【摘要】 26只兔被随机分为治疗组和对照组:颈动脉放血至血压5.3kPa,维持90 min,复制出血性休克模型。于休克前后,输液输血（对照组）和给药(治疗组,噻庚啶10 mg·kg^-1)后30nin分别由颈动脉采取血样,结果显示用药组血栓素B₂显著下降（P<0.05）,6-酮前列腺素F_1α升高不明显（P>0.05）。噻庚啶致血浆血栓素B₂水平下降是其抗休克作用机制之一。更多还原

【Abstract】 Profound hemorrhagic shock was produced in 26 rabbits by exsanguination via carotid artery until blood pressure (BP) = 5. 3 kPa (40 mmHg) for a period of 90 min. Rabbits were equally divided into a cyprohep-tadine (Cyp) treated group and a .control group. The blood samples before and 90 min after shock and 30 min after liquid and blood infusion and administering Cyp (10 mg·kg-1) were collected from the carotid artery. With radioimmunoassay, we measured the throm-boxane B2(TXB2) and 6-ketoprostaglandin F1a (6-keto-PGF1a) contents in plasma- The results indicated that the TXB2 and 6-keto-PGF1a levels during shock (1024 ±924, 30 ± 32) and after liquid and blood infusion (990± 943, 60±54) were higher than those (221 ± 134, 6±4) in normal rabbits (P<0. 01, P< 0.05). Cyp reduced obviously the TXA2 plasma level in rabbit with shock (304±299 vs990±943, P<0. 05). We conclude that the decrease of TXB2 content is one of the possible mechanisms of cyproheptadine anti-shock effect.更多还原