Biomedical subjects

C Gippner-Steppert

Publications and source records attributed to C Gippner-Steppert.

21 records · Page 2Linked to original sources

PubMed1997

Delayed treatment with desulfato-hirudin prevents fibrin formation in lipopolysaccharide-induced shock.

Previous work has shown that pre-treatment with the thrombin inhibitor recombinant desulfato-hirudin prevented fibrin formation and respiratory dysfunction in porcine lipopolysaccharide shock. We examined the effects of delayed administration of recombinant desulfato-hirudin in bacterial lipopolysaccharide shock. Miniature pigs were studied under anaesthesia and ventilation, and received a bacterial lipopolysaccharide infusion (2 microg/kg/h) for 7 h; recombinant desulfato-hirudin was started 1 h after bacterial lipopolysaccharide in 10 animals (bolus 12.9 nmol/kg; continuous infusion 6.5 nmol/ kg/h); 10 randomised control animals received saline instead of recombinant desulfato-hirudin. Fibrin and thrombin-antithrombin complex levels in plasma were significantly lower in bacterial lipopolysaccharide+recombinant desulfato-hirudin animals than in controls. Both groups displayed a similar rise in pulmonary vascular resistance and other parameters of lung dysfunction; only lung tissue wet/dry ratio was lower in recombinant desulfato-hirudin-treated than in control animals. Both groups had similar circulatory alterations. Recombinant desulfato-hirudin interrupted coagulation activation during ongoing bacterial lipopolysaccharide-induced shock in pigs even when administered with a delay of one hour after start of the bacterial lipopolysaccharide infusion. A protective effect of delayed recombinant desulfato-hirudin administration on bacterial lipopolysaccharide-induced acute lung injury and alterations in the systemic circulation could not be demonstrated in this experiment.

Animals↗

PubMed1997

Indicators of the posttraumatic inflammatory response correlate with organ failure in patients with multiple injuries.

BACKGROUND: Most prognostic indices for severely injured patients are based on anatomical findings and the vital signs. The posttraumatic organ failure, however, is thought to be triggered by the initial inflammatory response. The objective of this study was to evaluate the correlation between the early activation of inflammation and the rate of organ failure and death. METHODS: Sixty-six patients with multiple injuries (Injury Severity Score > 18, age 18-70 years, admission within 6 hours after accident, survival > 48 hours) were included in this prospective study. During a 14-day observation period, serial blood samples were collected starting within 30 minutes after admission. Plasma levels of neutrophil elastase, lactate, antithrombin III, and interleukin-6 and -8 were determined. The clinical course and the degree of organ failure were recorded daily until death or transfer to a general ward. RESULTS: The 66 severely injured patients had a mean Injury Severity Score of 40 points. Eleven patients died from multiple organ failure (group 1), 38 subjects survived a single or multiple organ failure (group 2), and 17 patients had an uneventful recovery (group 3). The initial plasma concentrations for neutrophil elastase (650 vs. 355 ng/mL), lactate (5.0 vs. 3.1 mmol/L), antithrombin III (48 vs. 62% from normal), interleukin-6 (703 vs. 177 pg/mL), and interleukin-8 (1,101 vs. 301 pg/mL) were significantly different between groups 2 and 3 already in the initial posttraumatic period. Patients from group 1 presented with significantly higher levels of these parameters as early as 24 hours after trauma compared with group 2. Different patterns were identified with respect to early versus late posttraumatic organ failure. CONCLUSIONS: These data show that the degree of the initial inflammatory response corresponds with the development of posttraumatic organ failure. Besides anatomically and physiologically based trauma scores, these parameters might be used as indicators for the injury severity.

Adolescent↗

PubMed1994

The role of phagocyte proteinases and proteinase inhibitors in multiple organ failure.

Although numerous other inflammatory mediators are important, the following review of our research and that of other authors reveals a prominent role for the phagocyte proteinases, polymorphonuclear (PMN) elastase and cathepsin B, in the development of multiple organ failure. The release of these enzymes in relation to the severity of trauma- and/or infection-induced inflammation was clearly verified in a variety of clinical studies. The amounts of the extracellularly discharged phagocyte proteinases were highly predictive of forthcoming organ failure and ultimate patient outcome. Moreover, the consumption of important proteinase inhibitors (e.g., alpha 1-proteinase inhibitor, antithrombin III) and other plasma proteins (e.g., fibrinogen), which are highly susceptible to proteolytic degradation, coincided with the occurrence of proteolytic activity, especially that of PMN elastase. Therefore, the therapeutic use of specific PMN elastase and/or thrombin inhibitors should prevent multiple organ failure or at least reduce severe signs of inflammation.

Animals↗