动物试验表明:在肾组织受损时,影响血管扩张剂前列环素和血管收缩剂血栓恶烷A_2(TxA_2)的合成,TxA_2可引起免疫性或毒性肾小球损害时尿蛋白的丢失。从患抗基底膜肾小球肾炎的鼠中分离出肾小球合成的TxA_2比正常肾小球显著增加,且合成的增多与蛋白尿有关。同样,从患阿霉素肾病(人类微小病变性肾病的模型)的鼠中分离出肾小球合成的TxA_2比正常鼠也显著增多,同时该鼠尿液中TxB_2的排泄亦 Animal experiments show that when renal tissue is impaired, the synthesis of prostacyclin and vasoconstrictor thromboxane A_2 (TxA_2), which is a vasodilator, can be affected. TxA 2 can cause the loss of urinary protein in immune or toxic glomerular lesions. Isolated from glomerular basement membrane glomerulonephritis rats glomerular synthesis of TxA 2 increased significantly than normal glomeruli, and the increased synthesis of proteinuria. Similarly, TxA 2 synthesis from glomerulus was significantly increased in rats with adriamycin nephropathy (a model of human minimal neoplastic disease) than in normal mice, and TxB 2 excretion