Objectives:Gastro-oesophageal reflux disease (GORD) is both common and troubling with a prevalence of 20-40%. We assessed the utility of a scintigraphic reflux study to evaluate the oesophageal and extra-oesophageal manifestation of disease compared to the standard tests such as pH monitoring and manometry.Methods:Patients were recruited into a prospective database of referrals to a tertiary referral center for either resistance to maximal medical therapy or extra-oesophageal symptoms of GORD. Data included 2 channel 24-hour pH monitoring and manometry results, as well as scintigraphic reflux data with late images assessing pulmonary aspiration of refluxate.Results:Study population included 250 patients (155 F, 95 M) with an average age of 60 years. Patients were clinically classified as either GORD (n=72) or laryngopharyngeal reflux (LPR) (n=178). Pulmonary aspiration of the refluxate was detected significantly more commonly in LPR patients (58/178 compared with GORD 10/72). Strong correlations were found between the scintigraphic time-activity curves in the upper oesophagus and pharynx, and ineffective oesophageal motility and pulmonary aspiration. pH studies correlated with the scintigraphic studies but did not predict aspiration similar to other modalities when evaluated by ROC analysis.Conclusion:Scintigraphic reflux studies offer a viable alternative test for GORD and extra-oesophageal manifestations of reflux disease. Strong correlations were found between measurable scintigraphic parameters and oesophageal motility and lung aspiration of refluxate. This may provide a more confident decision analysis in patients being considered for fundoplication for troubling extra-oesophageal symptoms.

Colonization with B. cepacia had a significant adverse effect on survival within the study population. Genomovar and strain typing contributed usefully in accessing the effectiveness of the hospital's segregation policy in preventing cross-colonization.

The purine nucleoside, adenosine, has been implicated as a neuromodulator in central respiratory depression during prolonged exposure to hypoxia. It may also be a mediator of hypoxic hyperpnoea, acting on the carotid bodies. As there may be adenosine-sensitive mechanisms of hypoxic respiratory control, we sought to determine whether adenosine might be involved as a respiratory modulator in another central but non-oxygen-related control mechanism, the ventilatory response to hyperoxic hypercapnia.Twelve normal subjects were studied following 3 days of oral treatment with placebo, dipyridamole (which potentiates adenosine effects by inhibiting cellular uptake), and theophylline (a specific adenosine antagonist of cell surface receptors). The drugs were given in a random order, double-blind fashion. Resting endtidal carbon dioxide tension (PET,CO 2 ) and the maximum rate of isometric inspiratory pressure change at the mouth ((dP/dt )max), an index of respiratory drive, were determined in all subjects on each treatment. Hyperoxic, hypercapnic ventilatory responses were determined in seven of these subjects using a rebreathing technique. For each hypercapnic response, minute ventilation (V 'E) and (dP/dt )max were plotted against PET,CO 2 breath-by-breath.Resting PET,CO 2 breathing room air was lower with theophylline (5.47 (SD 0.21) kPa) than with placebo (5.74 (0.26) kPa) or dipyridamole (5.86 (0.34) kPa), with no significant drug differences in resting (dP/dt )max. However, neither the slope nor the PET,CO 2 intercept of the relationship between ventilation or respiratory drive and PET,CO 2 were altered by the study drugs under hyperoxic conditions. We conclude that endogenous adenosine-related mechanisms are unlikely to be involved in determining either the sensitivity or the threshold of the ventilatory response to carbon dioxide under hyperoxic conditions. However, in normoxia, a centrally-acting, tonic, adenosine-mediated, respiratory modulation is not ruled out.

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1. Twelve healthy young men took part in this investigation of the effect of oral theophylline and dipyridamole (two drugs known to affect the pharmacological effects of the purine nucleoside adenosine) on the respiratory response to isocapnic hypoxia. 2. The subjects underwent hypoxic rebreathing manoeuvres after 3-day pretreatments with each of the drugs for 12 h and were at least 2 h postprandial. For each in-Minute ventilation, the maximum rate of isometric inspiratory pressure development at the mouth and the ratio of inspiratory duration to total breath duration were analysed breath-by-breath and regressions of these variables upon the haemoglobin oxygen saturation were performed. 3. The slopes and intercepts of the lines describing the relationships of minute ventilation and the maximum rate of isometric inspiratory pressure development at the mouth with haemoglobin oxygen saturation were unaffected by the study drugs, and no differences in the pattern of breathing were observed. 4. We conclude that oral administration of these drugs does not result in alteration of the response of the respiratory system to progressive isocapnic hypoxia. 5. This suggests that either adenosine has no physiological role in hypoxic respiratory control as measured, or that it has opposing peripheral chemoreceptor and central respiratory centre effects which could not be distinguished by the techniques used.