Fibroblasts in healthy adult lung are quiescent, synthesizing little collagen. We studied lung biopsies from 30 patients with pulmonary fibrosis, using immunohistochemistry with monoclonal antibodies against the propeptides of type I collagen to localize fibroblasts actively synthesizing collagen. Adjacent sections were stained with antibodies to type III and IV collagen, fibrin, cytokeratin, plasma fibronectin, or EDIIIa-containing "cellular" fibronectin (cFN). In rapid pulmonary fibrosis, including the proliferative phase of diffuse alveolar damage, organizing pneumonia, and subacute idiopathic fibrosis, collagen-synthesizing cells were numerous in organizing exudate filling airspaces but were also seen in the interstitium of the alveolar walls, interlobular septa, and walls of blood vessels. The new matrix deposited in the airspaces also contained type III collagen and EDIIIa-containing fibronectin. In chronic pulmonary fibrosis, more than half of the biopsies showed foci of collagen synthesis and cFN deposition near the air-tissue interface. The foci were consistently localized outside remnants of basal lamina and therefore within airspaces. The results indicate that (1) fibrosis in chronic idiopathic pulmonary fibrosis results mainly from organization of exudate within airspaces, just as it does after acute lung injury, and (2) during this process, fibroblasts increase their synthesis of collagen and fibronectin coordinately. Foci of active matrix deposition provide evidence for the progressive nature of chronic pulmonary fibrosis.

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Propofol-MCT/LCT showed a significant advantage compared to propofol-LCT considering the severity of injection pain, but not in reducing the incidence of pain. The use of lidocaine resulted in a significant reduction of incidence and severity of injection pain for both propofol solvents.

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In patients with cystic fibrosis undergoing minor ear, nose and throat surgery who do not show significant reduction in pulmonary function anesthesia can be safely carried out.

Eine Ausdehnung des Rettungswesens einschließlich einer nahezu flächendeckenden Luftrettung, eine Optimierung der Rettungskette bis zur klinischen Versorgung sowie eine Verbesserung der sich anschließenden operativen und intensivmedizinischen Therapie haben die Letalität Poytraumatisierter deutlich gesenkt. Trotzdem bleibt das Trauma die Hauptursache der Morbidität und Mortalität der unter 45−Jährigen. Die Ur− sachen eines letalen Verlaufs nach Polytrauma sind vielfältig und umfassen vor allem die gleichzeitige Hirnverletzung und die blutungsbedingte Hypovolämie (Abb. 1). Langfristig spielen Organversagen (z. B. Lunge) bzw. die Entwicklung eines Multi−Or− gan−Versagens (MOV) eine entscheidende Rolle für das outcome des Polytaumatisier− ten (Abb. 2).