Skip to main content

Complement Inhibitor Therapeutics and Lung Injury

  • Chapter
Vascular Endothelium

Part of the book series: NATO ASI Series ((NSSA,volume 294))

  • 86 Accesses

Abstract

Lung injury from any cause can have severe clinical outcomes. The Adult Respiratory Distress Syndrome (ARDS) was defined as a clinical entity in 1967.1 It is generally recognized as acute respiratory failure characterized by relatively normal cardiac function, an increase in vascular permeability leading to pulmonary edema manifested by diffuse pulmonary infiltrates on the chest X-ray and by a major oxygenation defect.2 Precipitating insults include severe sepsis, diffuse pneumonia, pancreatitis, multiple trauma, aspiration, near-drowning, burns, shock, hypotension, and coagulopathy. ARDS is a major contributor to the morbidity and mortality of patients in intensive care units with 30-day mortality rates varying from 55 to 65%.1–4 Current estimates are that more than 100,000 patients per year in the U.S. develop ARDS.5

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 169.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 219.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 219.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Ashbaugh DG, Bigelow DB, Petty TL, and Levine BE. Acute respiratory distress in adults. Lancet 1967; ii: 319–323.

    Article  Google Scholar 

  2. Hyers TM. Prediction of survival and mortality in patients with adult respiratory distress syndrome. New Horizons 1993; 1:466–470.

    PubMed  CAS  Google Scholar 

  3. Suchyta MR, Clemmer TP, Elliott CG, Orme JF, Jr., and Weaver LK. The adult respiratory distress syndrome: a report of survival and modifying factors. Chest 1992; 101:74–79.

    Article  Google Scholar 

  4. Artigas A, Calet J, Legall JR, et. al. Clinical presentation, prognostic factors and outcome of ARDS in the European Collaborative study (1985–1987). A preliminary report. In: Zapol W, LeMaire F, editors. Adult Respiratory Distress Syndrome, New York: Marcell Dekker, 1991:37–64.

    Google Scholar 

  5. Wheeler AP, Carroll FE, Bernard GR. Radiographic issues in adult respiratory distress syndrome. New Horizons 1993; 1:471–477.

    PubMed  CAS  Google Scholar 

  6. Ryan US. Structural bases for metabolic activity. Ann Rev Physiol 1982; 44:223–239.

    Article  CAS  Google Scholar 

  7. Ryan US, Ryan JW. Vital and functional activities of endothelial cells. In: Nossel HL, Vogel HJ, editors. Pathobiology of the Endothelial Cell. New York: Academic Press, 1982:455–469.

    Google Scholar 

  8. Ryan US, Ryan JW, Whitaker C, and Chiu A. Localization of angiotensin converting enzyme (kininase II): immunocytochemistry and immunofluorescence. Tissue & Cell 1976; 8:125–146.

    Article  CAS  Google Scholar 

  9. Crutchley DJ, Ryan JW, Ryan US, and Fisher GH. Bradykinin-induced release of prostacyclin and thromboxanes from bovine pulmonary artery endothelial cells. Studies with lower homologs and calcium antagonists. Biochem Biophys Acta 1983; 751:99–107.

    Article  PubMed  CAS  Google Scholar 

  10. Furchgott RF and Zawadzki JV. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetycholine. Nature 1980; 373:299.

    Google Scholar 

  11. Yanagisawa M, Kurihara H, Kimura S, et al. A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature 1988; 332:411–415.

    Article  PubMed  CAS  Google Scholar 

  12. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992; 20:864–874.

    Article  Google Scholar 

  13. Zilow G, Joka T, Obertacke U, Rother U, and Kirschfink M. Generation of anaphylatoxin C3a in plasma and bronchoalveolar lavage fluid in trauma patients at risk for the adult respiratory distress syndrome. Crit Care Med 1992; 20:468–473.

    Article  PubMed  CAS  Google Scholar 

  14. Hamilton KK, Hattori R, Esmon CT, and Sims PJ. Complement proteins C5b-9 induce vesiculation of the endothelial plasma membrane and expose catalytic surface for assembly of the prothrombinase enzyme complex. J Biol Chem 1990; 265:3809–3814.

    PubMed  CAS  Google Scholar 

  15. Halperin JA, Taratuska A, Nicholson-Weller A. Terminal complement complex C5b-9 stimulates mitogenesis in 3T3 cells. J Clin Invest 1993; 91:1974–1978.

    Article  PubMed  CAS  Google Scholar 

  16. Benzaquen LR, Nicholson-Weller A, and Halperin JA. Terminal complement proteins C5b-9 release basic fibroblast growth factor and platelet-derived growth factor from endothelial cells. J Exp Med 1994; 179:985–992.

    Article  PubMed  CAS  Google Scholar 

  17. Mulligan MS, Yeh CG, Rudolph AR, and Ward PA. Protective effects of soluble CR1 in complement-and neutrophil-mediated tissue injury. J Immunol 1992; 148:1479–1485.

    PubMed  CAS  Google Scholar 

  18. Rabinovici R., Yeh CG, Hillegass LM, Griswold DC, DiMartino MJ, Vernick J, et al. Role of complement in endotoxin/platelet-activating factor-induced lung injury. J Immunol 1992; 149:1744–1750.

    PubMed  CAS  Google Scholar 

  19. DiMartino MJ, Wolfe CE, Slivjak MJ, Minthorn EA, Feuerstein G. Effects of soluble complement receptor (sCR1, BRL55730) on thermal skin injury induced hemoconcentration and lung inflammation in rats. Pharmacol Commun 1993; 3:249–256.

    CAS  Google Scholar 

  20. Weisman HF, Bartow T, Leppo MK, et. al. Soluble human complement receptor type 1: In vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis. Science 1990; 249:146–151.

    Article  PubMed  CAS  Google Scholar 

  21. Smith EF, III, Griswold DE, Egan JW, Hillegass LM, Smith RAG, Hibbs MJ, et al. Reduction of myocardial reperfusion injury with soluble complement receptor I (BRL 55730). Eur J Pharmacol 1993; 236:477–481.

    Article  PubMed  CAS  Google Scholar 

  22. Dupe RJ, Goddard ME, Freeman AM, Hibbs MJ, Lifter J, Mossakowska DE, et al. Utility of complement inhibition during myocardial reperfusion: Pharmacology of soluble complement receptor 1. 13th Congress of the International Society of Thrombosis and Haemostasis. Thrombos Haemostasis 1991; 65:695.

    Google Scholar 

  23. Schaiff WT and Eisenberg PR. Pharmacologie activation of plasminogen directly induces and enhances complement activation. Suppl. to Circulation 1995; 92:I–342 Abstract.

    Google Scholar 

  24. Naka Y, Roy DK, Marsh HC, et. al. Protective effects of complement blockade in an isograft model of lung preservation and transplantation. Am Col of Cardiology 45th Annual Scientific Symposium 1996; Abstract.

    Google Scholar 

  25. Pruitt SK and Bollinger RR. The effect of soluble complement receptor type I on hyperacute allograft rejection. J Surg Res 1991; 50:350–355.

    Article  PubMed  CAS  Google Scholar 

  26. Pruitt SK, Baldwin WM, Marsh HC, Jr., Lin SS, Yeh CG, Bollinger RR. The effect of soluble complement receptor type I on hyperacute xenograft rejection. Transplantation 1991; 52:868–873.

    Article  PubMed  CAS  Google Scholar 

  27. Pruitt SK, Kirk AD, Bollinger RR, Marsh HC, Jr., Collins BH, Levin JL, et al. The effect of soluble complement receptor type I on hyperacute rejection of porcine xenografts. Transplantation 1994; 57:363–370.

    Article  PubMed  CAS  Google Scholar 

  28. Davis EA, Pruitt SK, Greene PS, Ibrahim S, Lam TT, Levin JL, et al. Inhibition of complement, evoked antibody, and cellular response prevents rejection of pig-to-primate cardiac xenografts. Transplantation 1996; 62:1018–1023.

    Article  PubMed  CAS  Google Scholar 

  29. Pratt JR, Hibbs MJ, Laver AJ, Smith RAG, Sacks SH. Allograft immune response with sCR1 intervention. Transplant Immunol 1996; 4:72–75.

    Article  CAS  Google Scholar 

  30. Pratt JR, Harmer AW, Smith RAG, and Sacks SH. Influence of complement inhibition with soluble complement receptor (sCR1) on the B cell response in experimental allograft rejection. Transplantation Society 1996; Barcelona, Spain: Abstract.

    Google Scholar 

  31. Kallio E, Koskinen P, Krebs R, Ryan U, Hayry P, and Lemstrom K. Soluble recombinant complement receptor type 1 significantly reduces the development of experimental obliterative bronchiolitis in rat tracheal allografts. Int Transplantation Society 1996; Abstract.

    Google Scholar 

  32. Ryan US. Complement inhibitory therapeutics and xenotransplantation. Nature Medicine 1995; 1:967–968.

    Article  PubMed  CAS  Google Scholar 

  33. Ryan US. Complement inhibition: the sine qua non of xenotransplantation? Xeno 1994; 2:19–22.

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1998 Springer Science+Business Media New York

About this chapter

Cite this chapter

Ryan, U.S. (1998). Complement Inhibitor Therapeutics and Lung Injury. In: Catravas, J.D., Callow, A.D., Ryan, U.S. (eds) Vascular Endothelium. NATO ASI Series, vol 294. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0133-0_3

Download citation

  • DOI: https://doi.org/10.1007/978-1-4899-0133-0_3

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4899-0135-4

  • Online ISBN: 978-1-4899-0133-0

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics