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在抗Ｔｈｙ１．１抗体所玫的大鼠系膜增殖性肾炎模型中，研究了白细胞衍生的ＴＸ及ＬＴ参与急性肾功能减迟的肾小球血液动力学机理。在肾炎鼠ｋｆ，ＧＦＲ及ＲＢＦ的急性降低伴有肾小球白细胞计数的升高及肾小球ＴＸＢ２，ＬＴＢ４的合成增多。除去白细胞可抑制ＴＸＢ２，ＬＴＢ４的合成外，能完全防止ＧＦＲ及ＲＢＦ的降低。合用ＴＸ合成酶抑制剂及花生四烯酸５－脂氧化酶抑制剂也防止了ＧＦＲ及ＲＢＦ的降低，分别抑制ＴＸ合成酶或５－脂氧化酶仅可部分防止ＧＦＲ及ＲＢＦ的降低。ＴＸ受体拮抗剂或５－脂氧化酶抑制剂可防止入球小动脉阻力的升高及ｋｆ的减少。结果表明，浸润于肾小球的白细胞所衍生的ＴＸ，ＬＴ通过收缩入球小动脉、减少ｋｆ，而参与系膜增殖性肾炎模型的急性肾功能减退。
In a rat mesangial proliferative glomerulonephritis model that is resistant to anti-Thy1.1 antibodies, glomerular hemodynamics of leukocyte-derived TX and LT are involved in the acute renal failure. In nephritis rats kf, GFR and RBF acute reduction accompanied by increased glomerular white blood cell count and glomerular TXB2, LTB4 synthesis increased. Removal of leukocytes can inhibit TXB2, LTB4 synthesis, can completely prevent the GFR and RBF reduction. Combination of TX synthase inhibitors and arachidonic acid 5-lipoxygenase inhibitors also prevented a reduction in GFR and RBF, and inhibition of TX synthase or 5-lipoxygenase, respectively, only partially prevented a decrease in GFR and RBF. TX receptor antagonists or 5-lipoxygenase inhibitors prevent increased arteriolar resistance and decreased kf. The results showed that leukocytes infiltrating glomerular derived TX and LT are involved in the acute renal dysfunction of mesangial proliferative glomerulonephritis model by contracting into the arterioles and reducing kf.