Anaphylactic release of thromboxane A 2, Prostaglandin D 2, and prostacyclin from human lung parenchyma

E. S. Schulman, H. H. Newball, L. M. Demers, F. A. Fitzpatrick, N. F. Adkinson

Research output: Contribution to journalArticle

127 Citations (Scopus)

Abstract

Antigen challenge of passively sensitized chopped human lung resulted in the generation of several arachidonic acid cyclooxygenase metabolites (AACM): thromboxane A 2 (TxA 2) as measured by its stable metabolite TxB 2, prostaglandin D 2 (PgD 2), prostacyclin (PgI 2) as measured by its table metabolite 6-keto-PgF(1α), prostaglandin F(2α) (PgF(2α)) and prostaglandin E (PgE). The kinetics of AACM release after antigen challenge paralleled histamine release. All AACM were released in an antigen dose-dependent manner and reached maximal release at antigen concentrations lower than those required for maximal histamine release. Quantitatively, of the AACM measured, PgD 2 and PgI 2 were found to predominate in anaphylactic reactions of human lung parenchyma. Generation of PgD 2 and PgI 2 were 3- to 7-fold greater than that of other AACM measured. Thromboxane B 2 was generated in quantities comparable to PgE and PgF(2α). Studies were designed to test the hypothesis that lung smooth muscle contraction per se can account for the generated AACM that are released during anaphylaxis of the lung. The studies compared antigen-induced AACM generation with methacholine-induced (10 -4M) AACM generation. The failure to confirm this hypothesis was especially evident for PgD 2 where release was dependent on mast cell activation. Thromboxane A 2, PgD 2, and PgI 2, have been reported to have potent effects on smooth muscle. Our data suggested that these AACM are generated in such sufficient quantities that they may function in important aspects of the modulation of hypersensitivity responses in human lungs.

Original languageEnglish (US)
Pages (from-to)402-406
Number of pages5
JournalAmerican Review of Respiratory Disease
Volume124
Issue number4
StatePublished - Dec 6 1981

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Prostaglandins D
Thromboxanes
Epoprostenol
Prostaglandin-Endoperoxide Synthases
varespladib methyl
Lung
Antigens
Histamine Release
Prostaglandins F
Anaphylaxis
Prostaglandins E
Smooth Muscle
Methacholine Chloride
Muscle Contraction
Mast Cells
Hypersensitivity

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Cite this

Schulman, E. S., Newball, H. H., Demers, L. M., Fitzpatrick, F. A., & Adkinson, N. F. (1981). Anaphylactic release of thromboxane A 2, Prostaglandin D 2, and prostacyclin from human lung parenchyma. American Review of Respiratory Disease, 124(4), 402-406.
Schulman, E. S. ; Newball, H. H. ; Demers, L. M. ; Fitzpatrick, F. A. ; Adkinson, N. F. / Anaphylactic release of thromboxane A 2, Prostaglandin D 2, and prostacyclin from human lung parenchyma. In: American Review of Respiratory Disease. 1981 ; Vol. 124, No. 4. pp. 402-406.
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Schulman, ES, Newball, HH, Demers, LM, Fitzpatrick, FA & Adkinson, NF 1981, 'Anaphylactic release of thromboxane A 2, Prostaglandin D 2, and prostacyclin from human lung parenchyma', American Review of Respiratory Disease, vol. 124, no. 4, pp. 402-406.

Anaphylactic release of thromboxane A 2, Prostaglandin D 2, and prostacyclin from human lung parenchyma. / Schulman, E. S.; Newball, H. H.; Demers, L. M.; Fitzpatrick, F. A.; Adkinson, N. F.

In: American Review of Respiratory Disease, Vol. 124, No. 4, 06.12.1981, p. 402-406.

Research output: Contribution to journalArticle

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N2 - Antigen challenge of passively sensitized chopped human lung resulted in the generation of several arachidonic acid cyclooxygenase metabolites (AACM): thromboxane A 2 (TxA 2) as measured by its stable metabolite TxB 2, prostaglandin D 2 (PgD 2), prostacyclin (PgI 2) as measured by its table metabolite 6-keto-PgF(1α), prostaglandin F(2α) (PgF(2α)) and prostaglandin E (PgE). The kinetics of AACM release after antigen challenge paralleled histamine release. All AACM were released in an antigen dose-dependent manner and reached maximal release at antigen concentrations lower than those required for maximal histamine release. Quantitatively, of the AACM measured, PgD 2 and PgI 2 were found to predominate in anaphylactic reactions of human lung parenchyma. Generation of PgD 2 and PgI 2 were 3- to 7-fold greater than that of other AACM measured. Thromboxane B 2 was generated in quantities comparable to PgE and PgF(2α). Studies were designed to test the hypothesis that lung smooth muscle contraction per se can account for the generated AACM that are released during anaphylaxis of the lung. The studies compared antigen-induced AACM generation with methacholine-induced (10 -4M) AACM generation. The failure to confirm this hypothesis was especially evident for PgD 2 where release was dependent on mast cell activation. Thromboxane A 2, PgD 2, and PgI 2, have been reported to have potent effects on smooth muscle. Our data suggested that these AACM are generated in such sufficient quantities that they may function in important aspects of the modulation of hypersensitivity responses in human lungs.

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Schulman ES, Newball HH, Demers LM, Fitzpatrick FA, Adkinson NF. Anaphylactic release of thromboxane A 2, Prostaglandin D 2, and prostacyclin from human lung parenchyma. American Review of Respiratory Disease. 1981 Dec 6;124(4):402-406.