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The Rehabilitation Research Network of Ulm on "Bausteine der Reha" consists of several departments of the University of Ulm, and various rehabilitation hospitals and cooperates with a pension insurance institute (LVA Wuerttemberg). The aim of this interdisciplinary approach is to evaluate process and outcome of rehabilitation measures considering specific clinical and rehabilitative questions with main emphasis on epidemiological and economic aspects. The Rehabilitation Research Nétwork of Ulm is subdivided into clinical projects and cross-sectional subjects. The clinical studies deal with cardiovascular and neurological rehabilitation and rehabilitation in disorders of the musculoskeletal system. The cross-sectional topics contain special fields such as biometry, health economics, epidemiology and occupational rehabilitation. All participating institutions have access to a central database with uniform structure of the data.

Since nitric oxide (NO) contributes to both circulatory disorders and host defense, we analyzed the NO production in (poly)trauma patients (pts) in a prospective (pre)clinical study starting as early as at the scene of accident. Upon approval of the local IRB/EC, 85 multiple injured pts were enrolled. Subsets were performed according to trauma severity (ISS) and injury pattern, and between survivors versus nonsurvivors. The first blood sample was collected at the scene of accident, then in hourly to daily intervals. NO production was assessed by measuring nitrate+nitrite plasma levels. To estimate dilution effects, all values were calculated according to the actual plasma protein content. The extent of trauma was appraised by C-reactive protein (CRP) levels. Immediately after trauma, NO2-+NO3- plasma levels were always elevated. This was most pronounced in thoracic injury, irrespective of whether it was combined with multiple trauma. Nitrate+nitrite levels returned to normal within 24 h. CRP generation increased during 12 h following trauma and was most marked in severest trauma (ISS >50). For the first time, we show very early data following major trauma that demonstrate that NO overproduction starts immediately after trauma. However, systemic NO2-+NO3- levels actually reflect the severity of injury only during the first 2 h. Thereafter, NO generation is rather related to the individual trauma pattern, e.g., chest trauma. Nonetheless, the role of NO after severe trauma and especially in thoracic injury remains unclear and should further be elucidated in a specific study.

Background: The molecule CD14 acts as a receptor for the protein-bound endotoxin (lipopolysaccharide [LPS]) complex and mediates the cellular effects of LPS. The soluble formation, sCD14, is supposed to neutralize circulating LPS (i.e., LPS antagonist) or transfer LPS effects to endothelial cells (i.e., LPS agonist)., Objective: To elucidate the release of sCD14 per se in patients with major trauma in the early posttrauma period. Our a priori hypothesis was that sCD14 release depends on the plasma LPS concentration simultaneously measured., Patients: In a prospective study, 65 patients with multiple injuries (Injury Severity Score, 9-75) were enrolled. The patients were rescued by the medical helicopter service and directly admitted to our clinics. The plasma concentrations of sCD14 (enzyme immunoassay) and LPS (chromogenic limulus amebocyte lysate test) were analyzed. The first blood sample was collected immediately at the accident site. The following samples were drawn at intervals from 2 hours to daily for 2 weeks., Results: Sixty-one patients survived the observation time. Immediately after trauma, their mean sCD14 level was not different from that of healthy individuals. Two hours later, a pronounced increase of sCD14 was observed and sustained throughout the observation period. Even nonsurvivors showed an increased sCD14 release, but less pronounced. In all patients, plasma LPS levels were elevated during the first 12 hours., Conclusions: Major trauma caused an increased release of sCD14. This elevation, however, was not correlated to LPS levels or to the severity of trauma (estimated by trauma scores). We found no evidence that sCD14 levels are of prognostic value regarding survival. Furthermore, the release of sCD14 did not occur in an LPS-neutralizing manner, but rendered possible an LPS-independent mechanism.

Membrane-fixed CD14 acts as a receptor for the protein-bound endotoxin (LPS) complex and mediates the cellular effects of endotoxin. Soluble CD14 (sCD14) is suggested to neutralize circulating LPS, i.e., acting as an endotoxin antagonist. The aim of this study was to elucidate the release of both sCD14 and endotoxin in traumatized patients, starting from the earliest phase after trauma. A total of 15 patients (O ISS = 19, 9-75) suffering major trauma were enrolled in this prospective study. Blood samples were collected as early as immediately at the site of accident, on hospital admission, and thereafter hourly, then daily. For patients (O ISS = 47) died within 24 h because of their severe injuries. Immediately after the accident as well as during the first 2 h after hospital admission, the mean sCD14 levels of surviving patients did not differ from those of healthy volunteers (n = 53). Thereafter, however, sCD14 increased continuously in the trauma group. The concentrations remained elevated throughout the entire observation period. There was, however, no relation between the sCD14 release and the pattern or the severity of injury. In contrast, endotoxin levels revealed a pattern-specific release. The highest plasma concentrations of LPS were observed in patients suffering from (additional) thoracic injury. On the basis of these results we conclude that the release of sCD14 after trauma does not reflect a strict principle such as action/reaction caused by the appearance of endotoxin immediately after the injury. Soluble CD14 is more likely release by an endotoxin-independent mechanism.

Prostanoids are inflammatory mediators which originate from endothelial cells following local tissue damage. That is why plasma levels of prostanoids are possible markers of inflammatory response and severity of trauma. We were able to demonstrate that the systemic release of prostanoids does not depend on the score values (ISS, PTS) but rather on different trauma patterns (chest trauma, head injury). Influencing vascular permeability and resistance elevated plasma levels of prostanoids may explain the impairment of pulmonary function in traumatized patients. It seems to be useful to re-evaluate the scoring systems with respect to chest trauma and head injury.