Topically applied glucocorticosteroids (GS) have been shown to cause local vasoconstriction in normal skin and this phenomenon is commonly used to assess the potency of topical GS (McKenzie skin blanching test). The purpose of the present study was to determine if an inhaled GS, fluticasone propionate (FP), similarly leads to vasoconstriction in the airway mucosa and if subjects with and without asthma have differential vascular responsiveness to GS. In 10 nonsmokers with stable asthma and 10 nonasthmatic nonsmokers, airway mucosal blood flow (Qaw) expressed per milliliter of anatomical dead space and the forced expiratory volume in 1 s (FEV (1)) were determined before and serially after inhalation of FP (88 to 1,760 microg) or placebo. Baseline mean (+/- SE) Qaw was 55.1 +/- 1.0 and 44.2 +/- 1.1 microl x min(-1) x ml(-1) in subjects with and without asthma, respectively (p < 0.001). The corresponding mean FEV(1) values were 2.34 +/- 0.13 and 3.22 +/- 0.12 L (p < 0.001). FP at 880 microg but not placebo produced a transient decrease in mean Qaw with a nadir at 30 min and return toward baseline at 90 min post-inhalation; the maximum mean decrease was 37% in subjects with asthma and 21% in unaffected subjects (p < 0.01); 880 microg of FP was the lowest effective dose. FEV(1) did not change after FP administration in either group. These results demonstrate a transient vasoconstrictive action of inhaled FP in the airway mucosa, with a greater vascular responsiveness in subjects with asthma than in unaffected subjects. The measurement of Qaw may provide a more relevant means of assessing the potency of inhaled GS than the McKenzie skin blanching test. In addition, our observation suggests that inhaled GS have potentially beneficial effects in asthma that is not related to their antiinflammatory action.

As an inflammatory airway disease, asthma is expected to be associated with an increase in airway blood flow. We therefore compared airway mucosal blood flow (Qaw) among normal subjects (n = 11) and patients with stable asthma receiving (n = 13) or not receiving (n = 10) long-term inhaled glucocorticosteroid (GS) therapy. Qaw was calculated from the uptake of dimethyl ether in the anatomic dead space minus the most proximal 50 ml (DS), and expressed as blood flow per ml DS. Mean (+/- SE) Qaw was 38.5 +/- 5. 3 microl . min-1 . ml-1 in normals, 68.2 +/- 7.9 microl . min-1 . ml-1 in GS-naive asthmatics (p < 0.01), and 55.4 +/- 5.3 microl . min-1 . ml-1 in GS-treated asthmatics (p < 0.05). Ten minutes after administration of 180 microg albuterol by metered dose inhaler, mean Qaw increased by 83 +/- 26% in normal subjects (p < 0.01), but did not change significantly in GS-naive (+5 +/- 8%) or GS-treated (+32 +/- 15%) asthmatics. These results demonstrate that Qaw is increased in stable asthmatics and resistant to further increase by a standard inhaled dose of a beta-adrenergic agonist.

We studied 20 patients with intraspinal tuberculosis (TB), to characterise the MRI features of tuberculous meningitis and myelitis. MRI leptomeningitis and intramedullary involvement in 11 patients, intramedullary lesions alone in 5, leptomeningitis alone in 2, and isolated extradural disease in 2. TB leptomeningitis was characterised by loculation of the cerebrospinal fluid (CSF), nerve root thickening and clumping (seen only in the lumbar region) or complete obliteration of the subarachnoid space on unenhanced images. Gd-DTPA-enhanced images proved useful in 6 cases, revealing linear enhancement of the surface of the spinal cord and nerve roots or plaque-like enhancement of the dura-arachnoid mater complex. Intramedullary lesions included tuberculomas (8), cord oedema (5) and cavitation (3). In seven cases of intramedullary tuberculoma multiple lesions with skip areas were seen, without significant cord swelling. One patient had an isolated lesion in the conus medullaris. The lesions were iso- or hypointense on T1-weighted images, iso-, hypo- or hyperintense on T2-weighted images and showed rim or nodular enhancement with contrast medium.

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