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1.  Blockade of CD49d (alpha4 integrin) on intrapulmonary but not circulating leukocytes inhibits airway inflammation and hyperresponsiveness in a mouse model of asthma. 
Journal of Clinical Investigation  1997;100(12):3083-3092.
Immunized mice after inhalation of specific antigen have the following characteristic features of human asthma: airway eosinophilia, mucus and Th2 cytokine release, and hyperresponsiveness to methacholine. A model of late-phase allergic pulmonary inflammation in ovalbumin-sensitized mice was used to address the role of the alpha4 integrin (CD49d) in mediating the airway inflammation and hyperresponsiveness. Local, intrapulmonary blockade of CD49d by intranasal administration of CD49d mAb inhibited all signs of lung inflammation, IL-4 and IL-5 release, and hyperresponsiveness to methacholine. In contrast, CD49d blockade on circulating leukocytes by intraperitoneal CD49d mAb treatment only prevented the airway eosinophilia. In this asthma model, a CD49d-positive intrapulmonary leukocyte distinct from the eosinophil is the key effector cell of allergen-induced pulmonary inflammation and hyperresponsiveness.
PMCID: PMC508521  PMID: 9399955
2.  Mechanisms of the adult respiratory distress syndrome: selectins. 
Thorax  1995;50(Suppl 1):S49-S52.
PMCID: PMC1129016  PMID: 7570464
3.  Sequelae of the adult respiratory distress syndrome. 
Thorax  1994;49(1):8-13.
Most survivors of ARDS have persistent mild reductions of TLCO even as long as a year after their episode. The lung volumes and flows return to normal in most instances, although a subset of patients will have persistent impairment. Both obstructive and restrictive deficits may be seen. This group may be predicted by the degree of acute lung injury assessed by the level of FIO2, PEEP, and gas exchange abnormality that exists in the first few days. In the first year after ARDS most physiological abnormalities will improve, but if deficits persist at one year further improvement is unlikely. Although many patients report dyspnoea following ARDS, the symptom does not correlate with abnormalities of pulmonary function. The possibility that conventional management may augment the degree of acute injury and worsen outcome must be considered. The effects of chronic hyperoxia in humans with acute lung injury or those of high levels of PEEP compared with low levels are not known. Exploring new ventilator management strategies while we await more specific treatment directed at the primary problem of acute lung inflammation will hopefully reduce acute mortality as well as acute and chronic morbidity.
PMCID: PMC474074  PMID: 8153946
4.  Increased surface tension favors pulmonary edema formation in anesthetized dogs' lungs. 
Journal of Clinical Investigation  1979;63(5):1015-1018.
The possibility that surface tension may affect the hydrostatic transmural pressure of pulmonary vessels and the development of pulmonary edema was studied in anesthetized, open-chested dogs. Isogravimetric pressure (the static intravascular pressure at which transmural osmotic and hydrostatic pressures are balanced such that net fluid flux is zero and lung weight is constant) was measured in nine animals under three conditions: (a) control, normal surface tension, at an alveolar pressure of 30 cm H2O with the apenic lung at room temperature; (b) after increasing surface tension by cooling and ventilating at a low functional residual capacity, at an alveolar pressure sufficient to produce the same lung volume present during control measurements; and (c) after restoring surface tension by rewarming while holding the lung at a high inflation volume, again at the control lung volume. Lung volumes were established from external dimensions and confirmed +/- 10% by deflation spirometry. The isogravimetric pressure (relative to alveolar pressure) was significantly less with increased surface tension than during either the initial control condition (P less than 0.01), or when the surface tension has been restored (P less than 0.01). Similar changes occurred in each of three additional studies performed with control alveolar pressures of 10 cm H2O. Thus, increased surface tension favors fluid leakage presumably because it increases the microvascular transmural pressure.
PMCID: PMC372043  PMID: 447823

Results 1-4 (4)