中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2010年
4期
371-375
,共5页
羟乙基淀粉%再灌注损伤%白细胞介素-8%内皮素-1%髓过氧化物酶
羥乙基澱粉%再灌註損傷%白細胞介素-8%內皮素-1%髓過氧化物酶
간을기정분%재관주손상%백세포개소-8%내피소-1%수과양화물매
Hydroxyethyl starch%Reperfusion injury%Interleukin-8%Endothelin-1%Myeloperoxidase
目的 观察羟乙基淀粉(HES130/0.4)对兔心肌缺血一再灌注损伤的白细胞介素-8(IL-8)、内皮素-1(ET-1)和髓过氧化物酶(MPO)活性的影响,探讨其可能的保护机制.方法 36只大白兔随机分为乳酸林格氏液组(A组,n=12);白蛋白组(B组,n:12);羟乙基淀粉组(C组,n=12).A,B,C三组再灌注前15 min分别静脉注入6 mL/kg乳酸林格氏液、5%人体白蛋白或6%羟乙基淀粉,于缺血前(I_0)、缺血30 min(I_1)、再灌注60 min(R_1)、180 min(R_2)四个时点采血,检测血清乳酸脱氢酶(LDH)、肌酸磷酸激酶(CPK)、白细胞介素-8(IL-8)和内皮素-1(ET-1)的浓度.再灌注180 min处死大白兔测定心肌水含量、心肌梗死面积及髓过氧化物酶(MPO)活性.组间比较采用单因素方差分析(SNK-q检验),采用SPSS 12.0统计软件处理,以P＜0.05为差异有统计学意义.结果 三组血清LDH,CPK,IL-8和ET-1随再灌注时间延长而逐渐升高,在R2时点,C组增高的程度明显低于A组[(181±17)U/L vs.(334±39)U/L;(1927±205)U/L v8.(2987±326)U/L;(5.03±1.16)ng/L vs.(6.96±1.21)ng/L;(380.9±78.4)ng/L vs.(667.2±82.1)ng/L,P＜0.05]和B组[(181±17)u/Lvs.(320±38)U/L;(1927±205)U/L vs.(2218±290)U/L;(5.03±1.16)ng/L vs.(5.90±1.03)ng/L;(380.9±78.4)ng/L vs.(615.6±80.2)ng/L,P＜0.05];C组缺血区MPO活性(0.20±0.09)ng/L明显低于A组(0.48±0.15)ng/L和B组(0.37±0.12)ng/L(P＜0.05);C组的心肌含水量(76±8.23)%和心肌梗死面积(11.53±1.02)%分别显著低于A组[(86±5.66)%,(26.48±2.33)%]和B组[(82±6.42)%,(19.76±4.32)%](P＜0.05).结论 羟乙基淀粉对通过抑制IL-8及ET-1的生成和释放,降低缺血区MPO活性和毛细血管通透性,对缺血-再灌注损伤的心肌具有保护作用.
目的 觀察羥乙基澱粉(HES130/0.4)對兔心肌缺血一再灌註損傷的白細胞介素-8(IL-8)、內皮素-1(ET-1)和髓過氧化物酶(MPO)活性的影響,探討其可能的保護機製.方法 36隻大白兔隨機分為乳痠林格氏液組(A組,n=12);白蛋白組(B組,n:12);羥乙基澱粉組(C組,n=12).A,B,C三組再灌註前15 min分彆靜脈註入6 mL/kg乳痠林格氏液、5%人體白蛋白或6%羥乙基澱粉,于缺血前(I_0)、缺血30 min(I_1)、再灌註60 min(R_1)、180 min(R_2)四箇時點採血,檢測血清乳痠脫氫酶(LDH)、肌痠燐痠激酶(CPK)、白細胞介素-8(IL-8)和內皮素-1(ET-1)的濃度.再灌註180 min處死大白兔測定心肌水含量、心肌梗死麵積及髓過氧化物酶(MPO)活性.組間比較採用單因素方差分析(SNK-q檢驗),採用SPSS 12.0統計軟件處理,以P＜0.05為差異有統計學意義.結果 三組血清LDH,CPK,IL-8和ET-1隨再灌註時間延長而逐漸升高,在R2時點,C組增高的程度明顯低于A組[(181±17)U/L vs.(334±39)U/L;(1927±205)U/L v8.(2987±326)U/L;(5.03±1.16)ng/L vs.(6.96±1.21)ng/L;(380.9±78.4)ng/L vs.(667.2±82.1)ng/L,P＜0.05]和B組[(181±17)u/Lvs.(320±38)U/L;(1927±205)U/L vs.(2218±290)U/L;(5.03±1.16)ng/L vs.(5.90±1.03)ng/L;(380.9±78.4)ng/L vs.(615.6±80.2)ng/L,P＜0.05];C組缺血區MPO活性(0.20±0.09)ng/L明顯低于A組(0.48±0.15)ng/L和B組(0.37±0.12)ng/L(P＜0.05);C組的心肌含水量(76±8.23)%和心肌梗死麵積(11.53±1.02)%分彆顯著低于A組[(86±5.66)%,(26.48±2.33)%]和B組[(82±6.42)%,(19.76±4.32)%](P＜0.05).結論 羥乙基澱粉對通過抑製IL-8及ET-1的生成和釋放,降低缺血區MPO活性和毛細血管通透性,對缺血-再灌註損傷的心肌具有保護作用.
목적 관찰간을기정분(HES130/0.4)대토심기결혈일재관주손상적백세포개소-8(IL-8)、내피소-1(ET-1)화수과양화물매(MPO)활성적영향,탐토기가능적보호궤제.방법 36지대백토수궤분위유산림격씨액조(A조,n=12);백단백조(B조,n:12);간을기정분조(C조,n=12).A,B,C삼조재관주전15 min분별정맥주입6 mL/kg유산림격씨액、5%인체백단백혹6%간을기정분,우결혈전(I_0)、결혈30 min(I_1)、재관주60 min(R_1)、180 min(R_2)사개시점채혈,검측혈청유산탈경매(LDH)、기산린산격매(CPK)、백세포개소-8(IL-8)화내피소-1(ET-1)적농도.재관주180 min처사대백토측정심기수함량、심기경사면적급수과양화물매(MPO)활성.조간비교채용단인소방차분석(SNK-q검험),채용SPSS 12.0통계연건처리,이P＜0.05위차이유통계학의의.결과 삼조혈청LDH,CPK,IL-8화ET-1수재관주시간연장이축점승고,재R2시점,C조증고적정도명현저우A조[(181±17)U/L vs.(334±39)U/L;(1927±205)U/L v8.(2987±326)U/L;(5.03±1.16)ng/L vs.(6.96±1.21)ng/L;(380.9±78.4)ng/L vs.(667.2±82.1)ng/L,P＜0.05]화B조[(181±17)u/Lvs.(320±38)U/L;(1927±205)U/L vs.(2218±290)U/L;(5.03±1.16)ng/L vs.(5.90±1.03)ng/L;(380.9±78.4)ng/L vs.(615.6±80.2)ng/L,P＜0.05];C조결혈구MPO활성(0.20±0.09)ng/L명현저우A조(0.48±0.15)ng/L화B조(0.37±0.12)ng/L(P＜0.05);C조적심기함수량(76±8.23)%화심기경사면적(11.53±1.02)%분별현저저우A조[(86±5.66)%,(26.48±2.33)%]화B조[(82±6.42)%,(19.76±4.32)%](P＜0.05).결론 간을기정분대통과억제IL-8급ET-1적생성화석방,강저결혈구MPO활성화모세혈관통투성,대결혈-재관주손상적심기구유보호작용.
Objective To observe the effects of hydroethyl starch (HES 130/0.4) on serum interleukin-8, endothelin-l(ET-1) and myocardial myeloperoxidase activity (MP0) in rabbits subjected to ischemia-reperfusion, and to explore its possible mechanism. Method Thirty-six rabbits were randomly divided into three groups: lac-tated Ringer's solution group (group A, n= 12), 5% human albumin group (group B, n= 12) and 6% hy-droethyl starch group (group C, n= 12) Hie myodardial ischemia/reperfusion (MI/R) model was established by clamping left anterior descending coronary artery for 30 minutes followed by reperfusion for 180 minutes. Fifteen minutes prior to reperfusion, animals of these 3 given groups were ifused vis right internal jugular vein with 6 ml/kg lactated Ringer'solution, 5% human albumin and hydroethyl starch, respectively. Blood samples were obtained before occlusion (I_0),30 minutes after occlusion (I_1), 60 minutes (R_1) and 180 (R_2) minutes after reperfusion to determine the activities of serum lactate dehydrogenase (LDH), serum creatine phosphokinase (CPK), serum interleukin-8(IL-8) and endotheun-1 (ET-1).The size of myocardial infarction (MI),myocardial water content and myoloperoxidase activity (MPO) were examined as well.Statistical analyses were performed by using SPSS 12.0 software. Multiple comparisons were analyzed by using one-way analysis of variance (SNK- qtest). P ＜ 0.05 was considered statistically significant. Results The serum IDH, CPK,IL-8 and ET-1 weregradually increased after reperfusion, however, 180 min after reperfusion all serum biomarkers in 6% hydroethylstarch group (group C) were significantly lower than those in Iactated Ringer's solution group (group A) [(181 ±17) U/lvs. (334±39) U/L; (1927±205) U/L vs. (2987±326) U/L; (5.03±1.16) ng/L vs. (6.96±1.21) ng/L; (380±78.4) ng/L vs. (667.2±82.1) ng/L. all P ＜0.05], and than those in 5% human albu-min group (group B) [(181 ±17) U/L vs. (320±38) U/L; (1727 ±205) U/L vs. (2218 ±290) U/L; (5.03 ±1.16) ng/L vs. (5.90±1.03) ng/L; (380.9±78.4) ng/L vs. (615.6±80.2) ng/L, all P ＜0.05]. Theactivity of MPO of ischemic area in group C (0.20 ± 0.09 ng/L) was significantly lower than that in group A(0.48±0.15 ng/L) and in group B (0.37 ±0.12 ng/L) (P ＜ 0.05). Myocardial water content and infarct sizeof heart found in group C were significantly smaller than those in both group A and group B (P ＜ 0.05). Conclu-sions The 6% hydroethyl starch exhibits its protective effects on myocardial ischemia-reperfusion injury by pre-venting the production and release of serum IL-8 and ET-1, decreasing neutrophil infiltration capillary permeabilityand improving microvascular circulation.
