Hui S C, Ogle C W, Wang Z, An Y, Hu Y H
Department of Pharmacology, Medical Faculty, University of Hong Kong.
Pharmacology. 1989;39(5):291-8. doi: 10.1159/000138612.
The vasodepressor responses to intravenous injections of arachidonic acid, and the formation of its metabolites, were studied in rats made diabetic 1 or 2 weeks after a 1-dose alloxan treatment. Arachidonic acid dose-dependently decreased the diastolic blood pressure in normal animals, but this hypotensive effect was significantly weaker in 2-week postalloxan-treated rats. Indometacin abolished arachidonic-acid-induced depressor responses in both normal and diabetic animals. Hypotension induced by sodium nitroprusside was of the same magnitude in non-diabetic and insulin deficient rats. Plasma levels of thromboxane B2 were significantly increased in both the 1- and 2-week diabetic rats, being greater in the latter group; those of 6-keto-PGF1 alpha remained unchanged during the 2-week diabetic period. It is concluded that the attenuation by diabetes of depressor responses to arachidonic acid could be due to changes in the thromboxane/prostacyclin balance, with thromboxane formation being elevated whereas prostacyclin generation remains unaffected.
在单次注射四氧嘧啶1或2周后制成糖尿病模型的大鼠中，研究了静脉注射花生四烯酸后的血管减压反应及其代谢产物的形成。花生四烯酸剂量依赖性地降低正常动物的舒张压，但在四氧嘧啶处理2周后的大鼠中，这种降压作用明显较弱。吲哚美辛消除了正常和糖尿病动物中花生四烯酸诱导的降压反应。硝普钠诱导的低血压在非糖尿病和胰岛素缺乏大鼠中的程度相同。1周和2周糖尿病大鼠的血栓素B2血浆水平均显著升高，后一组更高；在2周糖尿病期间，6-酮-前列环素F1α的血浆水平保持不变。结论是，糖尿病导致对花生四烯酸的降压反应减弱可能是由于血栓素/前列环素平衡的改变，血栓素形成增加而前列环素生成未受影响。
