重症中暑大鼠微血管血流改变及抗氧化剂的保护作用

Microcirculatory Disorders and Protective Role of Anti-oxidant in Severe Heat Stroke

目的:观察重症中暑大鼠脊斜肌微循环血流动力学变化,探索抗氧化剂对重症中暑血流动力学的保护作用。方法:67只Wistar雄性大鼠实验前12h禁食不禁水,取27只分3组:造模组(HS组)、SOD预处理后造模组(SOD+HS组)、NS预处理后造模组(NS+HS组);每组分为3个亚组:对照组、热打击至中心体温为38℃组及热打击至中心体温为41℃组,测量各组ROS水平。取40只大鼠随机分为4组:对照组(Control组)、热打击组(HS组)、SOD预处理后热打击组(SOD+HS组)、NS预处理后热打击组(NS+HS组),活体显微镜下动态观察大鼠脊斜肌内相同三级以下微血管血流速度、血管管径、血流量。结果:随中心体温增高,脊斜肌中ROS水平逐渐增高。热打击后各组大鼠的微动脉及微静脉血流量明显减低。SOD+HS组ROS水平明显低于HS组及NS+HS组。SOD+HS组微血管红细胞流速比HS组及NS+HS组高;SOD+HS组血流量明显高于HS组及NS+HS组。结论:热打击大鼠局部组织ROS水平增高为局部微循环障碍的重要诱因,抗氧化剂SOD通过降低热打击ROS水平增高对局部微循环发挥有效的保护作用。

Objective：This study aims to examine microcirculation hemodynamic disturbances in severe heat stroke （HS）. Method.Twenty-seven rats were divided into three groups, i. e. , HS group （HS group）, group pre- treated with SOD （SOD＋ HS group）,and group pre-treated with normal saline （NS ＋ HS group）. Each groups were devided into three sub-groups. Rats designated for heat stress were subjected to continuous heat stress in in- fant incubator （humidity ： 65%, temperature ： 40 ℃ ）. At the timebefore heat stress, core temperature （Tc） to 38 ℃ （Tc= 38℃ ） and heat stress to 41℃ （Tc= 41℃ ）, rats wererespectively sacrificed for detection ROS. 40 rats were divided into four groups,i, e. ,Control group （Control）, H S group （HS group） ,group pre-treated with SOD （SOD ＋HS group）, and group pre-treated with normal saline （NS＋HS group）. The velocity of microvessel, vascular di- ameter detected in real time. Result： ROS level increased during heat stress. Arteriolar RBC velocity was decreased with the rise in temperature and the changes in four groups were all significant（P〈0.05）. As the core temperature rising,no remarkable changes were observed in microvascular diameter. Micro-vascular blood flow rate of HS and NS＋HS groups appeared a statistically decrease when the temperature increased. ROS lever in SOD-t-HS group was lower than HS and NS--HS group （P〈0.01）. Micro-vascular blood flow rate in SOD＋ HS group was higher than HS group and NS--HS group. Conclusion： Heat stress could induce the up-regulation of ROS activity, which may be a important mechanism of microcirculation dysfunction. Anti-oxidant may improve microcirculation in the rats with heat stroke. The mechanism is that SOD can decrease the bad effort of the increasing ROS to the local microcirculation.