中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2009年
7期
425-428
,共4页
丹宁酸%失血性休克%大鼠%心血管功能
丹寧痠%失血性休剋%大鼠%心血管功能
단저산%실혈성휴극%대서%심혈관공능
tannic acid%hemorrhagic shock%rat%cardiovascular function
目的 探讨丹宁酸预处理对失血性休克大鼠心血管功能的影响.方法 SD大鼠随机分为休克组和丹宁酸预处理组.①在体实验:于放血前10 min静脉注射丹宁酸5 mg/kg,放血至平均动脉压(MAP)达40 mm Hg(1 mm Hg=0.133 kPa)维持120 min造成失血性休克模型,观察两组大鼠休克前及休克180 min内MAP及心肌收缩功能;另外选择大鼠于制模后回血60、120、180 min时静脉给予去甲肾上腺素(NE),观察血管反应性的变化.②离体实验:休克后取心脏,固定于离体心脏灌流系统,维持灌注压在100 mm Hg,观察丹宁酸预处理对失血性休克大鼠心肌收缩功能的作用.结果 ①在体实验显示,与休克组比较,丹宁酸预处理组MAP于60 min和150 min、左心室收缩压(LVSP)于60 min时显著升高;心率(HR)于120 min时明显减慢,左心室舒张期末压(LVEDP)于休克时明显下降,血管反应性于120 min时显著改善(P均<0.05).②离体实验显示,与休克组比较,丹宁酸预处理组HR于90 min时显著减慢,左室内压上升最大速率(+dp/dt max)于10 min和20 min时、左室内压下降最大速率(-dp/dt max)于10 min时明显增加(P均<0.05).结论 丹宁酸预处理对失血性休克大鼠心血管功能有一定程度的改善作用.
目的 探討丹寧痠預處理對失血性休剋大鼠心血管功能的影響.方法 SD大鼠隨機分為休剋組和丹寧痠預處理組.①在體實驗:于放血前10 min靜脈註射丹寧痠5 mg/kg,放血至平均動脈壓(MAP)達40 mm Hg(1 mm Hg=0.133 kPa)維持120 min造成失血性休剋模型,觀察兩組大鼠休剋前及休剋180 min內MAP及心肌收縮功能;另外選擇大鼠于製模後迴血60、120、180 min時靜脈給予去甲腎上腺素(NE),觀察血管反應性的變化.②離體實驗:休剋後取心髒,固定于離體心髒灌流繫統,維持灌註壓在100 mm Hg,觀察丹寧痠預處理對失血性休剋大鼠心肌收縮功能的作用.結果 ①在體實驗顯示,與休剋組比較,丹寧痠預處理組MAP于60 min和150 min、左心室收縮壓(LVSP)于60 min時顯著升高;心率(HR)于120 min時明顯減慢,左心室舒張期末壓(LVEDP)于休剋時明顯下降,血管反應性于120 min時顯著改善(P均<0.05).②離體實驗顯示,與休剋組比較,丹寧痠預處理組HR于90 min時顯著減慢,左室內壓上升最大速率(+dp/dt max)于10 min和20 min時、左室內壓下降最大速率(-dp/dt max)于10 min時明顯增加(P均<0.05).結論 丹寧痠預處理對失血性休剋大鼠心血管功能有一定程度的改善作用.
목적 탐토단저산예처리대실혈성휴극대서심혈관공능적영향.방법 SD대서수궤분위휴극조화단저산예처리조.①재체실험:우방혈전10 min정맥주사단저산5 mg/kg,방혈지평균동맥압(MAP)체40 mm Hg(1 mm Hg=0.133 kPa)유지120 min조성실혈성휴극모형,관찰량조대서휴극전급휴극180 min내MAP급심기수축공능;령외선택대서우제모후회혈60、120、180 min시정맥급여거갑신상선소(NE),관찰혈관반응성적변화.②리체실험:휴극후취심장,고정우리체심장관류계통,유지관주압재100 mm Hg,관찰단저산예처리대실혈성휴극대서심기수축공능적작용.결과 ①재체실험현시,여휴극조비교,단저산예처리조MAP우60 min화150 min、좌심실수축압(LVSP)우60 min시현저승고;심솔(HR)우120 min시명현감만,좌심실서장기말압(LVEDP)우휴극시명현하강,혈관반응성우120 min시현저개선(P균<0.05).②리체실험현시,여휴극조비교,단저산예처리조HR우90 min시현저감만,좌실내압상승최대속솔(+dp/dt max)우10 min화20 min시、좌실내압하강최대속솔(-dp/dt max)우10 min시명현증가(P균<0.05).결론 단저산예처리대실혈성휴극대서심혈관공능유일정정도적개선작용.
Objective To investigate the effects of tannic acid pretreatment on cardiovascular function during hemorrhagic shock in rats. Methods Sprague-Dawley (SD) rats were randomly divided into two groups of shock and tannic acid pretreatment+shock. ①In vivo experiment: the model of hemorrhagic shock in rats was reproduced by bleeding to 40 mm Hg (1 mm Hg=0.133 kPa) being maintained for 120 minutes. Tannic acid in the dosage of 5 mg/kg was injected intravenously 10 minutes before hemorrhagic shock in tannic acid pretreatment+shock group. The mean arterial pressure (MAP), myocardial contractility and vascular reactivity were measured before hemorrhagic shock and at 180 minutes after hemorrhagic shock. In another experiment, the rats subjected to hemorrhagic shock and blood reinfusion were injected with norepinephrine (NE) intravenously at 60,120 and 180 minutes, and the vascular reactivity was observed. ② In vitro experiment: the heart was harvested after shock and fixed on a Langendorff system. The perfusion pressure was maintained at 100 mm Hg. The effects of tannic acid pretreatment on myocardial contractility was observed. Results ①In vivo experiment showed that tannic acid pretreatment significantly increased MAP at 60 minutes and 150 minutes, and left ventricular systolic pressure (LVSP) at 60 minutes, and the heart rate was obviously slowed at 120 minutes, and left ventricular end diastolic pressure (LVEDP) was lowered (all P<0.05). The vascular reactivity was significantly improved at 120 minutes in tannic acid pretreatment+shock group compared with shock group (P<0.05). ② In vitro experiment proved that tannic acid pretreatment significantly slowed heart rate at 90 minutes as well as increased +dp/dtmax at 10 minutes and 20 minutes and -dp/dtmax at 10 minutes (all P<0.05). Conclusion Pretreatment with tannic acid improves cardiovascular function following hemorrhagic shock to some extent in rats.
