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U.S. Department of Energy
Office of Scientific and Technical Information

Thromboxane-mediated injury following radiation. Annual summary report No. 1, January-September 1984

Technical Report ·
OSTI ID:6438322
The hypothesis under investigation is that moderate levels of radiation exposure result in endothelial and other tissue damage which, in turn, increases in vivo synthesis of thromboxane A2 (TXA2) and/or decreases synthesis of prostacyclin (PGI2). It is proposed that this altered arachidonate metabolism results in vasoconstriction and decreased peripheral blood flow, thereby leading to further tissue damage which is proportional to the degree of radiation exposure. The observations described in this first annual report demonstrate that whole body gamma irradiation results in a indomethacin sensitive increase in urine TXB2 four to 120 hours after 10 Gy and four to 12 hours after 20 Gy whole body irradiation. Exposure to 20 Gy also increased in vivo synthesis of the PGI2 hydrolysis product, 6-keto PGFla. These studies also showed that radiation-induced increases in TXB2 are due to altered extrarenal synthesis, while the altered 6-keto PGFla levels appear to be due to changes in intrarenal arachidonate metabolism. The projected studies for the second year will include identification of the organs and tissues involved in radiation-induced alterations in urine cyclooxygenase product synthesis using regional shielding techniques.
Research Organization:
Georgetown Univ., Washington, DC (USA). Dept. of Physiology and Biophysics
OSTI ID:
6438322
Report Number(s):
AD-A-145187/1
Country of Publication:
United States
Language:
English