American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Mar 1997
The effects of post-treatment with lisofylline, a phosphatidic acid generation inhibitor, on sepsis-induced acute lung injury in pigs.
The effects of lisofylline [(R)-1-(5-hydroxyhexyl)-3,7-dimethylxanthine] (LSF), an inhibitor of de novo phosphatidic acid (PA) generation, on sepsis-induced acute lung injury was studied using Hanford minipigs weighing 18 to 25 kg. Sepsis was induced by an intravenous infusion of Pseudomonas aeruginosa (1 x 10(6)/colony-forming units/kg/min over 2 h). Saline was used as the control vehicle. ⋯ LSF treatment attenuated sepsis-induced pulmonary hypertension, neutropenia, and hypoxemia, and increased MPO activity and lung injury measurements in the Pre and Post-1 h groups, but its efficacy was blunted in the Post-2 h group. Plasma TNF-alpha was decreased only in the Pre group. Thus, inhibition of intracellular PA generation through de novo pathways attenuates sepsis-induced acute lung injury.
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Am. J. Respir. Crit. Care Med. · Mar 1997
Proteins and phospholipids in BAL from patients with hydrostatic pulmonary edema.
The purpose of the present study is twofold: to evaluate alterations in total phospholipid content and individual phospholipid classes of the surfactant, and to detect markers of inflammatory reaction in bronchoalveolar lavage (BAL) from patients with hydrostatic pulmonary edema (HPE). Mechanically ventilated patients with HPE (Group 1) were compared with mechanically ventilated patients without cardiopulmonary disease (Group 2), considered as the control group. Group 3, including patients with high-permeability pulmonary edema, was used for further comparison. ⋯ There was an inverse correlation between PAF-AcH and PAF. Quantitative reduction of total BAL phospholipids (PL) and qualititative deficiency was observed in both patients with HPE and ARDS. The findings of this study suggest that there is evidence of inflammation in the airspaces of patients with HPE.
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Am. J. Respir. Crit. Care Med. · Mar 1997
Phenotypic analysis of alveolar macrophages and monocytes in allergic airway inflammation. I. Evidence for activation of alveolar macrophages, but not peripheral blood monocytes, in subjects with allergic rhinitis and asthma.
Macrophages and monocytes play important proinflammatory roles in allergic inflammation. We hypothesized that these cells would express an activated phenotype in allergic disease of the airways. We therefore compared the expression of 17 activation markers on the surface of alveolar macrophages (AM) and peripheral blood monocytes (PBM) in 13 subjects with asymptomatic allergic asthma (AA), nine subjects with asymptomatic allergic rhinitis (AR), and 11 nonallergic (N). ⋯ In contrast, no significant differences were found among the three groups in the expression in eight other markers (CD11b, CD14, CD23, CD29, CD33, CD35, CD63, and CD64). Finally, similar analysis of PBM from these same subjects failed to find any difference between the three groups in any of the 17 activation markers studied. These data suggest that AM are activated in allergic respiratory diseases, and that levels of HLA Class I and CD44 on AM are altered during allergic inflammation in the upper and lower airways.
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Am. J. Respir. Crit. Care Med. · Mar 1997
Tris-hydroxymethyl aminomethane and sodium bicarbonate to buffer metabolic acidosis in an isolated heart model.
Metabolic acidosis induces a decrease in the developed force of cardiac muscle by affecting every step of the excitation--contraction coupling pathway. Due to transient worsening in intracellular acidosis, the value of administering sodium bicarbonate therapeutically during acute acidosis has been questioned. An alternative therapeutic drug, Tris-hydroxymethyl aminomethane (THAM) has the advantage of diffusing into the intracellular space. ⋯ The combination of THAM with sodium bicarbonate perfectly buffered acidosis without modifying PaCO2 and significantly improved contractility. The combination of THAM with sodium bicarbonate is based on the ability of THAM to capture the CO2 produced by the sodium bicarbonate buffer. This combination achieves a perfect correction of metabolic acidosis and improves myocardial performance.