Thromboxane-Mediated Injury Following Radiation.
Abstract
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). The observations indicate that the sources of the radiation-induced increases in TXB2 excretion are diverse, involving organs of both the thorax and upper abdomen. This conclusion is based on the attenuation in the radiation-induced increase in TXB2 excretion seen four hours after 20.0 Gy gamma irradiation with either the thorax or abdomen shielded. An isolated perfused rat kidney model was developed to determine if the kidneys contribute to the altered cyclooxygenase product release. Urine from the irradiated isolated kidney system showed an elevated excretion of TXB2, PGE2, and 6KPGFla compared to kidneys from sham irradiated animals. Whole body irradiation of rats also increased pulmonary release of TXB2 four hours after exposure. The data show that in vivo release of TXB2 involves more than one organ system and as a result, the use of TXB2 as a biological dosimeter requires knowledge as to the organ systems that were irradiated. These data also suggest that regional release of TXB2 varies and as such may provide a means of evaluating regional radiation injury. The results of the past year show that radiation can alter vascular reactivity to a cyclooxygenase product mimic and that this arachidonate metabolite release is increased following radiation exposure.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 31, 1985
- Accession Number
- ADA177824
Entities
People
- Peter A. Kot
Organizations
- Georgetown University