摘要
目的探讨慢性阻塞性肺疾病(COPD)患者低氧血症对血清肌钙蛋白I(CTnI)的影响.方法对137例急性发作期的COPD患者的血氧分压p(O2)和血清CTnI及心肌酶谱进行检测,按氧分压的水平分成3组,观察CTnI及心肌酶谱的变化,并分析COPD患者p(O2)与CTnI及各种心肌酶的相关关系.结果轻、中、重度低氧血症组的CTnI分别为(0.15±0.08)μg/L,(0.87±0.92)μg/L和(2.24±0.97)μg/L,3组间均有显著差异(P<0.05).而3组p(O2)水平与相对应的CTnI水平呈显著的负相关关系(r=0.968 1,P<0.05).死亡患者8例,平均CTnI为(3.62±1.08)μg/L,与存活病例比较显著升高(P<0.05).结论低氧血症可导致COPD患者血清CTnI显著升高,且与氧分压p(O2)呈显著负相关关系.当CTnI明显升高时,提示患者病情危重.
Objective To investigate the effects of press of Oxygen p (O 2) on serum cardiac tropnin I(CTnI) in patients suffering from chronic obstruct pulmonary disease(COPD).Methods Serum CTnI, the myocardial enxymes and p (O 2) were measured. In three groups, observe the changes and relations between CTnI and p (O 2).Results The values of CTnI were (0.15±0.08)μg/L in patients with mild hypoxemia COPD, (0.87±0.92)μg/L in patients with moderate hypoxemia COPD, (2.24±0.97)μg/L in the patients with severe hypoxemia COPD (2.24±0.97)μg/L. There were significant differences in three groups ( P < 0.05 ). p (O 2) in patients of three groups had a negative relation with CTnI( r =-0.968?1, P <0.05). CTnI in average were(3.62±1.08)μg/L. In 8 patients of death, the CTnI level were significantly higher than those of the survival patients( P <0.05) .Conclusion Hypoxemia may significantly lead to increase of CTnI of patients with COPD, but it had a significant negative relation with p (O 2) level. When level of CTnI increases, it may attention to severed symptom in the patients.
出处
《北华大学学报(自然科学版)》
CAS
2003年第1期43-44,46,共3页
Journal of Beihua University(Natural Science)
基金
吉林省卫生厅科学基金资助项目 (986 92 )