted, enrolling 2307 patients above the age of 12. No deaths occurred in this trial. Although the absolute event rates were low, patients taking higher formoterol doses appeared to experience more serious asthma-related events than those given lower doses of the drug or placebo Table 2 ; . What to do: LABAs are indicated for asthma maintenance therapy, and only the lowest effective dose should be used. Recent large trials, particularly of salmeterol, have shown that asthma and serzone.

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