急性一氧化碳中毒家兔红细胞微观血流变学变化及其意义的探讨

Microrheological changes of erythrocyte in cerebral circulation of rabbits with acute carbon monoxide poisoning and their significance

目的探讨急性一氧化碳（CO）中毒家兔红细胞微观血流变学变化及其在急性CO中毒迟发性脑病（DEACMP）发病中的作用。方法通过腹腔注射CO方法制备急性CO中毒模型,使血中HbCO浓度达到50%以上持续30~36 h。动态检测初次染毒后6 h及末次染毒后30 min、24 h、3 d、5 d、7 d、14 d时颈静脉血红细胞变形性、红细胞渗透脆性、红细胞膜流动性、红细胞电泳率、红细胞脂质过氧化产物丙二醛（MDA）等指标的变化并进行分析。结果与正常对照组相比,家兔末次染毒后30 min红细胞变形性、红细胞渗透脆性、膜流动性显著下降,逐渐恢复后,于第3天再次降低,持续约14 d;末次染毒后30 min,红细胞电泳率增快,而后逐渐恢复正常,但3 d后其值逐渐减慢,持续约14 d;红细胞脂质过氧化产物MDA含量于末次染毒后30 min明显升高,而后虽然出现下降趋势,但中毒3 d后再次升高,14 d时仍高于正常。结论急性CO中毒早期和后期均出现了红细胞变形性、膜流动性、渗透脆性、电泳率等流变学指标的异常变化;红细胞微观血流变学的此种异常变化不仅加速了急性CO中毒早期脑组织缺血缺氧性病变的发生,而且很有可能在急性CO中毒迟发性脑病的发病中发挥至关重要的作用;而红细胞脂质过氧化损伤则可能是造成红细胞上述流变学异常变化的病因学基础。

Objective To investigate the microrheological changes of erythrocytes in cerebral circulation of rabbits after acute carbon monoxide（CO）poisoning and their possible roles in etiology of acute CO poisoning and delayed encephalopathy.Methods The animal model was prepared by intraperitoneal injection of CO at regular interval and the level of HbCO in blood reached above 50% for 30～36 h.Then RBCs＇ deformability,osmotic fragility,membrane fluidity,viscoelasticity and MDA were measured at 6 h after the first exposure,30 min,1 d,3 d,5 d,7 d,and 14 d after the last exposure.Results Compared with control,the parameters including RBCs＇ deformability,osmotic fragility,membrane fluidity decreased significantly at 30 min after the last exposure and dropped again from 3 d and recovered to normal levels till 14 d.The RBC electrophoresis rate increased at 30 min and then recovered.The content of RBC lipid peroxidation product MDA augmented remarkably at 30 min and then dropped.But the high level of MDA was kept till 14 d.Conclusion We observed the abnormalities in hemorheological parameters in the early and late stages of acute CO poisoning.These hemorheological changes may not only accelerate the happening of ischemia in brain tissues at the early stage of acute CO poisoning but also play an important role in the etiology of DEACMP.The RBC lipid peroxidation may be the pathological basis for the abnormalities of hemorheology.