丹宁酸预处理对失血性休克大鼠心血管功能的影响

Effects of tannic acid pretreatment on cardiovascular function during hemorrhagic shock in rats

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10min静脉注射丹宁酸5mg／kg，放血至平均动脉压（MAP）达40mmHg（1mmHg=0．133kPa）维持120min造成失血性休克模型，观察两组大鼠休克前及休克180min内MAP及心肌收缩功能；另外选择大鼠于制模后回血60、120、180min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100mmHg，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60min和150min、左心室收缩压（LVSP）于60min时显著升高；心率（HR）于120min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120min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90min时显著减慢，左室内压上升最大速率（＋dp／dtmax）于10min和20min时、左室内压下降最大速率（-dp／dt max）于10min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。

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. （1）In 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 （1）In 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.