American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · May 1995
Cigarette smoke inhibits lung fibroblast proliferation and chemotaxis.
Cigarette smoking is the most clearly recognized cause of pulmonary emphysema. Since loss of lung tissue, which characterizes emphysema, represents a balance between injury and repair, we hypothesized that cigarette smoke might contribute to the development of emphysema by inhibiting fibroblast proliferation and migration. To evaluate this, we examined the effect of cigarette smoke extract (CSE) on the proliferation and migration of human lung fibroblasts in vitro. ⋯ Therefore, we also examined acrolein and acetaldehyde, which are volatile components of cigarette smoke, Micromolar concentrations of acrolein and millimolar concentrations of acetaldehyde induced significant inhibition of fibroblast proliferation. In contrast, removal of volatile components did not eliminate the inhibitory activity of CSE for fibroblast migration, although acetaldehyde and acrolein alone were also capable of inhibiting chemotaxis. Cigarette smoke-induced inhibition of fibroblast proliferation and migration may impair lung repair following lung injury, and may thus contribute to the development of pulmonary emphysema.
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Am. J. Respir. Crit. Care Med. · May 1995
Do lower respiratory tract infections in early childhood cause chronic obstructive pulmonary disease?
The hypothesis that lower respiratory tract infections (LRTI) in early childhood lead to chronic obstructive pulmonary disease (COPD) in late adult life has been difficult to test. However, a unique opportunity arose when records were discovered in the counties of Hertfordshire and Derbyshire, England, that contained information about childhood LRTI recorded 60 to 70 years ago. The lung function of some men still living in these counties was examined. ⋯ In Derbyshire men, pneumonia before 2 yr of age was associated with a large and highly significant reduction in mean FEV1, adjusted for age and height. These findings were independent of smoking and social class. These data support a causal relationship between LRTI in early life and subsequent COPD.
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Am. J. Respir. Crit. Care Med. · May 1995
Clinical Trial Controlled Clinical TrialEffect of inhaled nitric oxide on right ventricular function in adult respiratory distress syndrome.
To determine whether inhaled nitric oxide (NO) affects pulmonary circulation, thereby improving right ventricular (RV) function in adult respiratory distress syndrome (ARDS), we studied 13 patients with both a lung injury severity score of 2.5 or more and a mean pulmonary artery pressure higher than 30 mm Hg. RV function was assessed by a thermodilution technique using a pulmonary artery catheter equipped with a rapid response thermistor before and 15 min after initiation of inhalation of NO (5 ppm). ⋯ The resulting fall in pulmonary vascular resistance (211 +/- 43 versus 180 +/- 59 dyn-s/cm5, p < 0.05) was associated with an increase in RV, ejection fractions (32 +/- 5 versus 36 +/- 6%, p < 0.05), a trend toward decreased RV end-systolic (96 +/- 25 versus 85 +/- 19 ml/m2, NS) and end-diastolic (142 +/- 36 versus 131 +/- 27 ml/m2, NS) volumes, and a decrease in right atrial pressures (10.9 +/- 2.9 versus 9.6 +/- 3.2 mm Hg, p < 0.05). No relationship was seen between the improvement in arterial oxygenation and the decrease in pulmonary vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)