中国急救医学
中國急救醫學
중국급구의학
CHINESE JOURNAL OF CRITICAL CARE MEDICINE
2014年
10期
873-876
,共4页
脂肪乳%脓毒症%大鼠%心肌抑制%左室收缩峰压(LVSP)%左室压力最大上升速率(+dp/dt max)%左室最大压力下降速率(-dp/dt max)
脂肪乳%膿毒癥%大鼠%心肌抑製%左室收縮峰壓(LVSP)%左室壓力最大上升速率(+dp/dt max)%左室最大壓力下降速率(-dp/dt max)
지방유%농독증%대서%심기억제%좌실수축봉압(LVSP)%좌실압력최대상승속솔(+dp/dt max)%좌실최대압력하강속솔(-dp/dt max)
Intralipid%Sepsis%Rats%Myocardial dysfunction%Left ventricular systolic peak pressure ( LVSP)%+dp/dt max%-dp/dt max
目的：研究脂肪乳对脓毒症大鼠心肌抑制的保护作用。方法清洁级成年健康雄性Wistar大鼠46只，随机分为A组（对照组，n＝8）、B组（脓毒症组，n＝18）、C组（脂肪乳组，n＝18）。 A组仅行盲肠探查术，B、C组采用盲肠结扎穿孔（ CLP）制作大鼠脓毒症模型。 A、B组术后即刻静脉给予生理盐水18．6 mL／kg，C组术后即刻给予脂肪乳18．6 mL／kg。比较两组大鼠3、6、12、24 h的心肌力学指标左室收缩峰压（LVSP）、左室压力最大上升速率（＋dp／dt max）、左室压力最大下降速率（-dp／dt max ），以及24 h后线粒体改变。结果 B组3、6、12、24 h LVSP明显低于A组（P＜0．01）；C组3、6、12 h LVSP明显低于A组（P＜0．01），24 h LVSP低于A组（P＜0．05）。C组3、6、12、24 h LVSP明显高于B组（P＜0．01）。 B组和C组3、6、12、24 h＋dp／dt max和-dp／dt max均明显低于A组。但C组3、6、12、24 h的＋dp／dt max和-dp／dt max明显高于B组。 C组的线粒体破坏明显轻于B组。结论脂肪乳能明显改善脓毒症大鼠的心肌功能，保护线粒体。
目的：研究脂肪乳對膿毒癥大鼠心肌抑製的保護作用。方法清潔級成年健康雄性Wistar大鼠46隻，隨機分為A組（對照組，n＝8）、B組（膿毒癥組，n＝18）、C組（脂肪乳組，n＝18）。 A組僅行盲腸探查術，B、C組採用盲腸結扎穿孔（ CLP）製作大鼠膿毒癥模型。 A、B組術後即刻靜脈給予生理鹽水18．6 mL／kg，C組術後即刻給予脂肪乳18．6 mL／kg。比較兩組大鼠3、6、12、24 h的心肌力學指標左室收縮峰壓（LVSP）、左室壓力最大上升速率（＋dp／dt max）、左室壓力最大下降速率（-dp／dt max ），以及24 h後線粒體改變。結果 B組3、6、12、24 h LVSP明顯低于A組（P＜0．01）；C組3、6、12 h LVSP明顯低于A組（P＜0．01），24 h LVSP低于A組（P＜0．05）。C組3、6、12、24 h LVSP明顯高于B組（P＜0．01）。 B組和C組3、6、12、24 h＋dp／dt max和-dp／dt max均明顯低于A組。但C組3、6、12、24 h的＋dp／dt max和-dp／dt max明顯高于B組。 C組的線粒體破壞明顯輕于B組。結論脂肪乳能明顯改善膿毒癥大鼠的心肌功能，保護線粒體。
목적：연구지방유대농독증대서심기억제적보호작용。방법청길급성년건강웅성Wistar대서46지，수궤분위A조（대조조，n＝8）、B조（농독증조，n＝18）、C조（지방유조，n＝18）。 A조부행맹장탐사술，B、C조채용맹장결찰천공（ CLP）제작대서농독증모형。 A、B조술후즉각정맥급여생리염수18．6 mL／kg，C조술후즉각급여지방유18．6 mL／kg。비교량조대서3、6、12、24 h적심기역학지표좌실수축봉압（LVSP）、좌실압력최대상승속솔（＋dp／dt max）、좌실압력최대하강속솔（-dp／dt max ），이급24 h후선립체개변。결과 B조3、6、12、24 h LVSP명현저우A조（P＜0．01）；C조3、6、12 h LVSP명현저우A조（P＜0．01），24 h LVSP저우A조（P＜0．05）。C조3、6、12、24 h LVSP명현고우B조（P＜0．01）。 B조화C조3、6、12、24 h＋dp／dt max화-dp／dt max균명현저우A조。단C조3、6、12、24 h적＋dp／dt max화-dp／dt max명현고우B조。 C조적선립체파배명현경우B조。결론지방유능명현개선농독증대서적심기공능，보호선립체。
Objective To investigate the effects of intralipid on the myocardial dysfunction in septic rats.Methods Forty-six Wistar rats were divided into three groups randomly:group A ( sham group, n=8);group B (sepsis group, n=18) and group C (intralipid group, n=18).In group A, appendix exploration was done .In group B & C, the animals received cecal ligation and puncture (CLP).In group A & B, the animals were intravenous dropped saline of 18.6 mL/kg; group C was intravenous dropped intralipid of 18.6 ml/kg after the operation immediately .The left ventricular systolic peak pressure ( LVSP ) , the largest increased rate of left ventricular pressure ( +dp/dt max ) , and maximal negative change infilling pressure versus time (-dp/dt max) at 3 h, 6 h, 12 h and 24 h were measured in three groups .Chondriosome structure of myocardial was observed under Electron microscopy after 24 h in three groups.Res ults LVSP in group B were significantly lower than those in group A at 3 h, 6 h, 12 h and 24 h (P<0.01).LVSP in group C were significantly lower than those in group A at 3 h, 6 h and 12 h (P<0.01) and were statistically lower than that in group A at 24 h (P<0.05). LVSP in group C were significantly higher than those in group A at 3 h, 6 h, 12 h and 24 h ( P<0.01 ) .+dp/dt max and -dp/dt max in group B and group C were significantly lower than those in group A at 3 h, 6 h, 12 h and 24 h.However, +dp/dt max and -dp/dt max in group C were significantly higher than those in group B at 3 h,6 h, 12 h and 24 h .Chondriosome structure of myocardial under Electron microscopy in group C was better than that in group B .Conclusion The cardiomyocytes have been damaged at the early stage of septic rat .Intralipid can improve myocardial function significantly , and may have a certain protective effect on the chondriosome of myocardial .
