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Role of subcutaneous tissue endotoxin in the production of prostanoid-induced lung injury: comparison with intravenous endotoxin response.
Circ Shock. 1985; 17(2):147-61.CS

Abstract

Local injection of endotoxin into soft tissues of the flank results in hypoxia and pulmonary hypertension. Our purpose was to determine whether this was caused by tissue prostanoid production or production by the lung as is seen with endotoxemia. Twenty-six sheep were prepared with lung and flank tissue lymph fistulae. Thirteen sheep were given 2 micrograms/kg Escherichia coli endotoxin into the flank soft tissue, six of which were pretreated with ibuprofen, 12.5 mg/kg. Thirteen sheep were given intravenous endotoxin, 2 micrograms/kg, with six pretreated with ibuprofen. An early hypertensive phase was noted with both insults characterized by pulmonary hypertension, hypoxia, and increased lung lymph flow (QL). With subcutaneous tissue endotoxin, there was a significant increase in tissue lymph TxB2 and 6-keto-PGF1 alpha when compared to lung lymph and increased values in venous plasma compared to arterial plasma, indicating tissue to be the source. With intravenous endotoxin, lung lymph and aortic plasma levels were significantly higher than tissue lymph and venous plasma, respectively. The hypoxia, hypertension and increased prostanoids were prevented using ibuprofen. An increased lung permeability phase was noted with intravenous endotoxin but not with tissue endotoxin. As expected, this phase was not inhibited with ibuprofen and, therefore, not prostanoid-induced.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

3840417

Citation

Demling, R H., et al. "Role of Subcutaneous Tissue Endotoxin in the Production of Prostanoid-induced Lung Injury: Comparison With Intravenous Endotoxin Response." Circulatory Shock, vol. 17, no. 2, 1985, pp. 147-61.
Demling RH, Wenger H, Hechtman H, et al. Role of subcutaneous tissue endotoxin in the production of prostanoid-induced lung injury: comparison with intravenous endotoxin response. Circ Shock. 1985;17(2):147-61.
Demling, R. H., Wenger, H., Hechtman, H., & Wong, C. (1985). Role of subcutaneous tissue endotoxin in the production of prostanoid-induced lung injury: comparison with intravenous endotoxin response. Circulatory Shock, 17(2), 147-61.
Demling RH, et al. Role of Subcutaneous Tissue Endotoxin in the Production of Prostanoid-induced Lung Injury: Comparison With Intravenous Endotoxin Response. Circ Shock. 1985;17(2):147-61. PubMed PMID: 3840417.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of subcutaneous tissue endotoxin in the production of prostanoid-induced lung injury: comparison with intravenous endotoxin response. AU - Demling,R H, AU - Wenger,H, AU - Hechtman,H, AU - Wong,C, PY - 1985/1/1/pubmed PY - 1985/1/1/medline PY - 1985/1/1/entrez SP - 147 EP - 61 JF - Circulatory shock JO - Circ Shock VL - 17 IS - 2 N2 - Local injection of endotoxin into soft tissues of the flank results in hypoxia and pulmonary hypertension. Our purpose was to determine whether this was caused by tissue prostanoid production or production by the lung as is seen with endotoxemia. Twenty-six sheep were prepared with lung and flank tissue lymph fistulae. Thirteen sheep were given 2 micrograms/kg Escherichia coli endotoxin into the flank soft tissue, six of which were pretreated with ibuprofen, 12.5 mg/kg. Thirteen sheep were given intravenous endotoxin, 2 micrograms/kg, with six pretreated with ibuprofen. An early hypertensive phase was noted with both insults characterized by pulmonary hypertension, hypoxia, and increased lung lymph flow (QL). With subcutaneous tissue endotoxin, there was a significant increase in tissue lymph TxB2 and 6-keto-PGF1 alpha when compared to lung lymph and increased values in venous plasma compared to arterial plasma, indicating tissue to be the source. With intravenous endotoxin, lung lymph and aortic plasma levels were significantly higher than tissue lymph and venous plasma, respectively. The hypoxia, hypertension and increased prostanoids were prevented using ibuprofen. An increased lung permeability phase was noted with intravenous endotoxin but not with tissue endotoxin. As expected, this phase was not inhibited with ibuprofen and, therefore, not prostanoid-induced. SN - 0092-6213 UR - https://www.unboundmedicine.com/medline/citation/3840417/Role_of_subcutaneous_tissue_endotoxin_in_the_production_of_prostanoid_induced_lung_injury:_comparison_with_intravenous_endotoxin_response_ L2 - https://antibodies.cancer.gov/detail/CPTC-HLA-B-1 DB - PRIME DP - Unbound Medicine ER -