INTRAVASCULAR ANTI-IGE CHALLENGE IN PERFUSED LUNGS - MEDIATOR RELEASE AND VASCULAR PRESSOR-RESPONSE

Intravascular application of goat anti-rabbit immunoglobulin E (IgE) was used to stimulate parenchymal mast cells in situ in perfused rabbit lungs. Sustained pulmonary arterial pressure rise was evoked in the absence of lung vascular permeability increase and lung edema formation. Early prostaglandin (PG) D2 and histamine release into the perfusate was documented, accompanied by more sustained liberation of cysteinyl leukotrienes (LT), LTB4, and PGI2. The quantities of these inflammatory mediators displayed the following order: histamine > cysteinyl-LT > PGI2 > LTB4 > PGD2. Pressor response and inflammatory mediator release revealed corresponding bell-shaped dose dependencies. Cyclooxygenase inhibition (acetylsalicylic acid) suppressed prostanoid generation, increased LT release, and did not substantially affect pressor response and histamine liberation. BW755 C, a cyclo- and lipoxygenase inhibitor, blocked the release of cysteinyl-LT and markedly reduced the liberation of the other inflammatory mediators as well as the pressor response. The H-1-antagonist clemastine caused a moderate reduction of the anti-IgE-provoked pressure rise. We conclude that intravascular anti-IgE challenge in intact lungs provokes the release of an inflammatory mediator profile compatible with in situ lung parenchymal mast cell activation. Pulmonary hypertension represents the predominant vascular response, presumably mediated by cysteinyl-LT and, to a minor extent, histamine liberation.

Dexamethasone reduces pain, vomiting and overall complications following tonsillectomy in adults: a systematic review and meta-analysis of randomised controlled trials

Background: Tonsillectomy is one of the most common surgical procedures, but there is debate whether systemic steroids should be used to reduce pain and post-operative complications.

Do smokers with chronic obstructive pulmonary disease report their smoking status reliably?:A comparison of self-report and bio-chemical validation

Chronic obstructive pulmonary disease (COPD) is predominantly caused by cigarette smoking and is considered a worldwide preventable chronic illness. Smoking cessation is considered the primary intervention for disease management and nurses should play a major role in assisting patients to stop smoking. Currently there is a lack of professional consensus on how cessation interventions should be evaluated. The vast array of biochemical markers reported in the literature can be confusing and can make the comparisons of results difficult.

Mycobacterium triplex pulmonary infection in an immunocompetent patient

We present the case of a 47-year-old immunocompetent patient with clinical evidence of pulmonary mycobacterial disease which was found to be due to Mycobacterium triplex. This novel organism is an uncommon, emerging, pathogen for which few reports of clinical infection exist in the medical literature. © 2002 The British Infection Society.