摘要
目的 探讨内源性一氧化碳 (CO)在新生大鼠缺氧缺血性脑损伤 (HIBD)中的作用机制及锡原卟啉的保护作用。方法 取7日龄新生SD大鼠30只 ,平均分成3组,1组为正常对照组 ,另2组为干预组和非干预组 ,分别于HIBD模型建立后立即腹腔注射锡原卟啉和9g/L氯化钠溶液 ,24h后用分光光度法检测全血一氧化碳血红蛋白 (COHb)水平 ,然后对脑组织进行HE染色 ,在光镜下观察脑组织病理变化。 结果 非干预组血COHb水平为7.54 %±0.72% ,高于正常对照组 (0.88%±0.07% )和干预组 (1.15%±0.21% ,均P<0.01)。干预组脑组织病变发生率 (30% )低于非干预组 (80% ,P<0.01)。结论 CO可能作为一种内源性介质参与新生大鼠HIBD的发病过程 ,锡原卟啉对HIBD具有保护和治疗作用。
Objective To study the role of endogenous carbon monoxide(CO) in newborn rats with hypoxic-ischemic brain damage (HIBD) and the protective effect of Sn-protoporphyrin (SnPP).Methods The serum COHb levels were detected in newborn rats with (HIBD). The SnPP was injected i.p to the rats and the effect on brain damage was observed.Results The serum COHb levels in the newborn rats with HIBD group(7.54%±0.72%)were significantly higher than those in the normal controls(0.88%±0.07%) and the treatment group(1.15%±0.21%)(P<0.01). The percentage of brain damage in SnPP treatment group (30%) was much lower than that in control group(80%)(P<0.01).Conclusion The present study suggests that CO as an endogenous mediator may take part in the pathogenesis of neonatal HIBD, and SnPP may have the protective effect on HIBD.
出处
《浙江医学》
CAS
2003年第2期80-81,共2页
Zhejiang Medical Journal
