Search

Objectives: We administered aerosolized histamine to 32 subjects with tetraplegia to determine whether there were differences in spirometric and/or lung volume parameters between responders and nonresponders. Results: Baseline pulmonary function parameters revealed mild to moderate restrictive dysfunction. We found that 25 subjects (78%) were hyperreactive to histamine (mean provocative concentration of a substance causing a 20% fall in FEV[sub 1] [PC[sub 20]], 1.77 mg/mL). Responders (PC[sub 20], <8 mg/mL) had significantly lower values for forced expiratory flow between 25% and 75% of the outflow curve (FEF[sub 25-75]), FEF[sub 25-75] percent predicted, and FEF[sub 25-75]/FVC ratio. Among all 32 subjects, the natural logarithmic transformation performed on PC[sub 20] values (lnPC[sub 20]) correlated with FEF[sub 25-75] percent predicted, FEV[sub 1] percent predicted, and FEF[sub 25-75]/FVC ratio but not with FVC percent predicted. Responders with PC[sub 20] values <2 mg/mL (n = 13) had significantly reduced values for FVC, FVC percent predicted, FEV[sub 1], and FEV[sub 1] percent predicted compared to those with PC[sub 20] values between 2 mg/mL and 8 mg/mL. In addition, among responders, there was a significant correlation between lnPC[sub 20] and FVC percent predicted. A significant relationship was found between maximal inspiratory pressure (PImax) and both FEV[sub 1] percent predicted and FEF[sub 25-75] percent predicted, but not between lnPC[sub 20] and either PImax or maximal expiratory pressure (PEmax). Conclusions: These findings demonstrate that subjects with tetraplegia who exhibit airway hyperreactivity (AHR) have reduced baseline airway caliber and that lower values for lnPC[sub 20] are associated with parallel reductions in surrogate spirometric indexes of airway size (FEV[sub 1] percent predicted and FEF[sub 25-75] percent predicted) and airway size relative to lung size (FEF[sub 25-75]/FVC ratio). The absence of an association between lnPC[sub 20] and FVC percent predicted for the entire group or between lnPC[sub 20] and either PImax or PEmax indicates that reduced lung volumes secondary to respiratory muscle weakness cannot explain the mechanism(s) underlying AHR. Among responders, however, a possible role for reduction in lung volume, as it pertains to increasing AHR, cannot be excluded. Proposed mechanisms for reduced baseline airway caliber relative to lung size in subjects with tetraplegia include unopposed parasympathetic activity secondary to the loss of sympathetic innervation to the lungs and/or the inability to stretch airway smooth muscle with deep inhalation. [ABSTRACT FROM AUTHOR]

OBJECTIVE:&EMSP;:To further investigate mechanisms of airway hyperreactivity among subjects with chronic cervical spinal cord injury (SCI), we assessed airway responsiveness to aerosolized methacholine and histamine in subjects receiving chronic oxybutynin chloride therapy, and compared the findings with those not receiving the agent. Methods: Twenty-five male subjects with cervical SCI participated in this study; 12 were maintained on oral oxybutynin chloride and 13 served as age-matched controls. Six of the 12 subjects receiving oxybutynin were challenged with aerosolized methacholine, and six with histamine; seven of the 13 control subjects were challenged with aerosolized methacholine and the remaining six with histamine. Results: All 13 control subjects and all six oxybutynin/histamine subjects exhibited a significant bronchoconstrictor response (PC20<8 mg/ml), whereas mean PC20 values for the oxybutynin/methacholine group were 25 mg/ml. Conclusion: Our finding that the bronchoconstrictor effects of methacholine were blocked by oxybutynin chloride while those of histamine were not suggests that oxybutynin acts primarily through anticholinergic pathways rather than by causing generalized airway smooth muscle relaxation. [ABSTRACT FROM AUTHOR]

To determine the prevalence of respiratory symptoms in subjects with chronic spinal cord injury (SCI), 180 subjects completed a standard respiratory questionnaire modified for subjects with limited mobility. Subjects were categorized as high tetraplegia (HT:C5 and above not requiring mechanical ventilation), low tetraplegia (LT: C6 – 8), high paraplegia (HP: T1 – 7), or low paraplegia (LP: T8 – L3). Overall, 68% of subjects reported one or more respiratory symptom. Breathlessness, the most prevalent complaint, was associated with level of lesion: HT=73%, LT=58%, HP=43% and LP=29%, whereas complaints of cough, phlegm, cough and phlegm, and wheeze did not differ significantly among subjects in the four groups. Breathlessness occurred significantly more often in the group with HT during rest or following exposure to hot air or passive smoke. Awareness of phlegm or wheeze was reported with increased prevalence among subjects with tetraplegia who had complete injuries. Among subjects with tetraplegia, respiratory complaints did not differ significantly in current smokers, former smokers, and non-smokers, whereas among subjects with paraplegia, phlegm and wheeze were reported more frequently among current smokers. [ABSTRACT FROM AUTHOR]

Background: Acid fast cell wall deficient forms (CWDF) of bacteria have been grown from blood, bronchial washings, and ocular anterior chamber fluid from patients with sarcoidosis. A monoclonal antibody raised against Mycobacterium tuberculosis whole cell antigen (H37RV) was used to characterise further CWDF grown from the blood of patients with sarcoidosis.Methods: Blood from 20 patients with active sarcoidosis and from 20 controls was cultured using methods favourable for the growth of CWDF. Isolates were further characterised by indirect fluorescent antibody analysis using a monoclonal antibody highly reactive with M tuberculosis.Results: CWDF were grown from the blood of 19 of 20 subjects with sarcoidosis. All isolates stained positively with the monoclonal antibody and with a modified Kinyoun stain. No organisms were grown from the blood of controls.Conclusions: These data demonstrate that CWDF can be grown from the blood of nearly all patients with active sarcoidosis. The results confirm that the organisms are mycobacterial in origin and are similar, if not identical, to M tuberculosis. Their role in the pathogenesis of sarcoidosis is unknown. [ABSTRACT FROM AUTHOR]