中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2010年
11期
772-776
,共5页
姚彤%刘育英%胡白和%常欣%吴新民%韩晶岩
姚彤%劉育英%鬍白和%常訢%吳新民%韓晶巖
요동%류육영%호백화%상흔%오신민%한정암
羟乙基淀粉%脂多糖%内皮细胞%过氧化物
羥乙基澱粉%脂多糖%內皮細胞%過氧化物
간을기정분%지다당%내피세포%과양화물
Hydroxycthyl starch%Lipopolysaccharide%Endothelium%Peroxide
目的 探讨羟乙基淀粉(HES 130/0.4)对脂多糖(LPS)引起大鼠肠系膜细静脉血管内皮损伤的影响. 方法 雄性Wistar大鼠36只,体质量200~250 g,采用随机数表法分为3组(n=12),对照组(C组)静脉注射生理盐水0.5 ml后,持续静脉输注生理盐水16 ml·kg~(-1)·h~(-1);内毒素组(LPS组)静脉注射LPS 2 ms/ks(溶于生理盐水0.5 ml)后,持续静脉输注生理盐水16 ml·kg~(-1)·h~(-1);HES组静脉注射LPS 2 mg/kg后,持续静脉输注HES 16 ml·kg~(-1)·h~(-1).补液时间60 min.连续观察给药前及补液期间大鼠肠系膜细静脉内红细胞血流速度、血管管径以及细静脉管壁过氧化物产生情况.补液结束后于电镜下观察细静脉血管内皮细胞的超微结构. 结果 各组细静脉内红细胞血流速度、血管管径以及血管壁血流剪切率各时点组内和组间差异无统计学意义(P>0.05).与C组比较,LPS组和HES组过氧化物产生增加(P<0.05).与LPS组比较,HES组该指标降低(P<0.05).LPS组血管内皮细胞内小泡增加,血管外水肿.HES组上述变化较小. 结论 羟乙基淀粉(HES 130/0.4)对脂多糖引起的大鼠肠系膜细静脉血管内皮损伤有保护作用,该作用与其抑制过氧化物的产生有关.
目的 探討羥乙基澱粉(HES 130/0.4)對脂多糖(LPS)引起大鼠腸繫膜細靜脈血管內皮損傷的影響. 方法 雄性Wistar大鼠36隻,體質量200~250 g,採用隨機數錶法分為3組(n=12),對照組(C組)靜脈註射生理鹽水0.5 ml後,持續靜脈輸註生理鹽水16 ml·kg~(-1)·h~(-1);內毒素組(LPS組)靜脈註射LPS 2 ms/ks(溶于生理鹽水0.5 ml)後,持續靜脈輸註生理鹽水16 ml·kg~(-1)·h~(-1);HES組靜脈註射LPS 2 mg/kg後,持續靜脈輸註HES 16 ml·kg~(-1)·h~(-1).補液時間60 min.連續觀察給藥前及補液期間大鼠腸繫膜細靜脈內紅細胞血流速度、血管管徑以及細靜脈管壁過氧化物產生情況.補液結束後于電鏡下觀察細靜脈血管內皮細胞的超微結構. 結果 各組細靜脈內紅細胞血流速度、血管管徑以及血管壁血流剪切率各時點組內和組間差異無統計學意義(P>0.05).與C組比較,LPS組和HES組過氧化物產生增加(P<0.05).與LPS組比較,HES組該指標降低(P<0.05).LPS組血管內皮細胞內小泡增加,血管外水腫.HES組上述變化較小. 結論 羥乙基澱粉(HES 130/0.4)對脂多糖引起的大鼠腸繫膜細靜脈血管內皮損傷有保護作用,該作用與其抑製過氧化物的產生有關.
목적 탐토간을기정분(HES 130/0.4)대지다당(LPS)인기대서장계막세정맥혈관내피손상적영향. 방법 웅성Wistar대서36지,체질량200~250 g,채용수궤수표법분위3조(n=12),대조조(C조)정맥주사생리염수0.5 ml후,지속정맥수주생리염수16 ml·kg~(-1)·h~(-1);내독소조(LPS조)정맥주사LPS 2 ms/ks(용우생리염수0.5 ml)후,지속정맥수주생리염수16 ml·kg~(-1)·h~(-1);HES조정맥주사LPS 2 mg/kg후,지속정맥수주HES 16 ml·kg~(-1)·h~(-1).보액시간60 min.련속관찰급약전급보액기간대서장계막세정맥내홍세포혈류속도、혈관관경이급세정맥관벽과양화물산생정황.보액결속후우전경하관찰세정맥혈관내피세포적초미결구. 결과 각조세정맥내홍세포혈류속도、혈관관경이급혈관벽혈류전절솔각시점조내화조간차이무통계학의의(P>0.05).여C조비교,LPS조화HES조과양화물산생증가(P<0.05).여LPS조비교,HES조해지표강저(P<0.05).LPS조혈관내피세포내소포증가,혈관외수종.HES조상술변화교소. 결론 간을기정분(HES 130/0.4)대지다당인기적대서장계막세정맥혈관내피손상유보호작용,해작용여기억제과양화물적산생유관.
Objective To investigate the effect of hydroxyethyl starch (HES, 130/0.4) on lipopolysaccharide (LPS) - induced endothelial injury in rat mesenteric venules. Methods Thirty-six Wistar rats weighing 200-250 g were randomly divided into 3 groups, n = 12 for each group. Rats were given LPS(2mg/kg) and followed by normal saline 16 ml· kg~(-1)·h~(-1) in LPS group or HES 16 ml·kg~(-1)·h~(-1) in HES group for 60 min. Rats in control group received equal volume of saline. The dynamic changes in diameters of postcapillary venules, red blood cell velocities in venules, and hydrogen peroxide released from venules were evaluated. The uhrastructure of postcapillary venule was observed by electron microscopy. Results Mesenteric venular RBC velocities, vascular diameters and shear rates on the venular wall remained constant in any of the groups during the observation (P > 0.05). The hydrogen peroxide generation from venules increased in both HES and LPS groups (P < 0.05). In HES group, the hydrogen peroxide generation and cytoplasmic caveolae in postcapillary venule induced by LPS were significantly inhibited compared with LPS group (P < 0.05). Conclusions Hydroxyethyl starch (130/0.4) could reduce the LPS-induced endothelial injury in rat mesentery. The effect was related to the inhibition of hydrogen peroxide generation on venular wall.