CAJ | 학술논문

目的探讨丙酮酸盐腹腔复苏对失血性休克大鼠肠道损伤的影响.方法 SPF级健康雄性SD大鼠50只,体重200～250 g.采用经左股动脉放血,维持MAP 35～45 mm Hg的方法制备失血性休克模型.采用随机数字表法,将其分为5组(n=10):假手术组(S组)仅行手术操作,不制备失血性休克及复苏;常规静脉复苏组(CR组)于失血性休克1h后回输自体血及2倍失血量的生理盐水进行静脉复苏;不同液体腹腔复苏组(DPR1-3组)在常规静脉复苏同时,采用微量输液泵分别腹腔输注1.5％葡萄糖乳酸盐腹膜透析液、1.5％葡萄糖丙酮酸盐(40.00 mtmol/L)腹膜透析液、1.5％葡萄糖高浓度丙酮酸盐(80.00 mmol/L)腹膜透析液20 ml,输注时间30 min.于放血前、休克5、30、60 min、复苏结束后5、30、60、90、120 min时记录MAP.复苏结束后120 min检测动脉血乳酸浓度,取小肠组织,测定MDA含量、髓过氧化物酶(MPO)活性、肿瘤坏死因子-α(YNF-α)表达水平,光镜下观察小肠黏膜组织形态,并行小肠黏膜上皮损伤评分.结果与放血前比较,4组大鼠休克期间MAP降低(P＜0.05),复苏后MAP差异无统计学意义(P＞0.05).与S组比较,其余4组动脉血乳酸浓度、小肠组织MDA含量、MPO活性、TNF-α表达水平以及小肠黏膜上皮损伤评分升高(P＜0.05或0.01);与CR组比较,DPR1-3组动脉血乳酸浓度、小肠组织MDA含量、MPO活性、TNF-α表达水平以及小肠黏膜上皮损伤评分降低(P＜0.01);与DPR1组比较,DPR2.3组动脉血乳酸浓度、小肠组织MDA含量、MPO活性、TNF-α4表达水平以及小肠黏膜上皮损伤评分降低(P ＜0.05或0.01);与DPR2组比较,DPR3组动脉血乳酸浓度、小肠组织MDA含量和TNF-α表达水平降低(P＜0.05或0.01).结论丙酮酸盐腹腔复苏可减轻失血性休克大鼠肠道损伤,机制与抑制肠道脂质过氧化反应和炎性反应有关.
목적 탐토병동산염복강복소대실혈성휴극대서장도손상적영향.방법 SPF급건강웅성SD대서50지,체중200～250 g.채용경좌고동맥방혈,유지MAP 35～45 mm Hg적방법제비실혈성휴극모형.채용수궤수자표법,장기분위5조(n=10):가수술조(S조)부행수술조작,불제비실혈성휴극급복소;상규정맥복소조(CR조)우실혈성휴극1h후회수자체혈급2배실혈량적생리염수진행정맥복소;불동액체복강복소조(DPR1-3조)재상규정맥복소동시,채용미량수액빙분별복강수주1.5％포도당유산염복막투석액、1.5％포도당병동산염(40.00 mtmol/L)복막투석액、1.5％포도당고농도병동산염(80.00 mmol/L)복막투석액20 ml,수주시간30 min.우방혈전、휴극5、30、60 min、복소결속후5、30、60、90、120 min시기록MAP.복소결속후120 min검측동맥혈유산농도,취소장조직,측정MDA함량、수과양화물매(MPO)활성、종류배사인자-α(YNF-α)표체수평,광경하관찰소장점막조직형태,병행소장점막상피손상평분.결과 여방혈전비교,4조대서휴극기간MAP강저(P＜0.05),복소후MAP차이무통계학의의(P＞0.05).여S조비교,기여4조동맥혈유산농도、소장조직MDA함량、MPO활성、TNF-α표체수평이급소장점막상피손상평분승고(P＜0.05혹0.01);여CR조비교,DPR1-3조동맥혈유산농도、소장조직MDA함량、MPO활성、TNF-α표체수평이급소장점막상피손상평분강저(P＜0.01);여DPR1조비교,DPR2.3조동맥혈유산농도、소장조직MDA함량、MPO활성、TNF-α4표체수평이급소장점막상피손상평분강저(P ＜0.05혹0.01);여DPR2조비교,DPR3조동맥혈유산농도、소장조직MDA함량화TNF-α표체수평강저(P＜0.05혹0.01).결론 병동산염복강복소가감경실혈성휴극대서장도손상,궤제여억제장도지질과양화반응화염성반응유관.
Objective To investigate the effects of direct peritoneal resuscitation (DPR) with sodium pyruvate from hemorrhagic shock (HS) on intestinal injury in rats.Methods Fifty SPF male Sprague-Dawley rats,weighing 200-250 g,were used in this study.The animals were anesthetized with 1％ pentobarbital sodium 40 mg/kg,tracheostomized and mechanically ventilated.Femoral artery was cannulated for mean arterial pressure (MAP) monitoring,blood-letting,blood sampling and fluid infusion.HS was induced according to the method described by Wiggers.MAP was maintained at 35-40 mm Hg for 60 min.The animals were then randomly and equally divided into 5 groups:sham operation group (group S) ; conventional resuscitation group (group CR) ; DPR with different fluid groups (DPRt-3 groups).In group CR,at 1 h after HS,the animals were resuscitated with infusion of the blood withdrawn and normal saline (the volume was 2 times volume of blood loss).In DPR1-3 groups,conventional resuscitation was performed,at the same time,1.5 ％ glucose-based peritoneal dialysis solution containing lactate,1.5％ glucose-based peritoneal dialysis solution containing lactate (40.00 mmol/L),and 1.5％ glucosebased peritoneal dialysis solution containing high lactate (80.00 mmol/L) 20 ml were infused intraperitoneally over 30 min,respectively.MAP was recorded before blood letting,at 5,30 and 60 min of HS,and at 5,30,60,90 and 120 min after the end of resuscitation.At 120 min after the end of resuscitation,the lactate level in the arterial blood was measured.The animals were then sacrificed.Small intestinal samples were obtained for determination of malondialdehyde (MDA) content,myeloperoxidase (MPO) activity and tumor necrosis factor-α (TNF-α) expression,and for microscopic examination.The damage to the small intestinal mucosa was assessed and scored.Results Compared with MAP before blood letting,MAP during HS was significantly decreased,and no significant change in MAP was found after resuscitation in CR and DPR1-3 groups (P ＜ 0.05).The lactate level in the arterial blood,MDA content,MPO activity,TNF-α expression and intestinal mucosal damage scores were significantly higher in CR and DPR1-3 groups than in S group (P ＜ 0.05 or 0.01),while lower in DPR1-3 groups than in CR group (P ＜0.01),and in DPR2,3 groups than in DPR1 group (P ＜ 0.05 or 0.01).The lactate level in the arterial blood,MDA content and TNF-α expression were significantly lower in DPR3 group than in DPR2 group (P ＜ 0.05 or 0.01).Conclusion Direct peritoneal resuscitation with sodium pyruvate can reduce the intestinal injury induced by HS and inhibition of lipid peroxidation and inflammatory responses is involved in the mechanism in rats.