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Biomedical subjects

U Obertacke

Publications and source records attributed to U Obertacke.

At least 73 records · Page 4Linked to original sources

Alterations of the immune system following splenectomy in childhood.

After splenectomy due to blunt abdominal trauma, splenectomized children showed a restricted pattern of T-cell immunodeficiency compared to age and sex-matched normal children. Peripheral blood total (CD3) T-cell counts of 11 splenectomized children of 43%, double positive helper (CD4) inducer subpopulation (CD29) cell counts of nine splenectomized children of 7%, and phytohemagglutinin (PHA)-induced T-cell proliferation of 11 splenectomized children of 53,206 c.p.m. were significantly (p less than 0.05) lower than values of normal children (61% CD3 cells, n = 12; 13% CD4CD29 cells, n = 11; 107,832 c.p.m. PHA-induced proliferation, n = 12). The deficit of CD4CD29 cell numbers may be due to impaired maturation of these particular CD4 lymphocytes and may explain diminished PHA-induced proliferation in small children. The significantly higher B-lymphocyte counts of splenectomized children (21%, n = 11; 558 cells/mm3, n = 10) compared with 12 normal children (14%; 329 cells/mm3) may be due to loss of the reservoir function of the spleen.

Adolescent↗

Serum CD14 levels in polytraumatized and severely burned patients.

Recently it has been demonstrated that the CD14 molecule which is expressed on monocytes and macrophages serves as a receptor for lipopolysaccharide (LPS) bound to LPS-binding protein (LBP) and thus mediates LPS-induced tumour necrosis factor (TNF) production. Here we report that CD14 is found as a soluble (s) molecule in serum. In healthy volunteers sCD14 levels (mean +/- s.e.m.) were 3.7 +/- 0.05 micrograms/ml (n = 30, 25-50 years of age) as determined by ELISA (detection limit 20 ng/ml serum) using two monoclonal antibodies in a sandwich technique. In polytraumatized patients (n = 16) significantly decreased levels (1.7 +/- 0.3) were detected immediately after the trauma, which increased to 4.9 +/- 0.3 micrograms/ml within the first 6 days post trauma. sCD14 remained elevated during the first 14 days post trauma in patients with the most severe injuries (injury severity score greater than 45 points), whereas a return to normal levels was observed in patients with an injury score of less than 45 points. In addition, the levels of the high-density lipoproteins that partially inactivate free endotoxin are significantly decreased post trauma. No correlation between parameters of inflammation (C3a and neopterin levels, leucocyte counts, amount of band cells), liver function and sCD14 levels was established. Comparable to polytraumatized patients, increased sCD14 serum levels were observed in five patients with burn trauma (burned area greater than 35%) within the second week post trauma when clinical signs of septicaemia were evident.

Adolescent↗

[Post-traumatic alveolar changes in lung contusion].

Bronchoalveolar lavage (BAL) specimens taken from nine patients with lung contusion following multiple trauma were compared with specimens from different control groups. Early interstitial and intra-alveolar reactions are PMN degranulation, mediator release and high protein leakage. The alveolar reactions are similar in extent to the reaction found in post-traumatic ARDS.

Acute-Phase Proteins↗

[Alveolo-capillary permeability following multiple trauma--monitoring by bronchoalveolar lavage].

In trauma patients (ISS greater than 40 points) bronchoalveolar lavage (BAL) as well as the first clinical measurements was performed within the first 6 hours after admission to hospital. Thereafter BAL was carried out once per day, using 100 ml NaCl 0.9% (10 x 10 ml). BAL-protein-concentrations (i.e. albumin) were converted to epithelial lining fluid (ELF) according to Rennard, using urea as an internal standard. The limitations of this method were taken into account. The alveolo-capillary permeability (ACP) was described by the quotient of the protein concentrations in ELF and plasma. Progressive lung failure (ARDS) was defined using the criteria given by Murray. Lung contusion was an exclusion criteria. The study period was 14 days. This study evaluated data from 12 patients (m: 10, f: 2; age 30.4 (17-52); ISS 63.4). Five patients developed a progressive lung failure ("+ARDS"--age 32.2; ISS 71.5), 7 patient suffered no pulmonary failure during intensive care ("-ARDS")--age 29.5; ISS 59.2). No patient died in the course of the study. An increased ACP for albumin (combined endothelial-epithelial disturbance) was detectable for both +ARDS- und -ARDS-patients after the 6th hour, reaching a maximum around the 24th hour. +ARDS-patients showed a significant higher ACP. Further, beginning from the 48th hour to the 4th day, the ACP value for -ARDS-patients again dropped to a physiologic range. The degree of the increased ACP depends on the size of the marker protein, but it is independent of pulmonary hemodynamics. It is of value for the prediction of ARDS within 24 hours and for monitoring of pulmonary damage in posttraumatic course.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Surfactant abnormalities and adult respiratory failure.

Surfactant abnormalities have been implicated in the development of the acute respiratory distress syndrome in adults. Experimental studies show that surfactant inhibition by protein-leak into the alveolar space is of major importance under these circumstances. Fibrin(ogen)-surfactant-interaction appears to contribute to disturbances of surfactant function with subsequent alveolar instability and ventilation-perfusion-mismatch. In a prospective study in severely injured patients, the surfactant in serially obtained bronchoalveolar lavage fluids was investigated. An early leakage of plasma proteins into the alveolar space was noted in those patients, who developed severe ARDS. Moreover, deterioration of surfactant function was markedly more pronounced in those patients than in trauma victims who developed only mild pulmonary dysfunction. In addition to the protein-leakage, a progressive decrease of the surfactant-specific dipalmitoyl-phosphatidylcholine was noted, significantly correlated with the deterioration of surfactant function and the severity of respiratory failure. In conclusion, experimental and clinical studies show surfactant abnormalities in the adult respiratory distress syndrome. Plasma protein-leakage and progressive alteration of alveolar type II surfactant secretion appear to be of major importance.

Adult↗

Altered pulmonary surfactant in uncomplicated and septicemia-complicated courses of acute respiratory failure.

Pulmonary surfactant, which is crucial for alveolar stability, may also be involved in endogenous defense mechanisms of the lungs. Thus, alterations in pulmonary surfactant may promote infections, including pneumonia and septicemia. Because patients who have acute respiratory failure often develop pneumonia, thus septicemia, we investigated when surfactant is altered in these patients and whether there is a specific pattern of changes in surfactant phospholipid composition associated with septicemia in these patients. To answer these questions, we determined the phospholipid content and composition in lung washings obtained from alveolar sites (by bronchoalveolar lavage) and from tracheal sites (by aspiration). Both techniques were performed serially over a period of 18 days in 30 patients who had acute respiratory failure resulting from polytrauma, 18 of whom developed septicemia caused by pneumonia. We found that in lung washings obtained from the alveolar sites from all patients, the phosphatidylglycerol content was decreased and the phosphatidylinositol content was increased as early as 6 hr after trauma and normalized during recovery of the patients. In addition, alveolar phosphatidylcholine content was decreased 24 hr after trauma. In patients who developed septicemia during the observation time, but not in patients who had uncomplicated courses of acute respiratory failure, the concentrations of alveolar phosphatidylethanolamine (normally 4.8% of total phospholipids) and alveolar phosphatidylcholine (normally 62.8%) both approached the proportions found in the trachea (phosphatidylethanolamine 33.4%, phosphatidylcholine 35.6%), suggesting that surfactant phospholipid pool size had progressively decreased. Our results indicate that in patients who have acute respiratory failure, pulmonary surfactant is altered very early, and that when septicemia complicates the course of acute respiratory failure, the surfactant phospholipid pool size decreases progressively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Surfactant abnormalities in patients with respiratory failure after multiple trauma.

We present a prospective study, designed to evaluate surfactant abnormalities in severely injured patients during the course of post-traumatic pulmonary dysfunction. Serially obtained bronchoalveolar lavage fluids from noncontused lung areas (in total, 132 samples from 17 patients) were analyzed for alveolar phospholipid composition and surfactant function in vitro during the first 14 days after trauma. The data were compared with those of 29 lavage samples obtained from 10 healthy control subjects and correlated to severity of respiratory failure. In the traumatized patients, the total lavage phospholipid content was unchanged, but there was a progressive decrease in the relative amounts of phosphatidylcholine (%PC) and phosphatidylglycerol and an increase in phosphatidylinositol, phosphatidylethanolamine, and sphingomyelin. These alterations were paralleled by a marked decrease in the hysteresis area of the surface tension isotherm. The decrease in %PC and reduction of hysteresis area were significantly correlated. The alterations in alveolar phospholipid composition and in vitro surfactant function were more pronounced in patients with severe respiratory failure. There was a significant inverse correlation between severity of respiratory dysfunction and %PC or hysteresis area for all traumatized patients. Protein leakage into the alveolar space was significantly higher in patients with severe respiratory failure and appeared to precede surfactant abnormalities in such patients. The neutrophil content in the alveolar space was markedly increased in all patients with multiple injuries however, no significant correlation with the noted alterations in alveolar phospholipid composition or surfactant function was found. We concluded that surfactant abnormalities occur during the course of post-traumatic pulmonary dysfunction and are correlated with the severity of respiratory failure.

Adolescent↗

Distribution and function of alveolar cells in multiply injured patients with trauma-induced ARDS.

To determine whether alveolar cells are involved in the pathogenesis of adult respiratory distress syndrome (ARDS), we assessed the distribution and function of alveolar cells from 30 polytraumatized patients with trauma-induced respiratory failure, 5 of whom also had lung contusion. Cells were obtained by bronchoalveolar lavage performed daily beginning on the day of trauma and continuing for 14 days. Neutrophils constituted about 60% of lavage cells in ARDS patients with lung contusion 0-2 days after polytrauma and about 50% in ARDS patients without lung contusion. In ARDS patients with lung contusion the neutrophil fraction decreased to 52% 3-6 days after trauma and to 40% 7-14 days after trauma. In patients without lung contusion the neutrophil fraction increased to 77% and then decreased to 60% at these times. Total cell counts in ARDS patients with lung contusion were more than twice as high as in patients without lung contusion 0-2 days after trauma. The difference in total cell counts decreased during days 3-6 and disappeared by day 7. In all patients morphologically altered alveolar cells were observed 4 days and more after trauma. In non-survivors significantly more altered cells were found. The chemiluminescence-response pattern of the alveolar cells was enhanced throughout the study and correlated with the neutrophil fraction (r = 0.6). The neutrophil fraction also correlated with the pulmonary vascular resistance during the first two days after trauma (r = 0.53). We conclude that alveolar cells are involved in the pathogenesis of trauma-induced ARDS and that the alveolar cell distribution is different in patients with and without lung contusion during the development of posttraumatic respiratory failure.

Acute Disease↗

Adult respiratory distress syndrome as a specific manifestation of a general permeability defect in trauma patients.

To establish whether a general dysfunction, i.e., an increase in permeability, had occurred in 16 trauma patients (6 with adult respiratory distress syndrome [ARDS]), we measured beta 2-microglobulin (beta 2MG), myoglobin (MG), immunoglobulin G (IgG), and transferrin (TF) concentrations in bronchoalveolar lavage fluid (BAL), serum, and urine as well as extravascular lung water content (EVLW) over a period of 14 days. Our results show a positive correlation (p = 0.03) between increases of EVLW, reflecting lung edema, and beta 2MG concentrations in urine of all patients with ARDS, indicating systemically increased permeability. Generalized increase of permeability can also explain the elevation of MG urine concentrations (p = 0.03) together with an EVLW increase, and an increase of BAL protein concentrations (IgG, TF, p less than 0.01) in the early post-trauma phase during the first 48 h after admission. In contrast, commonly used kidney function tests remained unchanged over the time course of 14 days.

Adolescent↗

[Septic shock with multiple organ failure in the trauma surgery intensive care unit].

Septicaemia was recorded from 17 in 160 cases of multiple trauma. The classical signs of clinical sepsis were found to be no early markers. However, alveolar, cellular, and humoral alterations were recordable from broncho-alveolar lavage fluid four days prior to clinical manifestation of septicaemia. Early and late phases of septicaemia, too, could be differentiated from each other by alveolar alterations.

Acute-Phase Reaction↗

[Normal values of cell distribution and function in the human alveolus. Bronchoalveolar lavage as a diagnostic tool in intensive care medicine].

The cell distribution and cell function in the normal human alveolar were determined in 23 healthy subjects by obtaining the pulmonary lavage fluid from bronchoalveolar lavage. A uniform alveolar cell spectrum was found. (Alveolar macrophages 95-98%, polymorphonuclear neutrophils 2-3%, lymphocytes 0-2%.) The cell systems reacted reproducibly to a defined phagocytosis stimulation in luminol-enhanced chemoluminescence. The phospholipid lung profile, which is important for the function of the surfactant, was determined by means of high-pressure liquid chromatography. The typical inflammation mediators were not present in the humoral spectrum of the supernatant part of the lavage fluid. Albumin, transferrin, and alpha-1-antitrypsin were regularly seen in healthy adults in the bronchoalveolar lavage fluid. The results supply the basis for the interpretation of the findings in polytraumatised patients in adult respiratory distress syndrome.

Acute-Phase Proteins↗