中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2010年
10期
621-623
,共3页
王鹏军%宋荣蓉%张卓伯%申东方
王鵬軍%宋榮蓉%張卓伯%申東方
왕붕군%송영용%장탁백%신동방
基质金属蛋白酶-9%脑梗死,急性%溶栓
基質金屬蛋白酶-9%腦梗死,急性%溶栓
기질금속단백매-9%뇌경사,급성%용전
Matrix metallo proteinases-9%Acute cerebral infarction%Thrombolysis
目的 探讨血浆基质金属蛋白酶-9(MMP-9)在急性脑梗死患者溶栓治疗后的变化及临床意义.方法 测定34例急性脑梗死患者溶栓前后血浆MMP-9水平,并与健康对照组(34例)比较.结果 急性脑梗死患者溶栓前MMP-9水平较健康对照组无明显升高[(13.47±3.09)ng/L比(12.89±10.22)ng/L,P＞0.05],溶栓后MMP-9水平[(22.06±12.53)ng/L]较健康对照组和溶栓前均显著升高(均P＜0.05).溶栓后发生出血患者(发生率26.5%,9/34)MMP-9水平较溶栓前显著增加[(24.02±15.41)ng/L比(14.28±2.33)ng/L,P＜0.05];与无出血患者[(20.42±9.57)ng/L]相比有增高趋势,但差异无统计学意义(P＞0.05).溶栓后完全再通患者(再通率58.8%,20/34)MMP-9水平较溶栓前明显升高[(19.26±7.94)ng/L比(13.63±3.02)ng/L,P＜0.05];与不完全再通患者[(18.97±4.23)ng/L]相比有增高趋势,但差异无统计学意义(P＞0.05).结论 溶栓后激活了MMP-9,MMP-9增加溶栓后出血的风险并参与了溶栓后出血的机制.
目的 探討血漿基質金屬蛋白酶-9(MMP-9)在急性腦梗死患者溶栓治療後的變化及臨床意義.方法 測定34例急性腦梗死患者溶栓前後血漿MMP-9水平,併與健康對照組(34例)比較.結果 急性腦梗死患者溶栓前MMP-9水平較健康對照組無明顯升高[(13.47±3.09)ng/L比(12.89±10.22)ng/L,P＞0.05],溶栓後MMP-9水平[(22.06±12.53)ng/L]較健康對照組和溶栓前均顯著升高(均P＜0.05).溶栓後髮生齣血患者(髮生率26.5%,9/34)MMP-9水平較溶栓前顯著增加[(24.02±15.41)ng/L比(14.28±2.33)ng/L,P＜0.05];與無齣血患者[(20.42±9.57)ng/L]相比有增高趨勢,但差異無統計學意義(P＞0.05).溶栓後完全再通患者(再通率58.8%,20/34)MMP-9水平較溶栓前明顯升高[(19.26±7.94)ng/L比(13.63±3.02)ng/L,P＜0.05];與不完全再通患者[(18.97±4.23)ng/L]相比有增高趨勢,但差異無統計學意義(P＞0.05).結論 溶栓後激活瞭MMP-9,MMP-9增加溶栓後齣血的風險併參與瞭溶栓後齣血的機製.
목적 탐토혈장기질금속단백매-9(MMP-9)재급성뇌경사환자용전치료후적변화급림상의의.방법 측정34례급성뇌경사환자용전전후혈장MMP-9수평,병여건강대조조(34례)비교.결과 급성뇌경사환자용전전MMP-9수평교건강대조조무명현승고[(13.47±3.09)ng/L비(12.89±10.22)ng/L,P＞0.05],용전후MMP-9수평[(22.06±12.53)ng/L]교건강대조조화용전전균현저승고(균P＜0.05).용전후발생출혈환자(발생솔26.5%,9/34)MMP-9수평교용전전현저증가[(24.02±15.41)ng/L비(14.28±2.33)ng/L,P＜0.05];여무출혈환자[(20.42±9.57)ng/L]상비유증고추세,단차이무통계학의의(P＞0.05).용전후완전재통환자(재통솔58.8%,20/34)MMP-9수평교용전전명현승고[(19.26±7.94)ng/L비(13.63±3.02)ng/L,P＜0.05];여불완전재통환자[(18.97±4.23)ng/L]상비유증고추세,단차이무통계학의의(P＞0.05).결론 용전후격활료MMP-9,MMP-9증가용전후출혈적풍험병삼여료용전후출혈적궤제.
Objective To investigate the changes in the content of plasma matrix metallo proteinase-9 (MMP-9) in patients with acute cerebral infarction before and after thrombolytic therapy and its clinical significance. Methods The levels of MMP-9 were determined in 34 patients with acute cerebral infarction before and after thrombolytic therapy, and 34 healthy individuals served as healthy control. Results Compared with the healthy controls, the levels of plasma MMP-9 before thrombolytic therapy were not significantly increased [(13. 47 ± 3.09) ng/L vs. (12.89 ± 10. 22) ng/L, P＞ 0. 05]. In contrast, MMP-9 values were significantly increased after thrombolytic therapy [(22. 06±12. 53) ng/L] compared with that in either before or healthy control group (both P＜0. 05). MMP-9 values were significantly higher in patients with hemorrhage after thrombolytic therapy (incidence rate was 26.5%, 9/34) compared with before treatment [(24. 02± 15.41) ng/L vs. (14. 28± 2. 33) ng/L, P＜0. 05], and the values of MMP-9 were higher than those of patients without hemorrhage [(20. 42±9. 57) ng/L], but there was no statistically significant difference (P＞0. 05). In patients with complete revascularization (revascularization rate was 58. 8%, 20/34), MMP-9 level was markedly higher than before thrombolytic therapy after thrombolytic therapy [(19.26±7. 94) ng/L vs. (13. 63±3. 02) ng/L, P＜0. 05], and the values of MMP-9 were higher than the no-revascularization patients [( 18. 97 ± 4. 23) ng/L], but there was no statistically significant difference (P＞0. 05). Conclusion Thrombolytic therapy activated MMP-9, and MMP-9 increased the risk of hemorrhage after thrombolytic therapy, and it participated in the mechanisms of hemorrhagic tendency after thrombolysis.
