Abbas N A, Taube C, Hirschelmann R, Mest H J
Department of Pharmacology, School of Medicine, Martin Luther University Halle-Wittenberg, FRG.
Biomed Biochim Acta. 1991;50(7):937-41.
The thromboxane A2 (TXA2) plasma level in kappa-carrageenin (KC)-induced acronecrosis in the rat tail has been studied. TXB2 as stable metabolite of TXA2 was determined by a radioimmunoassay (RIA). 30 min after KC i.v. injection, the increase in the plasma TXB2 level was highest in Barby:Wistar rats but not in Halle:Wistar rats. Lambda-carrageenin (LC) increased the TXB2 levels in both strains of Wistar rats, although it did not induce acronecrosis. Drugs inhibiting TXB2 formation, namely dexamethasone, acetylsalicylic acid, Hoe 944, R 68070 or chlorpromazine, had only a small effect on acronecrosis frequency. Heparin inhibited TXB2 formation and acronecrosis frequency while the serotonin antagonist cyproheptadine decreased only the acronecrosis frequency but caused no change in TXB2 plasma level. These data demonstrate that the kappa-carrageenin-induced acronecrosis is followed by an increased formation of TXA2 in rats.
研究了κ-角叉菜胶(KC)诱导的大鼠尾部急性坏死中血栓素A2(TXA2)的血浆水平。通过放射免疫分析(RIA)测定作为TXA2稳定代谢产物的TXB2。静脉注射KC 30分钟后,巴比:Wistar大鼠血浆TXB2水平升高最高,但哈勒:Wistar大鼠则不然。λ-角叉菜胶(LC)增加了两种品系Wistar大鼠的TXB2水平,尽管它不会诱导急性坏死。抑制TXB2形成的药物,即地塞米松、乙酰水杨酸、Hoe 944、R 68070或氯丙嗪,对急性坏死频率只有很小的影响。肝素抑制TXB2形成和急性坏死频率,而血清素拮抗剂赛庚啶仅降低急性坏死频率,但不会改变TXB2血浆水平。这些数据表明,κ-角叉菜胶诱导的急性坏死之后,大鼠体内TXA2的形成会增加。