Zhang Q Z, Wang Q, Zhang C F, Ling X Z, Liu W Y, Jin L Y
Department of Pharmacology, Ji-ning Medical College, China.
Zhongguo Yao Li Xue Bao. 1994 May;15(3):226-8.
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 cyproheptadine (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 thromboxane B2(TXB2) and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) contents in plasma. The results indicated that the TXB2 and 6-keto-PGF1 alpha 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 vs 990 +/- 943, P < 0.05). We conclude that the decrease of TXB2 content is one of the possible mechanisms of cyproheptadine anti-shock effect.
通过颈动脉放血使26只兔子产生深度失血性休克,直至血压(BP)=5.3千帕(40毫米汞柱),持续90分钟。兔子被平均分为赛庚啶(Cyp)治疗组和对照组。在休克前、休克90分钟后以及液体和血液输注并给予赛庚啶(10毫克·千克-1)30分钟后,从颈动脉采集血样。采用放射免疫分析法,我们测定了血浆中血栓素B2(TXB2)和6-酮前列腺素F1α(6-酮-PGF1α)的含量。结果表明,休克期间(1024±924,30±32)以及液体和血液输注后(990±943,60±54)的TXB2和6-酮-PGF1α水平高于正常兔子(221±134,6±4)(P<0.01,P<0.05)。赛庚啶明显降低了休克兔子血浆中TXA2水平(304±299对990±943,P<0.05)。我们得出结论,TXB2含量降低是赛庚啶抗休克作用的可能机制之一。