Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sensitive and specific radioimmunoassay was used to measure interleukin 8 (IL-8) in bronchoalveolar lavage fluids from control subjects, patients with the adult respiratory distress syndrome (ARDS) and patients undergoing coronary bypass surgery, a risk factor for developing ARDS. Concentrations of IL-8, albumin, total protein and numbers of neutrophils were higher in both patient groups than in controls. Levels of IL-8 were significantly correlated with the influx of neutrophils, plasma protein extravasation and with the PaO2/FiO2 ratio. These data suggest that IL-8 may mediate the recruitment of neutrophils from the vascular compartment into the alveolar space and may therefore be an important determinant in neutrophil-mediated lung injury. Since increased levels of IL-8 were also found in BAL fluid from patients at risk in whom ARDS did not develop, other factors are likely to be involved and IL-8, as well as other markers of inflammation, are of little prognostic use.
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PMID:Interleukin 8 (IL-8) in the bronchoalveolar lavage fluid from patients with the adult respiratory distress syndrome (ARDS) and patients at risk for ARDS. 129 43

Severe respiratory failure is always associated with a defect in the surfactant system. Surfactant substitution in newborn infants with respiratory distress syndrome (RDS) has gained worldwide acceptance. In the present study, we have evaluated whether surfactant diagnostics are of use in choosing recipients of exogenous surfactant. In addition, we studied whether factors apparently unrelated to surfactant influence the degree of respiratory failure and surfactant responsiveness. In small preterm infants, the surfactant indices in amniotic fluid (L/S ratio and phosphatidylglycerol), within 3 days of birth, predicted the risk of RDS with a sensitivity of 90-100%, and a specificity of 50-85%. The surfactant indices, measured in BAL, predicted the risk of ARDS (which became evident 1 to 7 days later) with a sensitivity of 50-60% and a specificity of 59-65%. In small preterm infants with RDS, the amount of fluids given during the first day correlated positively with the degree of respiratory failure and negatively with the degree of surfactant responsiveness. According to an experimental study, in hydrostatic lung edema, exogenous surfactant is diluted by edema fluid and becomes sensitive to inhibitors of surfactant function. Beside dosage, quality, and time of administration, the management of patients largely dictates the responsiveness to exogenous surfactant.
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PMID:Lung surfactant in respiratory distress syndrome. 192 23

Evidence obtained by biochemical analysis of BAL fluids from patients with ARDS indicates that at least 2 important pathogenic events take place in the pulmonary tissues. These are the release of neutrophil elastase and the generation of oxidants. Both events can lead to severe pulmonary injury as has been demonstrated in experimental animals. To better understand the mechanisms of oxidant damaged cells, H2O2 was added to cultured cells. H2O2 compromises a multitude of cellular functions, the combination of which leads to cell death. DNA is an important target for oxidant-induced injury. The formation of DNA strand breaks leads to activation of pADP-RP which in turn causes depletion of NAD and ATP, followed by Ca++ influx and eventually cell lysis. Inhibition of pADP-RP prevented cell lysis, but not DNA damage. A similar sequence of events has been described for cell injury following DNA damage induced by gamma-irradiation and alkylating agents and was proposed to be a suicide mechanism for cells with irreversibly damaged DNA. Sublethal doses of H2O2 will delay cell replication, but not necessarily prevent it.
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PMID:Biochemical events associated with pulmonary failure in shock and trauma. 244 44

Levels of platelet-specific alpha-granule proteins, PF, BTG, and TSP were measured in BAL fluids of patients with the ARDS, ILD, and normal healthy subjects, comprising two separate cohorts. In both groups BAL showed elevated levels of BTG and thrombospondin in ARDS patients. Low levels of PF4 were found in BAL and did not differ between ARDS and control patients. The BTG:PF4 ratio was 2:1 or greater in BAL of ARDS patients and of control subjects with other lung diseases, suggesting in vivo release. In ARDS patients, the ratio of TSP to BTG exceeded that usually found in plasma. In ARDS patients in group 2, BAL levels of TSP, BTG, and total protein correlated strongly with the composite injury scores that were used to quantitate their degree of lung injury. Elevated levels of platelet-derived proteins, which modulate chemotaxis of inflammatory cells and promote connective tissue reorganization, occur in the alveolar compartment of ARDS and ILD patients but are usually undetectable in BAL of healthy control subjects. Levels in these patients in BAL fluid are nonspecific indices of the severity of lung injury in patients with ARDS.
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PMID:Platelet-specific alpha-granule proteins and thrombospondin in bronchoalveolar lavage in the adult respiratory distress syndrome. 253 64

A monoclonal antibody has been made to a peptide that is released by human alveolar macrophages. This enzyme-releasing peptide (ERP) causes neutrophils to secrete azurophilic granule enzymes. Normal subjects, patients with pulmonary fibrosis, and patients with sarcoidosis had similar concentrations of this peptide in their bronchoalveolar lavage fluids. However, patients with the adult respiratory distress syndrome (ARDS) had about 2.7 times higher concentrations in their lavage fluids. The enzyme-releasing activity in the lavage fluids was significantly correlated with 2 indices of the severity of the clinical illness in patients with ARDS, the APACHE score, and the chest radiograph score. The correlation was diminished or ablated by removing the peptide with the monoclonal antibody bound to staphylococcal Sepharose 4B. This peptide accounted for 62.08% (SD = 15.88%) of the enzyme-releasing activity in fluids from lungs of patients with ARDS and 86.39% (SD = 24.46%) of the activity in fluids from lungs of normal control subjects. Therefore, ERP is the major neutrophil enzyme-releasing agent in the bronchoalveolar lavage fluid from patients with ARDS and from normal persons. There was a significant correlation between the neutrophil enzyme-releasing activity and the ERP concentrations in BAL of patients with ARDS. These observations suggest that modulation of neutrophil function by ERP significantly controls the protease and peroxidase loads in the lungs of patients with ARDS.
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PMID:A peptide from alveolar macrophages that releases neutrophil enzymes into the lungs in patients with the adult respiratory distress syndrome. 284 27

Angiotensin converting enzyme (ACE) is present in the endothelial cells of the normal lung where it converts angiotensin I to angiotensin II and inactivates bradykinin. It has been suggested that during endothelial injury ACE is sloughed into the blood, and that if the alveolar capillary membrane is injured, also into the alveolar lining fluid. Seven patients with adult respiratory distress syndrome (ARDS), were compared to 11 normal control subjects, nine patients with sarcoidosis, and six with idiopathic pulmonary fibrosis. Total, differential cell counts and ACE determinations were performed on bronchoalveolar lavage fluid in the ARDS group. ACE was detectable in the BAL of all but one ARDS patient. It was concluded that BAL ACE is elevated in some ARDS patients, especially those with infectious causes of lung injury. Increased ACE may reflect endothelial damage or local increase in ACE production in response to sepsis.
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PMID:Angiotensin converting enzyme in bronchoalveolar lavage in ARDS. 302 28

BAL in patients with ARDS provides material containing the soluble and cellular constituents of the alveolar compartment, and hence is a useful tool for the study of the pathogenesis of ARDS. The technique is imperfect as it is prone to problems of data acquisition and interpretation. However, it is lung-specific and may be used in serial studies of patients over the course of their disease. A large amount of evidence is rapidly being accumulated which documents the presence of effectors of inflammation in the BAL fluids of patients with ARDS. Confirmation of the importance of such mediators, pathways, or cellular constituents of BAL fluid in establishing the pathogenesis of ARDS ultimately depends upon proof of the efficacy of specific clinical interventions which both arrest the activity of the effector and predictably alter the course of the disease.
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PMID:Bronchoalveolar lavage in patients with the adult respiratory distress syndrome. 390 47

Conventional treatment of the adult respiratory distress syndrome (ARDS) includes pressure-limited ventilation, permissive hypercapnia, posture changes, aggressive dehydration, selective lung ventilation, and extracorporeal gas exchange. New strategies such as nitric oxide inhalation, the implantation of an intravenous membrane oxygenator (IVOX), and surfactant replacement are currently under evaluation. Nitric oxide (NO) is an important endothelium-derived relaxing factor that is rapidly inactivated by binding to haemoglobin. Inhaling this substance has been shown to induce selective vasodilatation of ventilated lung regions. Thus, inhaled NO reduces pulmonary hypertension, increases right heart ejection fraction, and improves arterial oxygenation by redistributing blood flow away from areas with intrapulmonary shunts to areas with a normal ventilation/perfusion ratio. Dose-response analysis has revealed that effective doses for improvement of oxygenation are lower than for reduction of mean pulmonary artery pressure. The use of a miniaturised membrane lung, IVOX, for intracaval oxygen and carbon dioxide exchange is a new approach to augment gas exchange. The IVOX is inserted via an introducer into the femoral vein and is designed for placement in the full length of the vena cava. Initial experiences with this device show that the currently used prototype provides a maximum of one-third of basal gas exchange. Therefore, a more efficient device will be needed to significantly reduce high inspired oxygen concentrations and airway pressures. Moreover, there exists evidence that IVOX causes caval obstruction. Lung surfactant recovered in BAL from patients with ARDS demonstrates that fractional contents of phosphatidylcholine and phosphatidylglycerol are reduced, and that the total concentration of apoproteins is decreased. Furthermore, the surfactant surface tension-lowering activity is abnormal. Thus, administration of exogenous surfactant may have therapeutic benefits. However, the optimal surfactant preparation, the optimal amount required to restore lung surfactant activity, and the optimal method to deliver it to patients with ARDS are unknown and currently under evaluation.
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PMID:[Therapy of ARDS. 2. New management methods--first clinical experiences]. 804 71

In the last years pentoxifylline (PTXF) has been successfully used in reducing acute injury of the lung parenchyma in ARDS. The authors have studied the effect of PTXF on degree of papain induced lung injury. Papain was administered intratracheally in a dose of 2 mg, 4 mg, 6 mg in 1 ml of PBS. The effect of papain on bronchoalveolar lavage characteristics was also evaluated. Wistar rats of both sexes were used in the experiment. The degree of lung destruction, reflected by interstitial hemorrhage was assessed by measuring hemoglobin content in the fluid of the lavaged lungs. The hemoglobin levels were assessed spectrofluorometrically with the use of the 414 nm wave length. A reduction of hemoglobin content was seen after PTXF administration only in animals receiving the lowest dosage of papain. However in all animals a decrease in the BAL neutrophil count was demonstrated. The protective effect of PTXF on pulmonary tissue in papain induced injury models and situations leading to development of ARDS may suggest a similar pathomechanism in both entities.
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PMID:[The effect of pentoxifylline on the degree of lung parenchyma injury after papain]. 814 56

ARDS includes a complex series of events leading to alveolar damage, high permeability pulmonary edema, and respiratory failure. The endogenous pulmonary surfactant system is crucial to maintaining normal lung function, and only recently has it been appreciated that alterations in the surfactant system significantly contributed to the pathophysiology of the lung injury of patients with ARDS. Through a combination of analyzing BAL samples from patients with ARDS and extensive animal studies, there have been significant insights into the variety of surfactant abnormalities that can occur in injured lungs. These include altered surfactant composition and pool sizes, abnormal surfactant metabolism, and inactivation of alveolar surfactant by serum proteins present within the airspace. Positive effects of exogenous surfactant administration on acute lung injury have been reported. There is now a prospective, randomized clinical trial evaluating the efficacy of aerosolized exogenous surfactant in patients with ARDS. This trial has demonstrated improvements in gas exchange and a trend toward decreased mortality in response to the surfactant. Despite these encouraging results, there are multiple factors requiring further investigation in the development of optimal surfactant treatment strategies for patients with ARDS. Such factors include the development of optimal surfactant delivery techniques, determining the ideal time for surfactant administration during the course of injury, and the development of optimal exogenous surfactant preparations that will be used to treat these patients. With further clinical trials and continued research efforts, exogenous surfactant administration should play a useful role in the future therapeutic approach to patients with ARDS.
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PMID:Surfactant and the adult respiratory distress syndrome. 842 Apr 22


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