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Prostaglandin and Complement Interaction in Clinical Acute Respiratory Failure

Prostaglandin and Complement Interaction in Clinical Acute Respiratory Failure Abstract • This study investigated the interaction of plasma levels of circulating prostaglandins and activated complement in clinical acute respiratory failure (ARDS). Fifty patients at risk for ARDS were followed up for up to ten days. Arterial blood gases and plasma levels of complement components C3a and C5a, thromboxane B2 (TxB), and prostaglandin 6-keto-F1α, (PGI) and granulocyte aggregation (GA) were measured daily. Seventeen patients (34%) developed ARDS, with mortality of 41% vs 23% for patients without ARDS. Compared with patients without ARDS, the ARDS group had significantly increased plasma C3a (1,130 ±750 vs 636±368 ng/mL) and granulocyte aggregation (48 ± 10 vs 17 ± 4 percentage of the maximum light transmission [% max T]). Plasma C5a, TxB, or PGI did not change significantly with or without ARDS. No measured variable was significantly associated with mortality. Regression analysis revealed significant correlations between GA, TxB, PGI, and arterial oxygenation. Plasma C3a and GA are increased in ARDS, suggesting systemic complement activation. A complex series of interactions between the prostaglandins, complement, and GA appears to be involved in ARDS. (Arch Surg 1986;121:271-274) References 1. Blaisdell WB: Respiratory insufficiency syndrome: Clinical and pathological definition . J Trauma 1973;13:195-199.Crossref 2. Hammerschmidt DE, Weaver LJ, Hudson LD, et al: Association of complement activation and elevated plasma-C5a with adult respiratory distress syndrome . Lancet 1980;1:947-949.Crossref 3. Slotman GJ, Burchard KW, Gann DS: Thromboxane and prostacyclin in clinical acute respiratory failure . J Surg Res 1985;39:1-7.Crossref 4. Ranson JHC, Basternack BS: Statistical methods for quantifying the severity of clinical acute pancreatitis . J Surg Res 1977;22:79-91.Crossref 5. Fitzpatrick FA: Immunochemical assays of enzymes and metabolites . Methods Enzymol 1982;86:286-297. 6. Hensby CN, Jogee M, Elder MG, et al: A comparison of the quantitative analysis of 6-oxo-PGF1 in biological fluids by gas chromatography mass spectrometry and radioimmunoassay . Biomed Mass Spectrom 1981;8:111-117.Crossref 7. Hugli RW, Chenoweth DE: Biologically active peptide of complement: Techniques and significance of C3a and C5a measurement , in Nakamura RM (ed): Future Perspectives in Clinical Laboratory Immunoassays . New York, Alan R Liss Inc, 1980, pp 443-459. 8. Craddock PR, Hammerschmidt DE, Modlow CF, et al: Granulocyte aggregation as a manifestation of membrane interactions with complement: Possible role in leukocyte margination, microvascular occlusion, and endothelial damage . Semin Hematol 1979;16:140-147. 9. Hammerschmidt DE, Harris PE, Wayland JH, et al: Complementinduced granulocyte aggregation in vivo . Am Assoc Pathol 1981;10:146-150. 10. Winer BJ: Statistical Principles in Experimental Design , ed 2. New York, McGraw Hill International Book Co, 1971. 11. Slotman GJ, Quinn JV, Burchard KW, et al: Thromboxane interaction with cardiopulmonary dysfunction in graded bacterial sepsis . J Trauma 1984;24:803-810.Crossref 12. Slotman GJ, Quinn JV, Burchard KW, et al: Thromboxane, prostacyclin and the hemodynamic effects of graded bacteremic shock. Circ Shock, in press. 13. Smith ME, Gunther R, Gee M, et al: Leukocytes, platelets, and thromboxane in endotoxin-induced lung injury . Surgery 1981;90:102-107. 14. Rampart M, Bult H, Herman AG: Complement activation and blood levels of 6-oxo-prostaglandin F1a during endotoxin-induced hypotension in rabbits . Arch Int Pharmacodyn Ther 1981;249:328-329. 15. McDonald JWD, Ali M, Morgan E, et al: Thromboxane synthesis by sources other than platelets in association with complement-induced pulmonary leukostasis and pulmonary hypertension in sheep . Circ Res 1983;52:1-6.Crossref 16. Larsen GL, Mitchell BC, Harper TB, et al: The pulmonary response of C5 sufficient and deficient mice to Pseudomonas aeruginosa . Am Rev Respir Dis 1982;12:306-311. 17. Huval WV, Dunham MM, Lelcuk S, et al: Thromboxane mediation of cardiovascular dysfunction following aspiration . Surgery 1983;94:260-266. 18. Steinberg SM, Dehring DJ, Gower WR, et al: Prostacyclin in experimental septic acute respiratory failure . J Surg Res 1983;34:298-302.Crossref 19. O'Flaherty JT, Showell HJ, Becker EL, et al: Substances which aggregate neutrophils . Am J Pathol 1978;92:156-166. 20. Williams J, Yellin SA, Slotman GJ: Leukocyte aggregation response to quantitative plasma levels of C3a and C5a . Arch Surg 1986;121:305-307.Crossref 21. Chenowith DE, Hugli TE: Binding and degradation of C5a by human neutrophils , abstracted. J Immunol 1980;124:1517. 22. Solomkin JS, Cotta LA, Ogle JD, et al: Complement-induced expression of cryptic receptors on the neutrophil surface: A mechanism for regulation of acute inflammation in trauma . Surgery 1984;96:336-344. 23. Solomkin JS, Cotta LA, Brodt JK, et al: Regulation of neutrophil superoxide production in sepsis . Arch Surg 1985;120:93-98.Crossref 24. Heideman M, Hugli TE: Anaphylatoxin generation in multisystem organ failure . J Trauma 1984;24:1-5.Crossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Surgery American Medical Association

Prostaglandin and Complement Interaction in Clinical Acute Respiratory Failure

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Publisher
American Medical Association
Copyright
Copyright © 1986 American Medical Association. All Rights Reserved.
ISSN
0004-0010
eISSN
1538-3644
DOI
10.1001/archsurg.1986.01400030025002
Publisher site
See Article on Publisher Site

Abstract

Abstract • This study investigated the interaction of plasma levels of circulating prostaglandins and activated complement in clinical acute respiratory failure (ARDS). Fifty patients at risk for ARDS were followed up for up to ten days. Arterial blood gases and plasma levels of complement components C3a and C5a, thromboxane B2 (TxB), and prostaglandin 6-keto-F1α, (PGI) and granulocyte aggregation (GA) were measured daily. Seventeen patients (34%) developed ARDS, with mortality of 41% vs 23% for patients without ARDS. Compared with patients without ARDS, the ARDS group had significantly increased plasma C3a (1,130 ±750 vs 636±368 ng/mL) and granulocyte aggregation (48 ± 10 vs 17 ± 4 percentage of the maximum light transmission [% max T]). Plasma C5a, TxB, or PGI did not change significantly with or without ARDS. No measured variable was significantly associated with mortality. Regression analysis revealed significant correlations between GA, TxB, PGI, and arterial oxygenation. Plasma C3a and GA are increased in ARDS, suggesting systemic complement activation. A complex series of interactions between the prostaglandins, complement, and GA appears to be involved in ARDS. (Arch Surg 1986;121:271-274) References 1. Blaisdell WB: Respiratory insufficiency syndrome: Clinical and pathological definition . J Trauma 1973;13:195-199.Crossref 2. Hammerschmidt DE, Weaver LJ, Hudson LD, et al: Association of complement activation and elevated plasma-C5a with adult respiratory distress syndrome . Lancet 1980;1:947-949.Crossref 3. Slotman GJ, Burchard KW, Gann DS: Thromboxane and prostacyclin in clinical acute respiratory failure . J Surg Res 1985;39:1-7.Crossref 4. Ranson JHC, Basternack BS: Statistical methods for quantifying the severity of clinical acute pancreatitis . J Surg Res 1977;22:79-91.Crossref 5. Fitzpatrick FA: Immunochemical assays of enzymes and metabolites . Methods Enzymol 1982;86:286-297. 6. Hensby CN, Jogee M, Elder MG, et al: A comparison of the quantitative analysis of 6-oxo-PGF1 in biological fluids by gas chromatography mass spectrometry and radioimmunoassay . Biomed Mass Spectrom 1981;8:111-117.Crossref 7. Hugli RW, Chenoweth DE: Biologically active peptide of complement: Techniques and significance of C3a and C5a measurement , in Nakamura RM (ed): Future Perspectives in Clinical Laboratory Immunoassays . New York, Alan R Liss Inc, 1980, pp 443-459. 8. Craddock PR, Hammerschmidt DE, Modlow CF, et al: Granulocyte aggregation as a manifestation of membrane interactions with complement: Possible role in leukocyte margination, microvascular occlusion, and endothelial damage . Semin Hematol 1979;16:140-147. 9. Hammerschmidt DE, Harris PE, Wayland JH, et al: Complementinduced granulocyte aggregation in vivo . Am Assoc Pathol 1981;10:146-150. 10. Winer BJ: Statistical Principles in Experimental Design , ed 2. New York, McGraw Hill International Book Co, 1971. 11. Slotman GJ, Quinn JV, Burchard KW, et al: Thromboxane interaction with cardiopulmonary dysfunction in graded bacterial sepsis . J Trauma 1984;24:803-810.Crossref 12. Slotman GJ, Quinn JV, Burchard KW, et al: Thromboxane, prostacyclin and the hemodynamic effects of graded bacteremic shock. Circ Shock, in press. 13. Smith ME, Gunther R, Gee M, et al: Leukocytes, platelets, and thromboxane in endotoxin-induced lung injury . Surgery 1981;90:102-107. 14. Rampart M, Bult H, Herman AG: Complement activation and blood levels of 6-oxo-prostaglandin F1a during endotoxin-induced hypotension in rabbits . Arch Int Pharmacodyn Ther 1981;249:328-329. 15. McDonald JWD, Ali M, Morgan E, et al: Thromboxane synthesis by sources other than platelets in association with complement-induced pulmonary leukostasis and pulmonary hypertension in sheep . Circ Res 1983;52:1-6.Crossref 16. Larsen GL, Mitchell BC, Harper TB, et al: The pulmonary response of C5 sufficient and deficient mice to Pseudomonas aeruginosa . Am Rev Respir Dis 1982;12:306-311. 17. Huval WV, Dunham MM, Lelcuk S, et al: Thromboxane mediation of cardiovascular dysfunction following aspiration . Surgery 1983;94:260-266. 18. Steinberg SM, Dehring DJ, Gower WR, et al: Prostacyclin in experimental septic acute respiratory failure . J Surg Res 1983;34:298-302.Crossref 19. O'Flaherty JT, Showell HJ, Becker EL, et al: Substances which aggregate neutrophils . Am J Pathol 1978;92:156-166. 20. Williams J, Yellin SA, Slotman GJ: Leukocyte aggregation response to quantitative plasma levels of C3a and C5a . Arch Surg 1986;121:305-307.Crossref 21. Chenowith DE, Hugli TE: Binding and degradation of C5a by human neutrophils , abstracted. J Immunol 1980;124:1517. 22. Solomkin JS, Cotta LA, Ogle JD, et al: Complement-induced expression of cryptic receptors on the neutrophil surface: A mechanism for regulation of acute inflammation in trauma . Surgery 1984;96:336-344. 23. Solomkin JS, Cotta LA, Brodt JK, et al: Regulation of neutrophil superoxide production in sepsis . Arch Surg 1985;120:93-98.Crossref 24. Heideman M, Hugli TE: Anaphylatoxin generation in multisystem organ failure . J Trauma 1984;24:1-5.Crossref

Journal

Archives of SurgeryAmerican Medical Association

Published: Mar 1, 1986

References