American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Oct 1994
Comparative StudyAntigen-specific stimulation of histamine releasing factors in diisocyanate-induced occupational asthma.
Diisocyanate-induced asthma differs from occupational asthma (OA) caused by protein allergens in that specific IgE antibody responses are rarely identified. To investigate the immunopathogenesis of diisocyanate asthma, diisocyanate-exposed workers were evaluated for in vitro production of antigen-specific mononuclear cell-derived histamine releasing factor (HRF). The mean HRF response to diisocyanate-HSA antigens was significantly greater in patients with OA than in diisocyanate-exposed asymptomatic subjects (p < 0.05). ⋯ Analysis of HRF production by subpopulations of peripheral blood mononuclear cells (PBMC) showed that lymphocytes and adherent cells were major sources of both spontaneous and antigen-stimulated HRF. The results suggest that antigen-specific HRF produced by PBMCs are an important biomarker for diisocyanate-induced asthma. This is the first report of hapten-specific stimulation of PBMCs resulting in HRF production.
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Am. J. Respir. Crit. Care Med. · Oct 1994
Comparative StudyHyperpnea limits the volume recruited by positive end-expiratory pressure.
The effectiveness of positive end-expiratory pressure (PEEP) relates directly to alveolar recruitment. We tested the hypothesis that active use of expiratory muscles during labored breathing impairs the ability of PEEP to increase end-expiratory lung volume. ⋯ Hyperpnea also shifted the distribution of the recruited volume toward regions sampled by the rib cage band of the plethysmograph. Whatever advantage expiratory muscle activity may have for minimizing the workload of the inspiratory muscles, the cost may be reduced effectiveness of PEEP in increasing lung volume and improving oxygen exchange.
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Am. J. Respir. Crit. Care Med. · Oct 1994
Comparative StudyFish consumption may limit the damage of smoking on the lung.
High fish consumption is characteristic of Japanese-American men of the Honolulu Heart Program (HHP). Analyses of data from the Atherosclerosis Risk in Communities (ARIC) study suggest high fish intake protects the lung against smoking damage. Measurements of forced expiratory volume in 1 s (FEV1) and smoking status in the HHP cohort were done at the first examination in 1965-68. ⋯ However, the predicted FEV1 at < or = 30 cigarettes/d was 52 ml (95% CI: 17, 87) higher in the high fish consumption group. No significant difference in FEV1 was noted between groups at > 30 cigarettes/d. These findings suggest that the protective role of fish is "saturated" at higher "doses" of cigarette smoking.
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Am. J. Respir. Crit. Care Med. · Oct 1994
Comparative StudyNicotine prevents a reduction in neutrophil filterability induced by cigarette smoke exposure.
Decreased deformability of neutrophils exposed to cigarette smoke is considered a determinant of neutrophil sequestration within the pulmonary microvasculature, which may be a risk for the development of pulmonary emphysema. In this study we examined the effect of nicotine, a major cigarette component, on the reduction in neutrophil deformability, measured as cell filterability, after exposed to cigarette smoke. Neutrophils were exposed to smoke by incubating them in an aqueous solution of smoke extracts. ⋯ Addition of nicotine, glutathione, alpha-tocopherol, thymol, and erythrocytes prevented the increase in membrane resistance following gas-phase smoke exposure. Nicotine also protected against an increase in membrane resistance against the effect of chloramine-T and hydrogen peroxide, but it provided no protection from superoxide radical generated from a xanthine-xanthine oxidase mixture of N-formylmethionylleucylphenylalanine. These results suggest that nicotine prevents the reduction in neutrophil filterability, probably by scavenging oxidants present in the cigarette smoke.