Zhang Q Z, Zhang C F, Wang Q, Li J M, Ling X Z
Department of Pharmacology, Jining Medical College.
Chin Med J (Engl). 1994 May;107(5):323-5.
Profound hemorrhagic shock was produced in thirty rabbits by exsanguination via the carotid artery until blood pressure (BP) reached 5.3 kPa (40 mmHg) and was sustained for a period of 90 minutes. The rabbits were equally divided into cyproheptadine (Cyp) treated group and control group. Blood samples 30 minutes after liquid and blood infusion and administration of Cyp (10 mg/kg) were collected from the carotid artery, and the plasma superoxide dismutase (SOD) activity and malondialdehyde (MDA) content measured. The results showed that Cyp remarkably enhanced the plasma SOD activity (2462 +/- 338 vs 1955 +/- 596, P < 0.01) and reduced MDA content (2.68 +/- 0.24 vs 3.20 +/- 0.49, P < 0.01). We believe that the increase of O2 production plays an important role in the development of shock, the single blood and liquid infusion can not significantly improve the shock conditions. Scavenging oxygen free radicals and alleviating cellular damage and multiple organ failure are the possible mechanisms of cyproheptadine anti-shock effect.
通过颈总动脉放血使30只家兔产生严重失血性休克,直至血压(BP)降至5.3 kPa(40 mmHg)并维持90分钟。将家兔平均分为赛庚啶(Cyp)治疗组和对照组。在输注液体和血液并给予赛庚啶(10 mg/kg)30分钟后,从颈总动脉采集血样,测定血浆超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果显示,赛庚啶显著提高了血浆SOD活性(2462±338对1955±596,P<0.01)并降低了MDA含量(2.68±0.24对3.20±0.49,P<0.01)。我们认为,氧产生增加在休克发展中起重要作用,单纯输注血液和液体不能显著改善休克状况。清除氧自由基、减轻细胞损伤和多器官功能衰竭是赛庚啶抗休克作用的可能机制。