急性一氧化碳中毒后迟发性脑病患者血清NO与NOS水平及其临床意义

Clinical significance of serum levels of NO and NOS in patients with delayed encephalopathy after acute carbon monoxide poisoning.

目的探讨血清一氧化氮(nitric oxide,NO)、一氧化氮合酶(nitric oxide synthsae,NOS)的水平及其动态变化与急性一氧化碳中毒后迟发性脑病(delayed encephalopathy after acute carbon monoxide poisoning,DEACMP)患者病情变化的关系。方法应用比色法(colorimetric method)动态测定31例DEACMP患者血清NO及NOS水平,并与30例急性一氧化碳中毒(acute carbon monoxide poisoning,ACMP)后未发生迟发脑病患者和30例正常对照进行比较。结果 DEACMP患者急性期血清NO及NOS水平[(62.67±14.39)μmol/L,(27.68±6.14)U/mL]明显高于正常对照组[(50.18±9.95)μmol/L,(20.88±6.32)U/mL](均P<0.05),与ACMP组急性期[(62.00±16.46)μmol/L,(28.13±5.23)U/mL]比较无统计学差异(均P>0.05);DEACMP患者恢复期血清NO及NOS水平[(54.66±11.73)μmol/L,(21.74±5.88)U/mL]明显低于急性期(均P<0.05),与ACMP组随访期[(52.79±11.22)μmol/L,(20.64±5.92)U/mL]比较无统计学差异(均P>0.05)。结论 NO-NOS系统参与了DEACMP的发病机制,NO-NOS水平变化与病情变化基本一致。

Objective To investigate the association between serum nitric oxide （NO）, nitric oxide synthsae （NOS） level and their dynamic changes versus condition changes in patients with delayed encephalopathy after acute carbon monoxide poisoning （DEACMP）. Methods By using colorimetric method, the serum NO and NOS level in 31 patients with DEACMP were determined, in comparison with those in 30 patients of acute carbon monoxide poisoning without DEACMP and 30 normal controls, respectively. Results The serum NO and NOS levels [（62.67 ± 14.39） μmol/L, （27.68 ± 6.14） U/mL] in DEACMP group at acute stage were significantly higher than those [ （50.18 ± 9.95） μmol/L, （20.88± 6.32） U/mL in controls （All P 〈 0.05）, but were not significantly different from those [（62.00± 16.46） μ mol/L, （28.13 ± 5.23） U/mL in acute carbon monoxide poisoning （ACMP） group at acute stage （All P 〉 0.05）. The serum NO and NOS levels [（54.66± 11.73） μmol/L, （21.74± 5.88） U/roLl in DEACMP group at convalescent stage were significantly lower than those at acute stage （All P 〈 0.05）, but were not significantly different from those [（52.79± 11.22） μmol/L, （20.64 ± 5.92）U/mL] in ACMP group at follow-up stage （All P 〉 0.05）. Conclusions NO-NOS system was involved in the pathogenesis of DEACMP and the level variation of NO-NOS was consistent with the condition change.