CAJ | 학술논문

目的研究脑缺血后即时亚低温干预对脑缺血损伤的影响.方法将48只SD大鼠随机分为假手术组(8只)、常温(37～38℃)脑缺血组(8只)和哑低温(33～34℃)脑缺血组(32只),后者又根据亚低温持续作用时间细分为4个亚组(n=8).将常温脑缺血组和亚低温脑缺血组大鼠制成全脑缺血20 min、再灌注240 min模型.亚低温脑缺血组大鼠于脑缺血20 min时给予亚低温治疗,4个亚组亚低温持续作用时间分别为30,60,120,240 min.于脑缺血再灌注240 min后检查上述各组大鼠脑组织中一氧化氮(NO)代谢产物亚硝酸盐(NO2)、内皮素-1(ET1)、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β含量;同时对各组大鼠血液中乳酸脱氢酶(LDH)、肌酸激酶(CK)和天门冬氨酸氨基转移酶(AST)及肌酸激酶脑型同工酶(CK-BB)水平进行检测.结果常温脑缺血组大鼠脑组织中ET1、NO2、TNF-α和IL-1β水平均明显高于假手术组(P<0.01);亚低温持续作用30 min对脑缺血组织中ET1、NO2、TNF-α和IL-1β含量无明显影响(P>0.05);亚低温持续作用60～240 min可显著降低脑缺血组织中ET1、NO2、TNF-α和IL-1β水平(P<0.05或0.01).常温脑缺血组大鼠血液中LDH、AST、CK和CK-BB水平均明显高于假手术组(P<0.01);亚低温持续作用60～240 min可显著减少脑缺血大鼠血液中LDH、AST、CK和CK-BB含量(P<0.05或0.01).结论脑缺血后即时亚低温干预能明显减轻脑缺血损伤,亚低温持续作用时间以超过1 h为宜.
목적 연구뇌결혈후즉시아저온간예대뇌결혈손상적영향.방법 장48지SD대서수궤분위가수술조(8지)、상온(37～38℃)뇌결혈조(8지)화아저온(33～34℃)뇌결혈조(32지),후자우근거아저온지속작용시간세분위4개아조(n=8).장상온뇌결혈조화아저온뇌결혈조대서제성전뇌결혈20 min、재관주240 min모형.아저온뇌결혈조대서우뇌결혈20 min시급여아저온치료,4개아조아저온지속작용시간분별위30,60,120,240 min.우뇌결혈재관주240 min후검사상술각조대서뇌조직중일양화담(NO)대사산물아초산염(NO2)、내피소-1(ET1)、종류배사인자-α(TNF-α)화백세포개소-1β함량;동시대각조대서혈액중유산탈경매(LDH)、기산격매(CK)화천문동안산안기전이매(AST)급기산격매뇌형동공매(CK-BB)수평진행검측.결과 상온뇌결혈조대서뇌조직중ET1、NO2、TNF-α화IL-1β수평균명현고우가수술조(P<0.01);아저온지속작용30 min대뇌결혈조직중ET1、NO2、TNF-α화IL-1β함량무명현영향(P>0.05);아저온지속작용60～240 min가현저강저뇌결혈조직중ET1、NO2、TNF-α화IL-1β수평(P<0.05혹0.01).상온뇌결혈조대서혈액중LDH、AST、CK화CK-BB수평균명현고우가수술조(P<0.01);아저온지속작용60～240 min가현저감소뇌결혈대서혈액중LDH、AST、CK화CK-BB함량(P<0.05혹0.01).결론 뇌결혈후즉시아저온간예능명현감경뇌결혈손상,아저온지속작용시간이초과1 h위의.
Objective To study the effect of mild brain hyothermia on cerebral ischemic injury. Methods Global cerebral ischemia was established by modified Pulsinelli 4-vessel occlusion model. Forty-eight Sprague-Dawley rats were divided into 4 group: a sham-operated group, a normothermia (37～38℃) ischemic group and a mild is-chemic hypothermia (31～32℃) group; the mild ischemic hypothermia was subdivided into 4 groups with the hypo-thermia lasting for 30 min, 60 min, 120 min and 240 min, respectively. After 240 rain of reperfusion following 20 min cerebral ischemia, the levels of nitric oxide products nitrite (NO2) ,endothelin-1 (ET1) , tumor necrosis fac-tor alpha (TNFα) and interleukin-1 beta (IL-1β) in brain tissue and the lactate dehydrogenase (LDH), aspartate aminotransferase(AST) , creatine kinase(CK) and its brain band isoenzyme (CK-BB) in plasma were measured. Results The levels of IL-1β,TNFα, ET1 and NO2. in brain tissue, and the amounts of LDH, AST, CK and CK-BB in serum were higher in normothermia ischemic group than those in sham-operated group (P <0.05). Mild hypother-mia lasting for 60 min to 240 min markedly decreased the levels of IL-1β, TNF-α, ET1 and NO2 in brain tissue, and the amounts of LDH, AST, CK and CK-BB in serum in normothermia ischemic group, when compared with normo-thermia ischemic group (P < 0.05 or P < 0.01). Mild hypothermia lasting for 30 min did not influence the content of IL-1β, TNF-α, ET1 and NO2 in brain tissue when compared with normothermia isehemia group (P > 0.05). Con-clusion Mild brain hypothermia post-ischemia can significantly suppress the inflammation response in ischemic brain tissue and stabilize the function of cell membrane. The best neuroprotection of mild brain hypothermia must be carried out immediately and last for more than 60 minutes.