Metabolism of 3H-digoxin and some acetyl-digoxins: time-dependent formation of hydrophilic metabolites after oral application in man.
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Administration, Oral↗
Biomedical subjects
A Dwenger
Publications and source records attributed to A Dwenger.
Investigation of neutrophil--endothelial cell interaction in multiple trauma by chemiluminescence.
The trauma-induced activation of neutrophils and their functional alterations, i.e., increase in adherence and release of oxygen derived metabolites, is considered to play a central role in the initiation and amplification of capillary endothelial cell damage and following organ failure. In the present study neutrophil-endothelial cell interaction was studied using an in vitro model of human umbilical cord vein endothelial cells and human neutrophils. Production of oxygen-derived metabolites was determined by comparing mean peak chemiluminescence of neutrophils from multiply traumatized patients (n = 40) and mean peak chemiluminescence of neutrophils from blood donors (n = 160). Adherence and endothelial injury by neutrophils of multiply traumatized patients were compared with data of healthy blood donors. Chemiluminescence response of 70,000 neutrophils isolated from healthy control individuals was 699 +/- 98 x 10(3) cpm and could be increased significantly by endothelial cells to 1410 +/- 135 x 10(3) cpm (p < 0.05). Chemiluminescence response to neutrophils of polytraumatized patients was 1174 +/- 94 x 10(3) cpm and could not be significantly increased by endothelial cells (1419 +/- 120 x 10(3) cpm). Adherence of neutrophils of blood donors to endothelial cells was 12.31 +/- 0.77%. Adherence of neutrophils of polytraumatized patients was significantly increased to values of 24.83 +/- 2.03%. Injury of endothelial cells was not detectable with neutrophils from blood donors (1.11 +/- 1.09% 111in-release). Significantly increased 111in-release was apparent upon incubation with neutrophils of polytraumatized patients (5.76 +/- 1.28%). The data shows evidence of in vivo preactivation of neutrophils of polytraumatized patients, and supports the hypothesis that endothelial cells play an active role in neutrophil-endothelial cell interactions by modulating production of oxygen-derived metabolites.
Abdominal Injuries↗
Lipopolysaccharide-dependent enhancement of adherence-mediated chemiluminescence response of polymorphonuclear leukocytes.
Adherence of resting polymorphonuclear leukocytes to nylon fibre increased the chemiluminescence response (CL) from 99,400 to 910,300 cpm/25,000 PMNL. This effect could be amplified by lipopolysaccharide (LPS) priming of granulocytes in a dose-dependent fashion. The results of nylon fibre adherence experiments suggest an in vitro model that might approximate certain conditions of in vivo PMNL-endothelial adherence and respiratory burst activation, and these reactions of polymorphonuclear leukocytes may contribute to the pathomechanisms of the Adult Respiratory Distress Syndrome.
Cell Adhesion↗
Simultaneous measurement of endothelial cell damage, elastase release and chemiluminescence response during interaction between polymorphonuclear leukocytes and endothelial cells.
Using cultured human umbilical cord vein endothelial cells and human blood neutrophils, the interaction between neutrophils and endothelial cells, in vitro, was studied. The aim of the study was to examine whether a respiratory burst stimulation by neutrophils would be observed by neutrophil/endothelial cell interaction and whether the respiratory burst stimulation of neutrophils by endothelial cells could be enhanced by lipopolysaccharide stimulation of neutrophils. The second aim was whether such an effect, or secretion of elastase, could cause an endothelial cell damage in vitro. Chemiluminescence as an indicator of oxygen-derived metabolites produced by neutrophils, elastase release by neutrophils, and endothelial cell damage, based on 111 In-oxine release from labelled endothelial cells, were measured simultaneously. The present investigation demonstrates that neutrophils can be directly stimulated by endothelial cells. A further amplification of this process following lipopolysaccharide priming up to 10 ng/ml blood could be demonstrated. A slight endothelial cell damage occurs following neutrophil stimulation, although elastase secretion does not increase during interaction between neutrophils and endothelial cells. These results raise the possibility that oxygen-derived metabolites rather than elastase contribute to an endothelial cell damage which might occur in conditions such as endotoxin-induced adult respiratory distress syndrome.
Cell Communication↗
In vitro effect of ascorbic acid on neutrophil-endothelial cell interaction.
The effect of different concentrations (0.06, 0.6 and 6.0 mmol/L) of ascorbic acid on neutrophil-endothelial interaction was studied using an in vitro model of human umbilical cord vein endothelial cells and human neutrophils. The aim of the study was to determine changes in chemiluminescence response of neutrophils during adherence to endothelial cells. Because adherence of neutrophils to endothelial cells is an essential component in inflammatory processes leading to endothelial cell injury, the influence of ascorbic acid on adherence and endothelial cell injury have been investigated. Production of oxygen-derived metabolites, measured by chemiluminescence response of neutrophils, decreased significantly in the presence of 6 mmol/L ascorbic acid during coincubation of neutrophils and endothelial cells (p < 0.025). The adherence of neutrophils to endothelial cells was significantly decreased at a concentration of 6 mmol/L (p < 0.0005). The inhibition of neutrophil adherence to endothelial cells was correlated with a diminished neutrophil-mediated endothelial cell injury during incubation with 6 mmol/L ascorbic acid (p < 0.0005). The present results indicate that ascorbic acid might exert a protective effect on neutrophil-mediated endothelial cell injury by decreasing adherence of neutrophils to endothelial cells and by scavenging reactive oxygen metabolites. Moreover, the current investigation points to probable protective effect of ascorbic acid on oxidant-mediated cell damage in diseases (e.g., Adult Respiratory Distress Syndrome).
Ascorbic Acid↗
Effect of prostaglandin E1 on chemiluminescence response and adherence of human polymorphonuclear leukocytes to human cultured endothelial cells of prostaglandin E1 treated polytraumatized patients.
We investigated the effect of prostaglandin E1 on human polymorphonuclear leukocytes, in vivo. Polymorphonuclear leukocytes of a prostaglandin E1 and placebo study group were harvested and their function, as production of oxygen-derived metabolites and adherence to human cultured endothelial cells, was compared. Additionally, data obtained from polymorphonuclear leukocytes of a prostaglandin E1 and placebo group were compared with data obtained from polymorphonuclear leukocytes from 28 blood donors, who served as a control group. Production of oxygen-derived metabolites by polymorphonuclear leukocytes during contact with endothelial cells was measured by chemiluminescence. Chemiluminescence was significantly (p < 0.01) increased in the placebo group in comparison to the control group decreasing to values of control group after 6 d (post-trauma). Chemiluminescence response was not significantly suppressed in patients treated with prostaglandin E1 in comparison to the placebo group. Adherence of polymorphonuclear leukocytes (placebo group) to endothelial cells was significantly increased (p < 0.01) within the first 6d post-trauma. Following day 6, values were in the same range as values for the control group. Adherence was not significantly suppressed in patients treated with prostaglandin E1 in comparison to the placebo group. In conclusion, prostaglandin E1 at a dose of 20 ng/kg bw/min does not influence production of oxygen-derived metabolites and adherence in polytraumatized patients in comparison to a placebo group. Additionally, production of oxygen-derived metabolites by polymorphonuclear leukocytes in response to endothelial cells is shown and it is evident that endothelial cells might influence production of oxygen derived metabolites by polymorphonuclear leukocytes.
Alprostadil↗
Chemiluminescence response and adherence of neutrophils to cultured endothelial cells--influence of immunoglobulin G.
The effect of different concentrations (0.8, 4.35, 8.7, 17.5, 25 and 35 mg/mL) of intravenous immunoglobulin G (Endobulin) on neutrophil-endothelial cell interaction was studied using an in vitro model of human umbilical cord vein endothelial cells and human neutrophils. Because adherence of neutrophils to endothelial cells is an essential component in inflammatory processes leading to endothelial cell injury the influence of immunoglobulin G on adherence has been investigated. A second aim of the present study was to determine changes in chemiluminescence response of neutrophils during adherence to endothelial cells. Production of oxygen-derived metabolites, measured by chemiluminescence response of neutrophils, decreased significantly in the presence of 8.7 mg immunoglobulin/mL test during coincubation of neutrophils and endothelial cells (p < 0.025). The adherence of neutrophils to endothelial cells was significantly decreased at a concentration of 8.7 mg immunoglobulin/mL test (p < 0.025). The present results indicate that this preparation of immunoglobulin G might exert a protective effect on neutrophil-endothelial cell interaction by decreasing adherence of neutrophils to endothelial cells and by scavenging reactive oxygen metabolites. metabolites. Therefore, the current investigation points to a probable protective effect of immunoglobulin G in oxidative diseases, such as the adult respiratory distress syndrome.
Cell Adhesion↗
Early biochemical indicators of the obliterative bronchiolitis syndrome in lung transplantation.
The diagnosis of the obliterative bronchiolitis syndrome in lung transplantation is presently best established by evaluation of postoperative lung function tests. Unfortunately the decline in lung function occurs only when obliteration has progressed significantly and is therefore not an early predictive indicator. To distinguish patients at increased risk for the development of obliterative bronchiolitis, we regularly assessed the chemiluminescence response of polymorphonuclear leukocytes, opsonic capacity, and plasma elastase/beta-N-acetylglucosaminidase in 52 outpatients (25 women and 27 men; mean age 45 +/- 12 years) who underwent transplantation between January 1991 and January 1992. Recent onset bronchiolitis within the described observation period occurred in 16 patients (group obliterative bronchiolitis). A matched cohort of 16 patients was formed according to type of procedure, age and follow-up (control) from the remaining 36 patients. Data obtained from a period 6 months before clinical onset of the syndrome showed a significant drop of the opsonic capacity (group obliterative bronchiolitis = 87% +/- 7%; control = 100% +/- 9%; p < 0.023) and rise of the N-acetyl-D-glucosaminidase (group obliterative bronchiolitis = 7.5 +/- 2 U/L; control = 5.8 +/- 1.8 U/L; p < 0.04). No correlation was found between the number of infectious events or rejection episodes and the incidence of obliterative bronchiolitis. According to these results, it can be concluded that a decrease in the plasma opsonic capacity and a rise in beta-N-acetylglucosaminidase may be early markers before clinical onset of obliterative bronchiolitis. The nonspecific immune system may therefore play an important role in the development of obliterative bronchiolitis.
Acetylglucosaminidase↗