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Effect of LY171883 on endotoxin-induced lung injury in pigs.
J Appl Physiol (1985). 1990 Oct; 69(4):1315-22.JA

Abstract

We evaluated the role of sulfidopeptide leukotrienes as mediators of endotoxin-induced respiratory failure in pigs. Escherichia coli endotoxin (055-B5) was infused intravenously into anesthetized 10- to 14-wk-old pigs at 5 micrograms/kg the 1st h followed by 2 micrograms.kg-1.h-1 for 3 h in the presence and absence of LY171883, a specific leukotriene D4 (LTD4)/LTE4 receptor antagonist. Endotoxin caused hemoconcentration, granulocytopenia, decreased cardiac index, systemic hypotension, pulmonary hypertension, increased pulmonary vascular resistance, bronchoconstriction, hypoxemia, increased permeability of the alveolar-capillary membrane, pulmonary edema, and increased plasma concentrations of thromboxane B2 (TxB2), prostaglandin F2 alpha (PGF2 alpha), and 6-keto-PGF1 alpha. LY171883 did not modify endotoxin-induced cardiopulmonary and hematologic abnormalities, except for a modest attenuation of pulmonary hypertension (at 1 h) and increased pulmonary vascular resistance (at 1-2 h). Ex vivo stimulation of whole blood with calcium ionophore caused large increases in plasma concentrations of TxB2, PGF2 alpha, and LTB4. These increases were not significantly modified in blood derived from pigs treated with LY171883, indicating no inhibition of cyclooxygenase or 5-lipoxygenase. We conclude that LTD4 and LTE4 are not important mediators of endotoxin-induced lung injury in anesthetized pigs, although they may contribute modestly to pulmonary vasoconstriction.

Authors+Show Affiliations

Department of Anatomy, Physiological Sciences, and Radiology, College of Veterinary Medicine, North Carolina State University, Raleigh 27606.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

1979787

Citation

Olson, N C., et al. "Effect of LY171883 On Endotoxin-induced Lung Injury in Pigs." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 69, no. 4, 1990, pp. 1315-22.
Olson NC, Kruse-Elliott KT, Johnson L. Effect of LY171883 on endotoxin-induced lung injury in pigs. J Appl Physiol (1985). 1990;69(4):1315-22.
Olson, N. C., Kruse-Elliott, K. T., & Johnson, L. (1990). Effect of LY171883 on endotoxin-induced lung injury in pigs. Journal of Applied Physiology (Bethesda, Md. : 1985), 69(4), 1315-22.
Olson NC, Kruse-Elliott KT, Johnson L. Effect of LY171883 On Endotoxin-induced Lung Injury in Pigs. J Appl Physiol (1985). 1990;69(4):1315-22. PubMed PMID: 1979787.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of LY171883 on endotoxin-induced lung injury in pigs. AU - Olson,N C, AU - Kruse-Elliott,K T, AU - Johnson,L, PY - 1990/10/1/pubmed PY - 1990/10/1/medline PY - 1990/10/1/entrez SP - 1315 EP - 22 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J Appl Physiol (1985) VL - 69 IS - 4 N2 - We evaluated the role of sulfidopeptide leukotrienes as mediators of endotoxin-induced respiratory failure in pigs. Escherichia coli endotoxin (055-B5) was infused intravenously into anesthetized 10- to 14-wk-old pigs at 5 micrograms/kg the 1st h followed by 2 micrograms.kg-1.h-1 for 3 h in the presence and absence of LY171883, a specific leukotriene D4 (LTD4)/LTE4 receptor antagonist. Endotoxin caused hemoconcentration, granulocytopenia, decreased cardiac index, systemic hypotension, pulmonary hypertension, increased pulmonary vascular resistance, bronchoconstriction, hypoxemia, increased permeability of the alveolar-capillary membrane, pulmonary edema, and increased plasma concentrations of thromboxane B2 (TxB2), prostaglandin F2 alpha (PGF2 alpha), and 6-keto-PGF1 alpha. LY171883 did not modify endotoxin-induced cardiopulmonary and hematologic abnormalities, except for a modest attenuation of pulmonary hypertension (at 1 h) and increased pulmonary vascular resistance (at 1-2 h). Ex vivo stimulation of whole blood with calcium ionophore caused large increases in plasma concentrations of TxB2, PGF2 alpha, and LTB4. These increases were not significantly modified in blood derived from pigs treated with LY171883, indicating no inhibition of cyclooxygenase or 5-lipoxygenase. We conclude that LTD4 and LTE4 are not important mediators of endotoxin-induced lung injury in anesthetized pigs, although they may contribute modestly to pulmonary vasoconstriction. SN - 8750-7587 UR - https://www.unboundmedicine.com/medline/citation/1979787/Effect_of_LY171883_on_endotoxin_induced_lung_injury_in_pigs_ L2 - https://journals.physiology.org/doi/10.1152/jappl.1990.69.4.1315?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -