Abstract
A series of humoral alterations are a characteristic finding in sepsis, polytrauma, and other affections, which are often followed by an acute lung failure (ARDS, adult respiratory distress syndrome) or multiple organ failure (MOF). Based on experimental and clinical findings, the cooperation of a variety of mediators and mediator systems are responsible for causing the disturbance of vascular tone and permeability and inducing the morphological transformation which finally may result in the failure of vital organs. Beside the classical mediators, such as catecholamines, histamine, serotonin, and bradykinin, increasing attention has recently focused on metabolites of arachidonic acid, cytokines, and products from circulating or resident inflammatory cells. Of all these humoral and cellular alterations the activation and liberation of proteinases seems to play an essential role with regard to loss of capillary barrier function and interstitial edema formation.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Becker EL, Showeil HJ, Henson PM, Hsu LS (1974) The ability of chemotactic factors to induce lysosomal enzyme release. J Immunol 112:2047–2054
Belew M, Gerdin B, Porath J, Saldeen T (1978) Isolation of vasoactive peptides from human fibrin and fibrinogen degraded by plasmin. Thromb Res 13:983–994
Brigham KL, Meyrick B (1984) Interactions of granulocytes with the lungs. Circ Res 54:623–635
Cochrane CG, Spragg R, Revak SD (1983) Pathogenesis of the adult respiratory distress syndrome — evidence of oxidant activity in bronchoalveolar lavage fluid. J Clin Invest 71: 754–761
Craddock PR, Hammerschmidt D, White JG, Dalmasso AP, Jacob HS (1977) Complement (C5a)-induced granulocyte aggregation in vitro. J Clin Invest 60:260–264
Dittmer H, Jochum M, Fritz H (1986) Freisetzung von granulozytärer Elastase und Plasmaproteinveränderungen nach traumatisch-hämorrhagischem Schock. Unfallchirurg 89:160–169
Fritz H, Jochum M (1984) Granulocyte proteinases as mediators of unspecific proteolysis in inflammation: a review. In: Selected topics in clinical enzymology 2. De Gruyter, Berlin, pp 305–327
Joris I, Manjo G, Ryan GB (1972) Endothelial contraction in vivo: a study of the rat mesentery. Virchows Arch [B] 12:73–83
Manwaring D, Curreri PW (1982) Platelet and neutrophil sequestration after fragment D-induced respiratory distress. Circ Shock 9:75–80
Nathan CF (1987) Secretory products of macrophages. J Clin Invest 79:319–326
Neuhof H, Lasch H-G (1984) Interactions between intravascular coagulation and tissue perfusion. Clin Hemorheol 4:5–13
Neuhof H, Seeger W, Suttorp N (1987) Activation of the pulmonary arachidonic acid system and its consequences for hemodynamics and fluid balance. In: Schlag G, Redl H (eds) First Vienna shock forum: pathophysiological role of mediators and mediator inhibitors in shock. Liss, New York, pp 289–300
Schlag G, Voigt WH, Redl H, Glatzl A (1980) Vergleichende Morphologie des posttraumatischen Lungenversagens. Anasth Intensivther Notfallmed 15:315–339
Seeger W, Menger M, Walmrath D, Becker G, Grimminger F, Neuhof H (1987) Arachidonic acid lipoxygenase pathways and increased vascular permeability in isolated rabbit lungs. Am Rev Respir Dis 136:964–972
Seemüller U, Dodt J, Fink E, Fritz H (1986) Proteinase inhibitors of the leech Hirudo medicinalis (hirudins, bdellins, eglins). In: Barrett, Salvesen (eds) Proteinase inhibitors. Elsevier, Amsterdam pp 337–359
Shasby DM, Vanbenthuysen KM, Tate RM, Shasby SS, McMurtry I, Repine JE (1982) Granulocytes mediate acute edematous lung injury in rabbits and in isolated rabbit lungs perfused with phorbol myristate acetate: role of oxygen radicals. Am Rev Respir Dis 125:443–447
Smedly LA, Tonnesen MG, Sandhaus RA, Haslett C, Guthrie LA, Johnston RB (1986) Neutrophil-mediated injury to endothelial cells-enhancement by endotoxin and essential role of neutrophil elastase. J Clin Invest 77:1233–1243
Suttorp N, Nolte A, Neuhof H (1989) Bedeutung der granulozytären Elastase für die endotheliale Permeabilität. In: Suttorp N (ed) Zellbiologische Untersuchungen zur Pathogenese des akuten Atemnotsyndroms des Erwachsenen. Habilitationsschrift, University of Giessen
Tate RM, Vanbenthuysen KM, Shasby DM, McMurtry IF, Repine J (1982) Oxygen-radical-mediated permeability edema and vasoconstriction in isolated perfused rabbit lungs. Am Rev Respir Dis 126:802–806
Tate RM, Repine JE (1983) State of the art-neutrophils and the adult respiratory distress syndrome. Am Rev Respir Dis 128:552–559
Varani J, Fligiel SEG, Till GO, Kunkel RG, Ryan US, Ward PA (1985) Pulmonary endothelial cell killing by human neutrophils. Lab Invest 53:656–663
Yamamoto T, Cochrane CG (1981) Guinea pig hageman factor as a vascular permeability enhancement factor. Am J Pathol 105:164–175
Zaslow MC, Clark RA, Stone PJ, Calore JD, Snider GL, Franzblau C (1983) Human neutrophil elastase does not bind to alpha1 -protease inhibitor that has been exposed to activated human neutrophils. Am Rev Respir Dis 128:434–439
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1992 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Neuhof, H., Fritz, H. (1992). Proteinases as Mediators of the Disturbance of Pulmonary Vascular Permeability in Sepsis, Polytrauma, and ARDS. In: Rügheimer, E. (eds) New Aspects on Respiratory Failure. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74943-8_8
Download citation
DOI: https://doi.org/10.1007/978-3-642-74943-8_8
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-74945-2
Online ISBN: 978-3-642-74943-8
eBook Packages: Springer Book Archive