摘要
目的 :探讨急性冠状动脉综合征 (ACS)患者外周血可溶性细胞粘附分子 1(sICAM 1)和转化生长因子 β(TGF β)浓度变化及其意义。方法 :符合ACS诊断的 4 5例于入院后 1h内抽取肘静脉血5ml,测定sICAM 1和TGF β ,同时测定肌酸激酶 (CK)、乳酸脱氢酶 (LDH)、肌酸激酶同工酶 (CK MB) ,并设健康对照组。结果 :血浆sICAM 1水平显著升高 ,其中不稳定型心绞痛 (UAP)为 35 9.0 8± 35 .12 μg/L,非Q波性急性心肌梗死 (NQAMI)为 4 95 .34± 4 9.16 μg/L、Q波性急性心肌梗死(AMI)为 5 83.5 1± 5 4 .2 7μg/L,与对照组 (2 5 3.5 1± 38.4 3μg/L)比较有显著差异 (P <0 .0 0 1) ;血浆TGF β浓度明显下降 ,其中UAP为4 6 .72± 10 .15 μg/L,NQAMI为 4 1.6 9± 9.0 8μg/L,AMI为36 .72± 8.79μg/L,与对照组 (6 2 .10± 14 .4 6 μg/L)比较有显著差异 (P <0 .0 0 1)。sICAM 1与TGF β呈显著负相关 ;sICAM 1和CK、CK MB、LDH呈显著正相关 (P <0 .0 1)。结论 :血清sICAM 1和TGF β浓度的变化反映了ACS患者炎症和免疫状态 ,抑制致炎因子的作用 ,适度增强抗炎因子的作用 。
Objective: To investigate the changes and significance of plasma intercellular adhesion molecule 1 (sICAM 1) and transforming growth factor β (TGF β) in patients with acute coronary syndrome (ACS). Methods: 5 ml blood was drawn from cubital vein in 45 patients with ACS within the 1st hour of hospitalization. sICAM 1 and TGF β were measured while creatine kinase(CK), MB isoenzyme of creatine kinase(CK MB) and lactate dehydrogenase(LDH) were detected at same time. Healthy people were regarded as control group. Results: Plasma sICAM 1 level was increased significantly: unstable angina pectoris group (UAP) was 359.08±35.12 , non Q wave acute myocardial infarction group (NQMI) was 495.34±49.16 , Q wave acute myocardial infarction group (AMI) was 583.51±54.27 . As compared with the control group ( 253.51±38.43 ), there was a significant difference ( P < 0.001 ). Plasma TGF β level was decreased significantly (UAP 46.72±10.15 , NQMI 41.69±9.08 , AMI 36.72±8.79 ) in comparison with control group ( 62.10±14.46 ) ( P < 0.001 ). There was a significant negative correlation between sICAM 1 and TGF β( P < 0.01 ), and significant positive correlation between sICAM 1 and CK, CK MB, LDH ( P < 0.01 ). Conclusion: The changes of sICAM 1 and TGF β levels may reflect the immunological and inflammatory status of the patients with ACS. It might be a new way to prevent and treat ACS with suppression of the inflammatory cytokine and improve the action of anti inflammatory cytokines.
出处
《内科急危重症杂志》
2002年第4期190-192,共3页
Journal of Critical Care In Internal Medicine
