中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
Chinese Journal of Anesthesiology
2015年
9期
1131-1133
,共3页
蒋婷婷%孙佳凤%夏江燕%邱晓东%袁静%陆新建%孙永瀛
蔣婷婷%孫佳鳳%夏江燕%邱曉東%袁靜%陸新建%孫永瀛
장정정%손가봉%하강연%구효동%원정%륙신건%손영영
肝素裂合酶%内毒素血症%多糖包被%内皮细胞
肝素裂閤酶%內毒素血癥%多糖包被%內皮細胞
간소렬합매%내독소혈증%다당포피%내피세포
Heparin lyase%Endotoxemia%Glycocalyx%Endothelial cells
目的 评价肝素酶在内毒素血症致大鼠血管内皮糖萼破坏中的作用.方法 SPF级健康雄性SD大鼠48只,8~10周龄,体重200~ 250 g,采用随机数字表法,将其分为3组(n=16):对照组(C组)、脂多糖(LPS)组(L组)和LPS+肝素组(LH组).L组和LH组经股静脉注射LPS 15mg/kg制备内毒素血症模型,LH组同时静脉输注肝素钠注射液100 U· kg-1·h-1.于LPS注射后3、6h时,采集股静脉血样,测定血清硫酸肝素(HS)、多配体蛋白聚糖1抗体、E-选择素、细胞间粘附分子-1(ICAM-1)的浓度,取血样后处死取肺组织,HE染色后观察肺组织病理学改变,计算肺组织湿重/干重(W/D)比值.结果 与C组比较,L组血清HS、多配体蛋白聚糖1抗体、E-选择素、ICAM-1浓度和肺组织W/D比值升高,LH组血清HS、ICAM-1浓度升高(P<0.05).与L组比较,LH组血清HS、多配体蛋白聚糖1抗体、ICAM-1、E-选择素浓度和肺组织W/D比值降低(P<0.05).L组肺组织病理学损伤明显,LH组病理学损伤程度减轻.结论 肝素酶参与了内毒素血症致大鼠血管内皮糖萼破坏.
目的 評價肝素酶在內毒素血癥緻大鼠血管內皮糖萼破壞中的作用.方法 SPF級健康雄性SD大鼠48隻,8~10週齡,體重200~ 250 g,採用隨機數字錶法,將其分為3組(n=16):對照組(C組)、脂多糖(LPS)組(L組)和LPS+肝素組(LH組).L組和LH組經股靜脈註射LPS 15mg/kg製備內毒素血癥模型,LH組同時靜脈輸註肝素鈉註射液100 U· kg-1·h-1.于LPS註射後3、6h時,採集股靜脈血樣,測定血清硫痠肝素(HS)、多配體蛋白聚糖1抗體、E-選擇素、細胞間粘附分子-1(ICAM-1)的濃度,取血樣後處死取肺組織,HE染色後觀察肺組織病理學改變,計算肺組織濕重/榦重(W/D)比值.結果 與C組比較,L組血清HS、多配體蛋白聚糖1抗體、E-選擇素、ICAM-1濃度和肺組織W/D比值升高,LH組血清HS、ICAM-1濃度升高(P<0.05).與L組比較,LH組血清HS、多配體蛋白聚糖1抗體、ICAM-1、E-選擇素濃度和肺組織W/D比值降低(P<0.05).L組肺組織病理學損傷明顯,LH組病理學損傷程度減輕.結論 肝素酶參與瞭內毒素血癥緻大鼠血管內皮糖萼破壞.
목적 평개간소매재내독소혈증치대서혈관내피당악파배중적작용.방법 SPF급건강웅성SD대서48지,8~10주령,체중200~ 250 g,채용수궤수자표법,장기분위3조(n=16):대조조(C조)、지다당(LPS)조(L조)화LPS+간소조(LH조).L조화LH조경고정맥주사LPS 15mg/kg제비내독소혈증모형,LH조동시정맥수주간소납주사액100 U· kg-1·h-1.우LPS주사후3、6h시,채집고정맥혈양,측정혈청류산간소(HS)、다배체단백취당1항체、E-선택소、세포간점부분자-1(ICAM-1)적농도,취혈양후처사취폐조직,HE염색후관찰폐조직병이학개변,계산폐조직습중/간중(W/D)비치.결과 여C조비교,L조혈청HS、다배체단백취당1항체、E-선택소、ICAM-1농도화폐조직W/D비치승고,LH조혈청HS、ICAM-1농도승고(P<0.05).여L조비교,LH조혈청HS、다배체단백취당1항체、ICAM-1、E-선택소농도화폐조직W/D비치강저(P<0.05).L조폐조직병이학손상명현,LH조병이학손상정도감경.결론 간소매삼여료내독소혈증치대서혈관내피당악파배.
Objective To evaluate the role of heparanase in endotoxemia-induced destruction of vascular endothelial glycocalyx in rats.Methods Forty-eight pathogen-free male Sprague-Dawley rats, aged 8-10 weeks, weighing 200-250 g, were randomly divided into 3 groups (n=16 each) using a random number table: control group (group C), lipopolysaccharide (LPS) group (group L) and LPS+ heparin group (group LH).Endotoxemia was induced by intravenous LPS 15 mg/kg in L and LH groups, and heparin sodium 100 U · kg-1 · h-1 was infused simultaneously in group LH.At 3 and 6 h after LPS injection, blood samples were collected from the femoral vein for determination of the serum concentrations of serum heparin sulfate (HS), syndecan-1, E-selectin and intercellular adhesion molecule-1 (ICAM-1) concentrations.The rats were then sacrificed, and lungs were removed for microscopic examination and for determination of wet/dry lung weight ratio (W/D ratio).Results Compared with group C, the serum HS, syndecan-1, E-selectin and ICAM-1 concentrations and W/D ratio were significantly increased in group L, and the serum HS and ICAM-1 concentrations were increased in group LH (P<0.05).Compared with group L, the serum HS, syndecan-1, E-selectin and ICAM-1 concentrations and W/D ratio were significantly decreased in group LH (P<0.05).The pathological changes of lungs were obvious in group L, and were significantly mitigated in group LH.Conclusion Heparanase is involved in endotoxemiainduced destruction of vascular endothelial glycocalyx in rats.