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The Role of Prostacyclin and Thromboxane in Sepsis and Septic Shock

The Role of Prostacyclin and Thromboxane in Sepsis and Septic Shock Abstract • Prostacyclin, or prostaglandin I2 (PGI2), and thromboxane A2 (TXA2) are potent, endogenously produced, vasoactive substances that have been implicated as mediators in the pathophysiologic nature of septic shock. We investigated the contribution and production of PGI2 and TXA2 in sepsis and septic shock, using an intact rabbit model and an in vitro rabbit isolated cardiac perfusion model. Continuous hemodynamic monitoring of both experimental models, along with serial radioimmunoassays of the metabolites of PGI2 and TXA2, indicated that myocardial depression is a common finding in subjects with septic shock and that septic shock causes a suppression of PGI2 production while augmenting TXA2 production. In addition, PGI2 and TXA2 were mediators of some cardiovascular changes in septic shock but were themselves not the toxic factor(s) responsible for the associated myocardial depression. (Arch Surg 1984;119:189-192) References 1. Dusting CJ, Moncada S, Vane JR: Prostaglandins, the intermediates and precursors: Cardiovascular action and regulatory roles in normal and abnormal circulatory systems . Prog Cardiovasc Dis 1979;21:405-430.Crossref 2. Dusting CJ, Moncada S, Vane JR: Prostacyclin (PGX) is the endogenous metabolite responsible for relaxation of coronary arteries induced by arachidonic acid . Prostaglandins 1977;13:3-15.Crossref 3. Hamberg M, Svensson J, Samuelsson B: Thromboxanes: A new group of biologically active compounds derived from prostaglandin endoperoxides . Proc Natl Acad Sci USA 1975;72:2994-2998.Crossref 4. Northover BJ, Subramanian G: Analgesic anti-pyretic drugs as antagonists of endotoxic shock in dogs . J Pathol 1962;83:463-468.Crossref 5. Vane JR: Inhibition of prostaglandin synthesis as a mechanism of action for aspirin like drugs . Nature 1971;231:232-235. 6. Carmona RH, Catalano R, Trunkey DD: Septic shock , in Shires T (ed): Clinical Surgery International . London, Livingston Press, 1983. 7. Webb PJ, Westwick MF, Scully J, et al: Do prostacyclin and thromboxane play a role in endotoxic shock? Br J Surg 1981;68:720-724.Crossref 8. Moncada S, Vane JR: Pharmacology and endogenous roles of prostaglandin endoperoxides: Thromboxane A2 and prostacyclin . Pharmacol Rev 1979;30:293-331. 9. Levison MA, Tsao TC, Trunkey DD: Myocardial depression: The effect of Ca+ + and calcium flux during sepsis. Arch Surg, in press. 10. Harris RH, Zmudka M, Maddox Y, et al: Relationships of TXB2 and 6-keto-PGF1α to the hemodynamic changes during baboon endotoxic shock . Adv Prostaglandin Thromboxane Leukotriene Res 1980;7:843-849. 11. Roberts LJ, Brash AR, Oates JA: Metabolic fate of thromboxane A2 and prostacyclin , in Oates JA (ed): Prostaglandins and the Cardiovascular System . New York, Raven Press, pp 211-225. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Surgery American Medical Association

The Role of Prostacyclin and Thromboxane in Sepsis and Septic Shock

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Publisher
American Medical Association
Copyright
Copyright © 1984 American Medical Association. All Rights Reserved.
ISSN
0004-0010
eISSN
1538-3644
DOI
10.1001/archsurg.1984.01390140053009
Publisher site
See Article on Publisher Site

Abstract

Abstract • Prostacyclin, or prostaglandin I2 (PGI2), and thromboxane A2 (TXA2) are potent, endogenously produced, vasoactive substances that have been implicated as mediators in the pathophysiologic nature of septic shock. We investigated the contribution and production of PGI2 and TXA2 in sepsis and septic shock, using an intact rabbit model and an in vitro rabbit isolated cardiac perfusion model. Continuous hemodynamic monitoring of both experimental models, along with serial radioimmunoassays of the metabolites of PGI2 and TXA2, indicated that myocardial depression is a common finding in subjects with septic shock and that septic shock causes a suppression of PGI2 production while augmenting TXA2 production. In addition, PGI2 and TXA2 were mediators of some cardiovascular changes in septic shock but were themselves not the toxic factor(s) responsible for the associated myocardial depression. (Arch Surg 1984;119:189-192) References 1. Dusting CJ, Moncada S, Vane JR: Prostaglandins, the intermediates and precursors: Cardiovascular action and regulatory roles in normal and abnormal circulatory systems . Prog Cardiovasc Dis 1979;21:405-430.Crossref 2. Dusting CJ, Moncada S, Vane JR: Prostacyclin (PGX) is the endogenous metabolite responsible for relaxation of coronary arteries induced by arachidonic acid . Prostaglandins 1977;13:3-15.Crossref 3. Hamberg M, Svensson J, Samuelsson B: Thromboxanes: A new group of biologically active compounds derived from prostaglandin endoperoxides . Proc Natl Acad Sci USA 1975;72:2994-2998.Crossref 4. Northover BJ, Subramanian G: Analgesic anti-pyretic drugs as antagonists of endotoxic shock in dogs . J Pathol 1962;83:463-468.Crossref 5. Vane JR: Inhibition of prostaglandin synthesis as a mechanism of action for aspirin like drugs . Nature 1971;231:232-235. 6. Carmona RH, Catalano R, Trunkey DD: Septic shock , in Shires T (ed): Clinical Surgery International . London, Livingston Press, 1983. 7. Webb PJ, Westwick MF, Scully J, et al: Do prostacyclin and thromboxane play a role in endotoxic shock? Br J Surg 1981;68:720-724.Crossref 8. Moncada S, Vane JR: Pharmacology and endogenous roles of prostaglandin endoperoxides: Thromboxane A2 and prostacyclin . Pharmacol Rev 1979;30:293-331. 9. Levison MA, Tsao TC, Trunkey DD: Myocardial depression: The effect of Ca+ + and calcium flux during sepsis. Arch Surg, in press. 10. Harris RH, Zmudka M, Maddox Y, et al: Relationships of TXB2 and 6-keto-PGF1α to the hemodynamic changes during baboon endotoxic shock . Adv Prostaglandin Thromboxane Leukotriene Res 1980;7:843-849. 11. Roberts LJ, Brash AR, Oates JA: Metabolic fate of thromboxane A2 and prostacyclin , in Oates JA (ed): Prostaglandins and the Cardiovascular System . New York, Raven Press, pp 211-225.

Journal

Archives of SurgeryAmerican Medical Association

Published: Feb 1, 1984

References