中国医药
中國醫藥
중국의약
China Medicine
2015年
9期
1278-1281
,共4页
李杰宾%杜庆霞%丁宁%王宇
李傑賓%杜慶霞%丁寧%王宇
리걸빈%두경하%정저%왕우
心肺复苏%右美托咪定%炎性因子%大鼠
心肺複囌%右美託咪定%炎性因子%大鼠
심폐복소%우미탁미정%염성인자%대서
Cardiopulmonary resuscitation%Dexmedetomidine%Inflammatory cytokine%Rat
目的 探讨右美托咪定对大鼠心肺复苏后早期炎性因子释放的影响.方法 选取36只SD雄性大鼠,按随机数字表法分为3组,每组12只.假手术组仅进行麻醉和气管插管、血管穿刺,不进行窒息及心肺复苏;心肺复苏组和右美托咪定组均采用窒息法制备大鼠心脏骤停模型,行标准心肺复苏,待自主循环恢复(ROSC)后,右美托咪定组即刻缓慢静脉注射右美托咪定50 μg/kg,心肺复苏组即刻给予等体积0.9％氯化钠注射液.分别在基础状态及ROSC后3、12、24 h抽取3组大鼠动脉血,采用酶联免疫吸附试验测定肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、细胞间黏附分子1(ICAM-1)及血管细胞黏附分子1(VCAM-1)的水平并进行比较.结果 假手术组大鼠均存活至ROSC后24 h;心肺复苏组大鼠经复苏后有11只恢复自主循环,其中9只存活至ROSC后24 h;右美托咪定组大鼠经复苏后有10只恢复自主循环,10只大鼠全部存活至ROSC后24 h.3组大鼠在基础状态下TNF-α、IL-1β、ICAM-1及VCAM-1水平比较差异无统计学意义(P＞0.05).心肺复苏组和右美托咪定组大鼠复苏后的炎性因子水平均增高,但右美托咪定组大鼠ROSC后3、12、24 h的TNF-α及IL-1β水平明显低于心肺复苏组[TNF-α,3 h:(23±5)ng/L比(40 ±6) ng/L,12 h:(39±9) ng/L比(84±10) ng/L,24 h:(49±9) ng/L比(92±9) ng/L; IL-1β,3 h:(65±24) ng/L比(101 ± 24) ng/L,12 h:(95±25) ng/L比(162±46) ng/L,24 h:(120±42) ng/L比(212±42) ng/L],差异均有统计学意义(均P＜0.05);右美托咪定组大鼠在复苏后24 h的ICAM-1和VCAM-1水平明显低于心肺复苏组大鼠[(7.9±2.3)μg/L比(18.6±6.3)μg/L,(9.9 ±3.7)μg/L比(20.5±7.3)μg/L],差异均有统计学意义(均P＜0.05).结论 右美托咪定能够抑制大鼠心肺复苏后早期炎性因子的释放,可能是其减轻全身炎性反应的作用机制之一.
目的 探討右美託咪定對大鼠心肺複囌後早期炎性因子釋放的影響.方法 選取36隻SD雄性大鼠,按隨機數字錶法分為3組,每組12隻.假手術組僅進行痳醉和氣管插管、血管穿刺,不進行窒息及心肺複囌;心肺複囌組和右美託咪定組均採用窒息法製備大鼠心髒驟停模型,行標準心肺複囌,待自主循環恢複(ROSC)後,右美託咪定組即刻緩慢靜脈註射右美託咪定50 μg/kg,心肺複囌組即刻給予等體積0.9％氯化鈉註射液.分彆在基礎狀態及ROSC後3、12、24 h抽取3組大鼠動脈血,採用酶聯免疫吸附試驗測定腫瘤壞死因子α(TNF-α)、白細胞介素1β(IL-1β)、細胞間黏附分子1(ICAM-1)及血管細胞黏附分子1(VCAM-1)的水平併進行比較.結果 假手術組大鼠均存活至ROSC後24 h;心肺複囌組大鼠經複囌後有11隻恢複自主循環,其中9隻存活至ROSC後24 h;右美託咪定組大鼠經複囌後有10隻恢複自主循環,10隻大鼠全部存活至ROSC後24 h.3組大鼠在基礎狀態下TNF-α、IL-1β、ICAM-1及VCAM-1水平比較差異無統計學意義(P＞0.05).心肺複囌組和右美託咪定組大鼠複囌後的炎性因子水平均增高,但右美託咪定組大鼠ROSC後3、12、24 h的TNF-α及IL-1β水平明顯低于心肺複囌組[TNF-α,3 h:(23±5)ng/L比(40 ±6) ng/L,12 h:(39±9) ng/L比(84±10) ng/L,24 h:(49±9) ng/L比(92±9) ng/L; IL-1β,3 h:(65±24) ng/L比(101 ± 24) ng/L,12 h:(95±25) ng/L比(162±46) ng/L,24 h:(120±42) ng/L比(212±42) ng/L],差異均有統計學意義(均P＜0.05);右美託咪定組大鼠在複囌後24 h的ICAM-1和VCAM-1水平明顯低于心肺複囌組大鼠[(7.9±2.3)μg/L比(18.6±6.3)μg/L,(9.9 ±3.7)μg/L比(20.5±7.3)μg/L],差異均有統計學意義(均P＜0.05).結論 右美託咪定能夠抑製大鼠心肺複囌後早期炎性因子的釋放,可能是其減輕全身炎性反應的作用機製之一.
목적 탐토우미탁미정대대서심폐복소후조기염성인자석방적영향.방법 선취36지SD웅성대서,안수궤수자표법분위3조,매조12지.가수술조부진행마취화기관삽관、혈관천자,불진행질식급심폐복소;심폐복소조화우미탁미정조균채용질식법제비대서심장취정모형,행표준심폐복소,대자주순배회복(ROSC)후,우미탁미정조즉각완만정맥주사우미탁미정50 μg/kg,심폐복소조즉각급여등체적0.9％록화납주사액.분별재기출상태급ROSC후3、12、24 h추취3조대서동맥혈,채용매련면역흡부시험측정종류배사인자α(TNF-α)、백세포개소1β(IL-1β)、세포간점부분자1(ICAM-1)급혈관세포점부분자1(VCAM-1)적수평병진행비교.결과 가수술조대서균존활지ROSC후24 h;심폐복소조대서경복소후유11지회복자주순배,기중9지존활지ROSC후24 h;우미탁미정조대서경복소후유10지회복자주순배,10지대서전부존활지ROSC후24 h.3조대서재기출상태하TNF-α、IL-1β、ICAM-1급VCAM-1수평비교차이무통계학의의(P＞0.05).심폐복소조화우미탁미정조대서복소후적염성인자수평균증고,단우미탁미정조대서ROSC후3、12、24 h적TNF-α급IL-1β수평명현저우심폐복소조[TNF-α,3 h:(23±5)ng/L비(40 ±6) ng/L,12 h:(39±9) ng/L비(84±10) ng/L,24 h:(49±9) ng/L비(92±9) ng/L; IL-1β,3 h:(65±24) ng/L비(101 ± 24) ng/L,12 h:(95±25) ng/L비(162±46) ng/L,24 h:(120±42) ng/L비(212±42) ng/L],차이균유통계학의의(균P＜0.05);우미탁미정조대서재복소후24 h적ICAM-1화VCAM-1수평명현저우심폐복소조대서[(7.9±2.3)μg/L비(18.6±6.3)μg/L,(9.9 ±3.7)μg/L비(20.5±7.3)μg/L],차이균유통계학의의(균P＜0.05).결론 우미탁미정능구억제대서심폐복소후조기염성인자적석방,가능시기감경전신염성반응적작용궤제지일.
Objective To investigate the influence of dexmedetomidine (DEX) on early release of inflammatory cytokines in rat models of cardiopulmonary resuscitation (CPR).Methods Thirty-six male SD rats were randonly divided into sham operation group,CPR group and DEX group.The rats in sham operation group only underwent anesthesia,endotracheal intubation and vascular puncture without asphyxia and CPR; the cardiac arrest model were established by using asphyxia method,then CPR was done in CPR group and DEX group; DEX group was injected with 50 μg/kg dexmedetomidine and CPR group was injected with the same volume 0.9％ sodium chloride immediately after recovery of spontaneous circulation (ROSC).The levels of serum tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β),intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were detected before CPR,3,12 and 24 h after ROSC by using enzyme-linked immunoabsorbent assay.Results All the rats in sham operation group survived for 24 hours ; in CPR group,11 rats recovered spontaneous circulation after CPR and 9 of them survived for 24 hours; in DEX group,10 rats recovered spontaneous circulation after CPR and all survived for 24 hours.Baseline levels of TNF-α,IL-1β,ICAM-l and VCAM-1 were not significantly different among the three groups (P ＞ 0.05).The levels of TNF-α,IL-1β,ICAM-l and VCAM-1 were all increased gradually in CPR group and DEX group after CPR; the levels of TNF-α,IL-1β were significantly lower in DEX group than those in CPR group 3,12 and 24 h after ROSC[TNF-α,3 h:(23 ±5) ng/L vs (40 ± 6) ng/L,12h:(39±9) ng/L vs (84±10) ng/L,24h:(49±9) ng/L vs (92±9) ng/L; IL-1β,3 h:(65± 24) ng/L vs (101 ±24) ng/L,12 h:(95 ±25) ng/L vs (162 ±46) ng/L,24 h:(120 ±42) ng/L vs (212 ± 42) ng/L] (all P ＜ 0.05) ; the levels of ICAM-l and VCAM-1 were significantly lower in DEX group than those in CPR group 24 h after ROSC [(7.9 ±2.3) μg/L vs (18.6 ±6.3) μg/L,(9.9±3.7) μg/L vs (20.5 ± 7.3) μg/L] (both P ＜0.05).Conclusion DEX can significantly inhibit early release of inflammatory cytokines after cardiopulmonary resuscitation,which may be one of the mechanisms for relieving systemic inflammatory reaction.
