急性一氧化碳中毒大鼠血肌酸激酶同工酶BB的变化及治疗

Changes of CK-BB induced by acute carbon monoxide poisoning in rat models and the effects of hyperbaric oxygenation

目的 观察急性一氧化碳中毒 (ACOP)后大鼠血清肌酸激酶同工酶BB(creatinekinaseBB ,CK BB)的动态变化及高压氧 (hyperbaricoxygenation ,HBO)的影响。方法 制作大鼠一氧化碳中毒模型 ,随机分成 2个亚组 ,ACOP组和ACOP +HBO组 ,每个亚组再按观察时间分为ACOP和ACOP +HBO后 1、3、5、10和 2 0d组 ,正常对照 1组 ,预期处死后心脏取血测定不同组别血清CK BB的变化。结果 ACOP组 :ACOP后第 1dCK BB显著升高 ,与对照组比较差异有显著意义 ,P <0 .0 0 1;第 3d起明显下降 ,与对照组比较差异无显著性意义 ,P >0 .0 5 ;第 10d再次明显升高 ,P <0 .0 0 1;第 2 0d下降 ,与对照组比较差异无显著意义 ,P >0 .0 5。ACOP后立即进行高压氧治疗 (ACOP +HBO组 ) :CK BB活性虽有所升高 ,但与对照组比较差异无显著意义 ,P >0 .0 5。结论 ACOP后大鼠血清CK BB活性迅速明显升高 ,高压氧治疗组血清CK BB无明显升高 ,提示高压氧治疗是减轻ACOP急性脑损伤有效的治疗方法。

Objective To investigate the changes of plasma CK BB induced by acute carbon monoxide poisoning(ACOP) and the effect of hyperbaric oxygenation(HBO). Methods Murine models of ACOP were randomly divided into two groups: group ACOP and group ACOP+ HBO. Each group was supdivided groups of 1、 3、 5、 10 and 20 day, with one normal control group. Intracardiac blood sampling were initiated upon rat sacrificing duly for the determination of CK BB.Results In group ACOP, CK BB increased significantly compared with control 1 day after ACOP ( P <0.001), which decreased significantly 3 days latter ( P >0.05). the concentration of CK BB increased once again 10 days after ACOP ( P <0.001), which decreased significantly 20 days latter ( P >0.05). In group ACOP+HBO, CK BB insignificant increased ( P >0.05). Conclusion In rats with ACOP, CK BB increased significantly as a marker of ACOP induced cerebral injury. By the treatment with HBO, the injury was reversed indicating that HBO is an effective method for the treatment of ACOP.