Altered prostaglandin synthesis in isolated lungs of rats with streptozotocin-induced diabetes.
Metabolism of exogenous and endogenous arachidonic acid (AA) to several cyclo-oxygenase products has been studied by bioassay, radioimmunoassay and radiochemical assay in isolated lungs from rats made diabetic with streptozotocin and compared with that occurring in lungs from untreated rats. From exogenous AA, more PGE2, PGF2 alpha and PGD2 were formed in diabetic lungs than in control lungs, although amounts of PGI2 and TxA2 formed did not differ between the two sets of lungs. From endogenous AA, the synthesis of PGI2 in diabetic lungs was nearly half that in controls lungs. Such a deficiency in the unstimulated synthesis of a potent anti-aggregatory substance would contribute to the hyperaggregable state observed in diabetes.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D015237:Dinoprost; D015232:Dinoprostone; D011464:Epoprostenol / Q000096:biosynthesis; D006651:Histocytochemistry / Q000379:methods; D066298:In Vitro Techniques; D008168:Lung / Q000378:metabolism*; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000096:biosynthesis; D011460:Prostaglandins F / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D013928:Thromboxane A2 / Q000096:biosynthesis
D001095:Arachidonic Acids; D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D013928:Thromboxane A2; D015237:Dinoprost; D011464:Epoprostenol; D015232:Dinoprostone