经颅高压电烧伤对微血管内白细胞流变行为的影响及相关机制
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摘要
目的:随着电能在生产和生活中的广泛应用,电烧伤发病率呈逐年上升趋势,已成为危害人类健康的主要创伤之一。高压电烧伤是电烧伤的主要组成部分,其病理变化复杂,对机体的影响广泛,具有较高的死亡率和致残率。因而,高压电烧伤的基础和临床研究受到医学界重视。
高压电对机体的损伤机制涉及“电热效应”、“容积导电”、“真性电损伤”、“微循环障碍”等,其中微循环障碍在高压电烧伤后机体的进一步损害过程中起重要作用。同时高压电烧伤所致的微循环障碍大部分具有可逆性,经过正确治疗,可使微循环障碍解除或减轻,以达到保护受伤组织、器官和挽救生命的目的。
白细胞流变行为异常是导致微循环障碍的重要原因之一。以往对高压电烧伤微循环的研究主要集中在微血管形态和微血流动力学上,并发现了高压电对机体外周组织和脏器微循环均有不同程度的影响,也发现了在微静脉内有白细胞增多的现象,但对白细胞流变行为变化及相关机制尚未进行深入和系统的研究。因此,本研究通过复制大鼠经颅高压电烧伤模型,以肠系膜为微循环观察窗,研究动物活体状态下白细胞在微静脉内的流变行为,检测电伤后P-选择素、E-选择素、L-选择素、可溶性细胞间黏附分子-1(sICAM-1)及CD11b/CD18的变化,并采用乌斯他丁及己酮可可碱治疗,探讨白细胞流变行为异常在高压电烧伤微循环障碍中的作用及相关机制,并为高压电烧伤微循环障碍的治疗提供实验依据。
方法:成年雄性SD大鼠369只。随机分为对照1组、电伤1组、治疗1组(前三组),每组各15只,用于电伤后白细胞流变行为的研究;对照2组、电伤2组、治疗2组(中三组),每组60只,每组分6个时相组,每个时相组10只,用于研究电伤后选择素家族对白细胞流变行为的影响;对照3组、电伤3组、治疗3组(后三组),每组48只,每组分6个时相组,每个时相组8只,用于研究电伤后免疫球蛋白超家族的CD11b/CD18及血清sICAM-1对白细胞流变行为的影响。电伤三个组和治疗三个组均复制2kV经颅高压电烧伤大鼠模型;治疗1组和治疗3组采用乌斯他丁于电伤即刻一次性给药治疗,治疗2组采用己酮可可碱于电伤即刻一次性给药治疗;对照组采用只连线不通电的方法处理。观察时相分别为伤前15min、伤后5min、1h、2h、4h、8h。前三组使用微循环显微镜按时相观测肠系膜微静脉白细胞流变学变化,观察指标:滚动白细胞数(个/ min)、白细胞滚动速度(μm/s)、白细胞黏附数、白细胞-内皮细胞接触时间(TLECT);中三组按时相采用酶联免疫吸附法(ELISA)测定血浆P-选择素、E-选择素及和L-选择素含量,采用激光多普勒微循环图像仪(LDPI)检测皮肤微循环灌流量,采用微循环显微镜观测肠系膜微静脉白细胞黏附数;后三组按时相采用流式细胞仪检测中性粒细胞CD11/CD 18表达量,采用ELISA法检测血清sICAM-1含量,采用激光多普勒微循环图像仪(LDPI)检测皮肤微循环灌流量,采用微循环显微镜观测肠系膜微静脉白细胞黏附数。实验数据用x±s表示,采用SPSS 16.0统计软件进行两因素方差分析。以P<0.05为显著性检验水准。
结果:
1前三组大鼠微静脉内滚动白细胞数的比较
对照1组伤后(假电)各时相的滚动白细胞数与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相的滚动白细胞数均明显多于伤前15min(P﹤0.05),伤后5min达(51. 40±3. 20)个,伤后1h滚动白细胞数减少,之后又呈逐渐增多趋势。治疗1组伤后各时相滚动白细胞数均明显多于伤前15min(P﹤0.05),伤后5min达(24. 60±1. 88)个,伤后1h滚动白细胞数减少,之后又呈逐渐增多趋势。
三组间伤前15min滚动白细胞数的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的滚动白细胞数均多于对照1组(P﹤0.05)。治疗1组伤后各时相的滚动白细胞数均少于电伤1组(P﹤0.05)。
2前三组大鼠微静脉内白细胞滚动速度的比较
对照1组伤后(假电)各时相的白细胞滚动速度与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相白细胞滚动速度均明显低于伤前15min(P﹤0.05),伤后5min下降至(90.29±8.72)μm/ s,伤后1h白细胞滚动速度有所增加,之后呈逐渐增加趋势。治疗1组伤后各时相白细胞滚动速度均明显低于伤前15min(P﹤0.05),伤后5min达(175.22±13.42)μm/ s,伤后1h白细胞滚动速度有所加快,之后呈逐渐加快趋势。三组间伤前15min白细胞滚动速度的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的白细胞滚动速度均慢于对照1组(P﹤0.05)。治疗1组伤后各时相的白细胞滚动速度均快于电伤1组(P﹤0.05)。
3前三组大鼠微静脉内白细胞黏附数的比较
对照1组伤后(假电)各时相的白细胞黏附数与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min增多至(23. 13±3. 34)个,伤后1h白细胞黏附数有所减少,之后呈逐渐增多趋势。治疗1组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min达(5.87±1.60)个,伤后1h白细胞黏附数有所减少,之后呈逐渐增多趋势。
三组间伤前15min白细胞黏附数的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的白细胞黏附数均多于对照1组(P﹤0.05)。治疗1组伤后各时相的白细胞黏附数均少于电伤1组(P﹤0.05)。
4前三组大鼠微静脉内TL ECT的比较
对照1组伤后(假电)各时相的TLECT值与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相TLECT值均明显高于伤前15min(P﹤0.05),伤后5min下降至(14.45±1.99)s/ min,伤后1h TLECT值有所下降,之后呈逐渐增加趋势。治疗1组伤后各时相TLECT值均明显高于伤前15min(P﹤0.05),伤后5min达(3. 66±0. 96)s/ min,伤后1h TLECT值有所下降,之后呈逐渐增加趋势。三组间伤前15min TLECT值的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的TLECT值均多于对照1组(P﹤0.05)。治疗1组伤后各时相的TLECT值均小于电伤1组(P﹤0.05)。
5中三组大鼠P-选择素含量的变化及比较
对照2组伤后(假电)各时相P-选择素含量与伤前15min无显著性差异(P﹥0.05)。电伤2组伤后各时相的P-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。治疗2组伤后各时相的P-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。
三组间伤前15min的P-选择素含量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的P-选择素含量均高于对照2组(P﹤0.05)。治疗2组伤后各时相的P-选择素含量均低于电伤2组(P﹤0.05)。
6中三组大鼠E-选择素含量的变化及比较
对照2组伤后(假电)各时相的E-选择素含量与伤前15min无显著性差异(P﹥0.05)。电伤2组伤后5min的E-选择素含量在与伤前15min比较无显著性差异(P﹥0.05),伤后1h、2h、4h及8h E-选择素含量均明显高于伤前15min(P﹤0.05),呈逐渐上升趋势。治疗2组伤后5min的E-选择素含量在与伤前15min比较无显著性差异(P﹥0.05),伤后1h、2h、4h及8h E-选择素含量均明显高于伤前15min(P﹤0.05),呈逐渐上升趋势。
三组间伤前15min和伤后5min的E-选择素含量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后1h、2h、4h及8h的E-选择素含量均高于对照2组(P﹤0.05)。治疗组伤后1h、2h、4h及8h的E-选择素含量均低于电伤2组(P﹤0.05)。
7中三组大鼠L-选择素含量的变化及比较
对照2组伤后(假电)各时相L-选择素含量与伤前15min无显著性差异(P﹥0.05)。电伤2组伤后各时相的L-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。治疗2组伤后各时相的L-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。
三组间伤前15min的L-选择素含量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的L-选择素含量均高于对照2组(P﹤0.05)。治疗2组伤后各时相的L-选择素含量均低于电伤2组(P﹤0.05)。
8中三组大鼠微静脉内白细胞黏附数比较
对照2组伤后(假电)各时相的白细胞黏附数与伤前15min均无显著性差异(P﹥0.05)。电伤2组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min即明显增多,伤后1h有所减少,之后呈逐渐增多趋势。治疗2组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min开始增多,之后的变化趋势同电伤2组。
三组间伤前15min白细胞黏附数的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的白细胞黏附数均多于对照2组(P﹤0.05)。治疗2组伤后各时相的白细胞黏附数均少于电伤2组(P﹤0.05)。
9中三组大鼠胸壁皮肤微循环灌流量比较
对照2组伤后(假电)各时相的微循环灌流量与伤前15min均无显著性差异(P﹥0.05)。电伤2组伤后各时相微循环灌流量均低于伤前15min(P﹤0.05),以伤后1h下降幅度最大。治疗2组伤后各时相微循环灌流量均低于伤前15min(P﹤0.05)。
三组间伤前15min微循环灌流量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的微循环灌流量均低于对照2组(P﹤0.05)。治疗2组伤后各时相的微循环灌流量均高于电伤2组(P﹤0.05)。
10后三组大鼠sICAM-1的变化及比较
对照3组伤后(假电)各时相的sICAM-1含量与伤前15min无显著性差异(P﹥0.05)。电伤3组伤后各时相的sICAM-1含量均明显高于伤前15min(P﹤0.05),以伤后5min为最高,以后呈逐渐下降趋势。治疗3组伤后各时相的sICAM-1含量均明显高于伤前15min(P﹤0.05),其变化趋势同电伤3组。
三组间伤前15min的sICAM-1含量的相互比较均无显著性差异(P﹥0.05)。电伤3组和治疗3组伤后各时相的sICAM-1含量均高于对照3组(P﹤0.05)。治疗3组伤后各时相的sICAM-1含量均低于电伤3组(P﹤0.05)。
11后三组大鼠CD11b/CD18的变化及比较
对照3组伤后(假电)各时相的CD11b/CD18表达量伤前15min无显著性差异(P﹥0.05)。电伤3组伤后各时相的CD11b/CD18表达量均明显高于伤前15min(P﹤0.05),以伤后5min为最高,以后呈逐渐下降趋势。治疗3组伤后各时相的CD11b/CD18表达量均明显高于伤前15min(P﹤0.05),其变化趋势同电伤3组。
三组间伤前15min的CD11b/CD18表达量的相互比较均无显著性差异(P﹥0.05)。电伤3组和治疗3组伤后各时相的CD11b/CD18表达量均高于对照3组(P﹤0.05)。治疗3组伤后各时相的CD11b/CD18表达量均低于电伤3组(P﹤0.05)。
12后三组大鼠微静脉内白细胞黏附数比较
其变化趋势同中三组。
13后三组大鼠胸壁皮肤微循环灌流量比较
其变化趋势同中三组
结论:
1高压电烧伤可引起大鼠肠系膜微循环白细胞流变行为异常,表现为滚动白细胞数量增多、白细胞滚动速度下降、白细胞黏附数增多、TLECT值延长。
2乌斯他丁可减少高压电烧伤后肠系膜微静脉内滚动白细胞数,增加白细胞滚动速度,减少白细胞黏附数,缩短TLECT。
3高压电烧伤可引起大鼠血浆P-选择素、E-选择素及L-选择素含量增加,同时肠系膜微静脉内白细胞黏附数增加,胸部皮肤微循环灌流量下降。
4己酮可可碱可降低高压电烧伤后血浆P-选择素、E-选择素及L-选择素含量,减少肠系膜微静脉内白细胞黏附数,增加胸部皮肤微循环灌流量。
5高压电烧伤可引起大鼠血浆sICAM-1含量增加、中性粒细胞CD11b/CD18表达量增加,同时肠系膜微静脉内白细胞黏附数增加,胸部皮肤微循环灌流量下降。
6乌斯他丁可降低大鼠血浆sICAM-1含量,降低中性粒细胞CD11b/CD18表达,减少肠系膜微静脉内白细胞黏附数,增加胸部皮肤微循环灌流量。
7高压电烧伤可导致微循环白细胞流变行为异常,P-选择素、E-选择素、L-选择素、sICAM-1、CD11b/CD18等黏附分子在高压电烧伤后的白细胞黏附过程中发挥重要作用。乌斯他丁及己酮可可碱可改善高压电烧伤后白细胞流变行为异常。
Objective: As the generally application of electrical in production and life, the incidence rate of electrical burn is increasing annually, and become one of the key heals that endanger people health. High voltage electrical burn, the main component of electrical burn, has high death rate and maim rate for its complex patholo gical variation. So, electrical burn basis and clinical study is being attached importance in medical area.
The damage mechanism of electrical burn involves electric-hot, volume-electric conduct, actual electrical damage、micro-circulation obstruction and so on, among microcirculation plays an important part in further damage after high voltage electrical. At the same time, most microcirculation obstruction is reversible. Microcirculation obstruction could be relieved or abate to protect damaged tissues、organs and save lifes after correct treatment.
Leucocytes rheological behavior change is an important cause of microcirculation obstruction. Former high-voltage burns microcirculation research focuses on microvascular form and micro hemodynamics, people found that high voltage electrical affect peripheral tissues and visceral microcirculation in different extent, and Leucocytes multiply in micro-veins. but didn’t study Leucocytes rheological behavior and related mechanism deeply and systematically yet. This experiment duplicates rats transcranial high voltage electrical burn models through the big, observes mesenteric micro-vessel, studys Leucocytes rheological behavior in micro-veins when the animals is live, and detects the change of P-selectin、E-selectin、L-selectin、sICAM-1 and CD11b/CD18. With Ulinastatin and PTX,this study researchs the affect and related mechanism of Leucocytes rheological behavior in microcirculation obstruction caused from high voltage electrical burn, and applys experiment evidences for the treatment to microcirculation obstruction caused from high voltage electrical burn.
Methods: The study consist of three steps, the first to study rheology characters of leukocytes after high-voltage electricity burns (HEB), 45 SD rats were randomly divided into three groups, consisting of control one group, electricical burns one group and treatment one group, 15 for each. The second step to study the effect of every selectin on rheology characters of leukocytes after HEB, 180 SD rats were randomly divided into three groups, consisting of control two group, electricical burns two group and treatment two group, 60 for each, every group was falled into six phases to study, 10 rats for each phase. The third step to study the effect of CD11b/CD18 and sICAM-1 on rheology characters of leukocytes after HEB, 144 SD rats were randomly divided into three groups, consisting of control three group, electricical burns three group and treatment three group, 48 for each, every group was falled into six phases to study, 8 rats for each phase. Used the system made by TC-30-20KV A type voltage regulator and YDJ-10KV A type transformer to reproduce the 2KV high-voltage electricity burns (HEB) animal model in electricical burns groups and treatment groups. Treatment group 1 and group 3 using Ulinastatin at electrical burn immediate time, the treatment group 2 using Pentoxifylline at electrical burn immediate time, the control group no electricity and medicine. At 15mins before HEB and 5mins,1,2,4,8h after HEB to observe. With WX-9 microscope and its image analytical system to observe leucocyte rheological change in mesentery veinule of anterior three groups. Observing indexes: rolling leucocyte count (a/min), rolling leucocyte speed (m/s), adhesion leukocytes, leucocyte-endothelial contact time (TLECT); by enzyme-linked immunosorbent method (ELISA)to measure selectin-P、selectin-E、selectin-L of center three groups , used the LISCA Laser Doppler Hemoperfusion image instrument(LDPI) to observe skin perfusion and used WX-9 microscope to to observe adhesion leukocytes. Used flow cytometric to detect CD11 / CD expression in neutrophils of aboral three groups, by ELISA to measure sICAM - 1 content, used the LISCA Laser Doppler Hemoperfusion image instrument(LDPI) to observe skin perfusion and used WX-9 microscope to to observe adhesion leukocytes. SPSS statistics software were used in the statistic analysis of the data (P < 0.05 level for examination) .
Results:
1 The comparison of rolling leucocyte count in anterior three groups . The rolling leucocyte count of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the rolling leucocyte count in the electrical burn group 1 were significantly more than before the burn 15min, at 5min after HEB, the rolling leucocyte count was 51.40±3.20, have a trend of increase gradually 1h later after HEB. The treatment group 1 and the electrical burn group 1 have same trend, at 5min after HEB, the rolling leucocyte count in treatment group 1 was 24.60±1.88.
The rolling leucocyte count of three groups at 15min before burn intercomparison(P﹥0.05). The rolling leucocyte count of electrical burn group 1 and treatment group 1 in each phase were more than the control group 1(P﹤0.05). The treatment group 1 each phase are less than the electrical burn group 1 (P﹤0.05).
2 The comparison of rolling leucocyte speed in anterior three groups. The rolling leucocyte speed of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the rolling leucocyte speed in the electrical burn group 1 after HEB were slower significantly than before the burn 15min, at 5min after HEB, the rolling leucocyte speed was (90.29±8.72)μm/ s, have a trend of increase gradually 1h later after HEB. The treatment group 1 and the electrical burn group 1 have same trend, at 5min after HEB, the rolling leucocyte speed in treatment group 1 was (175.22±13.42)μm/ s.
The rolling leucocyte speed of three groups at 15min before burn intercomparison (P﹥0.05). The rolling leucocyte speed of electrical burn group 1 and treatment group 1 in each phase were slower than the control group 1(P﹤0.05). The treatment group 1 each phase were faster than the electrical burn group 1 (P﹤0.05).
3 The comparison of adhesion leukocytes in anterior three groups.
The adhesion leukocytes of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the adhesion leukocytes in the electrical burn group 1 after HEB were significantly more than before the burn 15min, at 5min after HEB, the adhesion leukocytes was 23.13±3.34, have a trend of increase gradually 1h later after HEB. The treatment group 1 and the electrical burn group 1 have same trend, at 5min after HEB, the adhesion leukocytes in treatment group 1 was 5.87±1.60.
The adhesion leukocytes of three groups at 15min before burn intercomparison (P﹥0.05). The adhesion leukocytes of electrical burn group 1 and treatment group 1 in each phase were more than the control group 1(P﹤0.05). The treatment group 1 each phase were less than the electrical burn group 1 (P﹤0.05).
4 The comparison of leucocyte-endothelial contact time (TLECT) in anterior three groups.
The TLECT of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference(P﹥0.05). But the TLECT in the electrical burn group 1 were significantly more than before the burn 15min, at 5min after HEB, the TLECT was (14.45±1.99)s/ min, have a trend of increase gradually 1h later after HEB. the treatment group 1 and the electrical burn group 1 have same trend. at 5min after HEB, the TLECT in treatment group 1 was(3. 66±0. 96)s/ min.
The TLECT of three groups at 15min before burn intercomparison (P﹥0.05). The TLECT of electrical burn group 1 and treatment group 1 in each phase were more than the control group 1(P﹤0.05). The treatment group 1 each phase were less than the electrical burn group 1 (P﹤0.05).
5 The comparison of selectin-P in center three groups.
The selectin-P of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the selectin-P in the electrical burn group 2 after HEB were significantly higher than before the burn 15min, have a trend of increase gradually. The treatment group 2 and the electrical burn group 2 have same trend.
The selectin-P of three groups at 15min before burn intercomparison (P﹥0.05). The selectin-P of electrical burn group 2 and treatment group 2 in each phase were higher than the control group 2(P﹤0.05). The treatment group 2 each phase were lower than the electrical burn group 2 (P﹤0.05).
6 The comparison of selectin-E in center three groups.
The selectin- E of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). The selectin- E in electrical burn group 2 at 5min after HEB compared with 15min before the burn , no significant difference (P﹥0.05). But 1h later after HEB, have increasing trend and higher than before the burn. The treatment group 2 and the electrical burn group 2 have same trend.
The selectin- E of three groups at 15min before burn and 5 min after HEB intercomparison (P﹥0.05). The selectin- E of electrical burn group 2 and treatment group 2 in each phase(1h later ) were higher than the control group 2(P﹤0.05). The treatment group 2 each phase(1h later ) were lower than the electrical burn group 2 (P﹤0.05).
7 The comparison of selectin-L in center three groups .
The selectin-L of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the selectin-L in the electrical burn group 2 after HEB were significantly higher than before the burn 15min, have a trend of increase gradually. The treatment group 2 and the electrical burn group 2 have same trend.
The selectin-L of three groups at 15min before burn intercomparison (P﹥0.05). The selectin-L of electrical burn group 2 and treatment group 2 in each phase were higher than the control group 2(P﹤0.05). The treatment group 2 each phase were lower than the electrical burn group 2 (P﹤0.05).
8 The comparison of adhesion leukocytes in center three group.
The adhesion leukocytes of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the adhesion leukocytes in the electrical burn group 2 after HEB were significantly more than before the burn 15min, most at 5min after HEB, the adhesion leukocytes have a trend of increase gradually 1h later after HEB. The adhesion leukocytes in the treatment group 2 after HEB were significantly more than before the burn 15min, and have a trend of increase gradually 5min later after HEB.
The adhesion leukocytes of three groups at 15min before burn intercomparison (P﹥0.05). The adhesion leukocytes of electrical burn group 2 and treatment group 2 in each phase were more than the control group 2(P﹤0.05). The treatment group 2 each phase were less than the electrical burn group 2 (P﹤0.05).
9 The comparison of chest wall skin perfusion in center three group.
The skin perfusion of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the skin perfusion in the electrical burn group 2 after HEB were significantly less than before the burn 15min, least at 1h after HEB. The skin perfusion in the treatment group 2 after HEB were significantly less than before 15min.
The skin perfusion of three groups at 15min before burn intercomparison (P﹥0.05). The skin perfusion of electrical burn group 2 and treatment group 2 in each phase were lower than the control group 2(P﹤0.05). The treatment group 2 each phase were more than the electrical burn group 2 (P﹤0.05) .
10 The comparison of sICAM-1 in aboral three groups.
The sICAM-1 of each phase in control group 3 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the sICAM-1 in the electrical burn group 3 after HEB were significantly higher than before the burn 15min, most at 5min after HEB, the sICAM-1 have a trend of decrease gradually 1h later after HEB. The sICAM-1 in the treatment group 3 after HEB were significantly hegher than before the burn 15min.
The sICAM-1 of three groups at 15min before burn intercomparison (P﹥0.05). The sICAM-1 of electrical burn group 3 and treatment group 3 in each phase were hegher than the control group 3(P﹤0.05). The treatment group 3 each phase were less than the electrical burn group 3 (P﹤0.05). 11 The comparison of CD11b/CD18 in aboral three groups.
The CD11b/CD18 of each phase in control group 3 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the CD11b/CD18 in the electrical burn group 3 after HEB were significantly higher than before the burn 15min, most at 5min after HEB, the CD11b/CD18 have a trend of decrease gradually later. The CD11b/CD18 in the treatment group 3 after HEB were significantly hegher than before the burn 15min.
The CD11b/CD18 of three groups at 15min before burn intercomparison (P﹥0.05). The CD11b/CD18 of electrical burn group 3 and treatment group 3 in each phase were hegher than the control group 3(P﹤0.05). The treatment group 3 each phase were less than the electrical burn group 3 (P﹤0.05).
12 The adhesion leukocytes in aboral three groups and center three groups have same trend.
13 The skin perfusion in aboral three groups and center three groups have same trend.
Conclusion:
1 High-voltage electrical burns can cause leucocyte rheological abnormity change : count increase, rolling speed decrease, adhesion leukocytes increase, TLECT value extend.
2 Ulinastatin can reduce abnormity leucocyte rheological that were caused by high-voltage electrical.
3 High-voltage electrical burns can increased selectin-P, and selectin-E, and selectin-L and adhesion leukocytes in mesentery venuel, decreased chest wall skin perfusion.
4 Pentoxifylline can reduce selectin-P, and selectin-E, and selectin-L ,decrease adhesion leukocytes in mesentery venuel , increase chest wall skin perfusion.
5 High-voltage electrical burns can increase sICAM-1, and CD11b/CD18, and adhesion leukocytes and decrease chest wall skin perfusion.
6 Ulinastatin can decrease sICAM-1, and CD11b/CD18, and adhesion leukocytes and increase chest wall skin perfusion.
7 High-voltage electrical burns can cause leucocyte rheological abnormity change, selectin-P, and selectin-E, and selectin-L, and sICAM-1, and CD11b/CD18 et al play an important role in leukocyte adhesion. Ulinastatin and Pentoxifylline can reduce leucocyte rheological abnormity change.
高压电对机体的损伤机制涉及“电热效应”、“容积导电”、“真性电损伤”、“微循环障碍”等,其中微循环障碍在高压电烧伤后机体的进一步损害过程中起重要作用。同时高压电烧伤所致的微循环障碍大部分具有可逆性,经过正确治疗,可使微循环障碍解除或减轻,以达到保护受伤组织、器官和挽救生命的目的。
白细胞流变行为异常是导致微循环障碍的重要原因之一。以往对高压电烧伤微循环的研究主要集中在微血管形态和微血流动力学上,并发现了高压电对机体外周组织和脏器微循环均有不同程度的影响,也发现了在微静脉内有白细胞增多的现象,但对白细胞流变行为变化及相关机制尚未进行深入和系统的研究。因此,本研究通过复制大鼠经颅高压电烧伤模型,以肠系膜为微循环观察窗,研究动物活体状态下白细胞在微静脉内的流变行为,检测电伤后P-选择素、E-选择素、L-选择素、可溶性细胞间黏附分子-1(sICAM-1)及CD11b/CD18的变化,并采用乌斯他丁及己酮可可碱治疗,探讨白细胞流变行为异常在高压电烧伤微循环障碍中的作用及相关机制,并为高压电烧伤微循环障碍的治疗提供实验依据。
方法:成年雄性SD大鼠369只。随机分为对照1组、电伤1组、治疗1组(前三组),每组各15只,用于电伤后白细胞流变行为的研究;对照2组、电伤2组、治疗2组(中三组),每组60只,每组分6个时相组,每个时相组10只,用于研究电伤后选择素家族对白细胞流变行为的影响;对照3组、电伤3组、治疗3组(后三组),每组48只,每组分6个时相组,每个时相组8只,用于研究电伤后免疫球蛋白超家族的CD11b/CD18及血清sICAM-1对白细胞流变行为的影响。电伤三个组和治疗三个组均复制2kV经颅高压电烧伤大鼠模型;治疗1组和治疗3组采用乌斯他丁于电伤即刻一次性给药治疗,治疗2组采用己酮可可碱于电伤即刻一次性给药治疗;对照组采用只连线不通电的方法处理。观察时相分别为伤前15min、伤后5min、1h、2h、4h、8h。前三组使用微循环显微镜按时相观测肠系膜微静脉白细胞流变学变化,观察指标:滚动白细胞数(个/ min)、白细胞滚动速度(μm/s)、白细胞黏附数、白细胞-内皮细胞接触时间(TLECT);中三组按时相采用酶联免疫吸附法(ELISA)测定血浆P-选择素、E-选择素及和L-选择素含量,采用激光多普勒微循环图像仪(LDPI)检测皮肤微循环灌流量,采用微循环显微镜观测肠系膜微静脉白细胞黏附数;后三组按时相采用流式细胞仪检测中性粒细胞CD11/CD 18表达量,采用ELISA法检测血清sICAM-1含量,采用激光多普勒微循环图像仪(LDPI)检测皮肤微循环灌流量,采用微循环显微镜观测肠系膜微静脉白细胞黏附数。实验数据用x±s表示,采用SPSS 16.0统计软件进行两因素方差分析。以P<0.05为显著性检验水准。
结果:
1前三组大鼠微静脉内滚动白细胞数的比较
对照1组伤后(假电)各时相的滚动白细胞数与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相的滚动白细胞数均明显多于伤前15min(P﹤0.05),伤后5min达(51. 40±3. 20)个,伤后1h滚动白细胞数减少,之后又呈逐渐增多趋势。治疗1组伤后各时相滚动白细胞数均明显多于伤前15min(P﹤0.05),伤后5min达(24. 60±1. 88)个,伤后1h滚动白细胞数减少,之后又呈逐渐增多趋势。
三组间伤前15min滚动白细胞数的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的滚动白细胞数均多于对照1组(P﹤0.05)。治疗1组伤后各时相的滚动白细胞数均少于电伤1组(P﹤0.05)。
2前三组大鼠微静脉内白细胞滚动速度的比较
对照1组伤后(假电)各时相的白细胞滚动速度与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相白细胞滚动速度均明显低于伤前15min(P﹤0.05),伤后5min下降至(90.29±8.72)μm/ s,伤后1h白细胞滚动速度有所增加,之后呈逐渐增加趋势。治疗1组伤后各时相白细胞滚动速度均明显低于伤前15min(P﹤0.05),伤后5min达(175.22±13.42)μm/ s,伤后1h白细胞滚动速度有所加快,之后呈逐渐加快趋势。三组间伤前15min白细胞滚动速度的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的白细胞滚动速度均慢于对照1组(P﹤0.05)。治疗1组伤后各时相的白细胞滚动速度均快于电伤1组(P﹤0.05)。
3前三组大鼠微静脉内白细胞黏附数的比较
对照1组伤后(假电)各时相的白细胞黏附数与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min增多至(23. 13±3. 34)个,伤后1h白细胞黏附数有所减少,之后呈逐渐增多趋势。治疗1组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min达(5.87±1.60)个,伤后1h白细胞黏附数有所减少,之后呈逐渐增多趋势。
三组间伤前15min白细胞黏附数的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的白细胞黏附数均多于对照1组(P﹤0.05)。治疗1组伤后各时相的白细胞黏附数均少于电伤1组(P﹤0.05)。
4前三组大鼠微静脉内TL ECT的比较
对照1组伤后(假电)各时相的TLECT值与伤前15min无显著性差异(P﹥0.05)。电伤1组伤后各时相TLECT值均明显高于伤前15min(P﹤0.05),伤后5min下降至(14.45±1.99)s/ min,伤后1h TLECT值有所下降,之后呈逐渐增加趋势。治疗1组伤后各时相TLECT值均明显高于伤前15min(P﹤0.05),伤后5min达(3. 66±0. 96)s/ min,伤后1h TLECT值有所下降,之后呈逐渐增加趋势。三组间伤前15min TLECT值的相互比较均无显著性差异(P﹥0.05)。电伤1组和治疗1组伤后各时相的TLECT值均多于对照1组(P﹤0.05)。治疗1组伤后各时相的TLECT值均小于电伤1组(P﹤0.05)。
5中三组大鼠P-选择素含量的变化及比较
对照2组伤后(假电)各时相P-选择素含量与伤前15min无显著性差异(P﹥0.05)。电伤2组伤后各时相的P-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。治疗2组伤后各时相的P-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。
三组间伤前15min的P-选择素含量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的P-选择素含量均高于对照2组(P﹤0.05)。治疗2组伤后各时相的P-选择素含量均低于电伤2组(P﹤0.05)。
6中三组大鼠E-选择素含量的变化及比较
对照2组伤后(假电)各时相的E-选择素含量与伤前15min无显著性差异(P﹥0.05)。电伤2组伤后5min的E-选择素含量在与伤前15min比较无显著性差异(P﹥0.05),伤后1h、2h、4h及8h E-选择素含量均明显高于伤前15min(P﹤0.05),呈逐渐上升趋势。治疗2组伤后5min的E-选择素含量在与伤前15min比较无显著性差异(P﹥0.05),伤后1h、2h、4h及8h E-选择素含量均明显高于伤前15min(P﹤0.05),呈逐渐上升趋势。
三组间伤前15min和伤后5min的E-选择素含量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后1h、2h、4h及8h的E-选择素含量均高于对照2组(P﹤0.05)。治疗组伤后1h、2h、4h及8h的E-选择素含量均低于电伤2组(P﹤0.05)。
7中三组大鼠L-选择素含量的变化及比较
对照2组伤后(假电)各时相L-选择素含量与伤前15min无显著性差异(P﹥0.05)。电伤2组伤后各时相的L-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。治疗2组伤后各时相的L-选择素含量均明显高于伤前15min(P﹤0.05),且呈逐渐升高趋势。
三组间伤前15min的L-选择素含量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的L-选择素含量均高于对照2组(P﹤0.05)。治疗2组伤后各时相的L-选择素含量均低于电伤2组(P﹤0.05)。
8中三组大鼠微静脉内白细胞黏附数比较
对照2组伤后(假电)各时相的白细胞黏附数与伤前15min均无显著性差异(P﹥0.05)。电伤2组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min即明显增多,伤后1h有所减少,之后呈逐渐增多趋势。治疗2组伤后各时相白细胞黏附数均明显多于伤前15min(P﹤0.05),伤后5min开始增多,之后的变化趋势同电伤2组。
三组间伤前15min白细胞黏附数的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的白细胞黏附数均多于对照2组(P﹤0.05)。治疗2组伤后各时相的白细胞黏附数均少于电伤2组(P﹤0.05)。
9中三组大鼠胸壁皮肤微循环灌流量比较
对照2组伤后(假电)各时相的微循环灌流量与伤前15min均无显著性差异(P﹥0.05)。电伤2组伤后各时相微循环灌流量均低于伤前15min(P﹤0.05),以伤后1h下降幅度最大。治疗2组伤后各时相微循环灌流量均低于伤前15min(P﹤0.05)。
三组间伤前15min微循环灌流量的相互比较均无显著性差异(P﹥0.05)。电伤2组和治疗2组伤后各时相的微循环灌流量均低于对照2组(P﹤0.05)。治疗2组伤后各时相的微循环灌流量均高于电伤2组(P﹤0.05)。
10后三组大鼠sICAM-1的变化及比较
对照3组伤后(假电)各时相的sICAM-1含量与伤前15min无显著性差异(P﹥0.05)。电伤3组伤后各时相的sICAM-1含量均明显高于伤前15min(P﹤0.05),以伤后5min为最高,以后呈逐渐下降趋势。治疗3组伤后各时相的sICAM-1含量均明显高于伤前15min(P﹤0.05),其变化趋势同电伤3组。
三组间伤前15min的sICAM-1含量的相互比较均无显著性差异(P﹥0.05)。电伤3组和治疗3组伤后各时相的sICAM-1含量均高于对照3组(P﹤0.05)。治疗3组伤后各时相的sICAM-1含量均低于电伤3组(P﹤0.05)。
11后三组大鼠CD11b/CD18的变化及比较
对照3组伤后(假电)各时相的CD11b/CD18表达量伤前15min无显著性差异(P﹥0.05)。电伤3组伤后各时相的CD11b/CD18表达量均明显高于伤前15min(P﹤0.05),以伤后5min为最高,以后呈逐渐下降趋势。治疗3组伤后各时相的CD11b/CD18表达量均明显高于伤前15min(P﹤0.05),其变化趋势同电伤3组。
三组间伤前15min的CD11b/CD18表达量的相互比较均无显著性差异(P﹥0.05)。电伤3组和治疗3组伤后各时相的CD11b/CD18表达量均高于对照3组(P﹤0.05)。治疗3组伤后各时相的CD11b/CD18表达量均低于电伤3组(P﹤0.05)。
12后三组大鼠微静脉内白细胞黏附数比较
其变化趋势同中三组。
13后三组大鼠胸壁皮肤微循环灌流量比较
其变化趋势同中三组
结论:
1高压电烧伤可引起大鼠肠系膜微循环白细胞流变行为异常,表现为滚动白细胞数量增多、白细胞滚动速度下降、白细胞黏附数增多、TLECT值延长。
2乌斯他丁可减少高压电烧伤后肠系膜微静脉内滚动白细胞数,增加白细胞滚动速度,减少白细胞黏附数,缩短TLECT。
3高压电烧伤可引起大鼠血浆P-选择素、E-选择素及L-选择素含量增加,同时肠系膜微静脉内白细胞黏附数增加,胸部皮肤微循环灌流量下降。
4己酮可可碱可降低高压电烧伤后血浆P-选择素、E-选择素及L-选择素含量,减少肠系膜微静脉内白细胞黏附数,增加胸部皮肤微循环灌流量。
5高压电烧伤可引起大鼠血浆sICAM-1含量增加、中性粒细胞CD11b/CD18表达量增加,同时肠系膜微静脉内白细胞黏附数增加,胸部皮肤微循环灌流量下降。
6乌斯他丁可降低大鼠血浆sICAM-1含量,降低中性粒细胞CD11b/CD18表达,减少肠系膜微静脉内白细胞黏附数,增加胸部皮肤微循环灌流量。
7高压电烧伤可导致微循环白细胞流变行为异常,P-选择素、E-选择素、L-选择素、sICAM-1、CD11b/CD18等黏附分子在高压电烧伤后的白细胞黏附过程中发挥重要作用。乌斯他丁及己酮可可碱可改善高压电烧伤后白细胞流变行为异常。
Objective: As the generally application of electrical in production and life, the incidence rate of electrical burn is increasing annually, and become one of the key heals that endanger people health. High voltage electrical burn, the main component of electrical burn, has high death rate and maim rate for its complex patholo gical variation. So, electrical burn basis and clinical study is being attached importance in medical area.
The damage mechanism of electrical burn involves electric-hot, volume-electric conduct, actual electrical damage、micro-circulation obstruction and so on, among microcirculation plays an important part in further damage after high voltage electrical. At the same time, most microcirculation obstruction is reversible. Microcirculation obstruction could be relieved or abate to protect damaged tissues、organs and save lifes after correct treatment.
Leucocytes rheological behavior change is an important cause of microcirculation obstruction. Former high-voltage burns microcirculation research focuses on microvascular form and micro hemodynamics, people found that high voltage electrical affect peripheral tissues and visceral microcirculation in different extent, and Leucocytes multiply in micro-veins. but didn’t study Leucocytes rheological behavior and related mechanism deeply and systematically yet. This experiment duplicates rats transcranial high voltage electrical burn models through the big, observes mesenteric micro-vessel, studys Leucocytes rheological behavior in micro-veins when the animals is live, and detects the change of P-selectin、E-selectin、L-selectin、sICAM-1 and CD11b/CD18. With Ulinastatin and PTX,this study researchs the affect and related mechanism of Leucocytes rheological behavior in microcirculation obstruction caused from high voltage electrical burn, and applys experiment evidences for the treatment to microcirculation obstruction caused from high voltage electrical burn.
Methods: The study consist of three steps, the first to study rheology characters of leukocytes after high-voltage electricity burns (HEB), 45 SD rats were randomly divided into three groups, consisting of control one group, electricical burns one group and treatment one group, 15 for each. The second step to study the effect of every selectin on rheology characters of leukocytes after HEB, 180 SD rats were randomly divided into three groups, consisting of control two group, electricical burns two group and treatment two group, 60 for each, every group was falled into six phases to study, 10 rats for each phase. The third step to study the effect of CD11b/CD18 and sICAM-1 on rheology characters of leukocytes after HEB, 144 SD rats were randomly divided into three groups, consisting of control three group, electricical burns three group and treatment three group, 48 for each, every group was falled into six phases to study, 8 rats for each phase. Used the system made by TC-30-20KV A type voltage regulator and YDJ-10KV A type transformer to reproduce the 2KV high-voltage electricity burns (HEB) animal model in electricical burns groups and treatment groups. Treatment group 1 and group 3 using Ulinastatin at electrical burn immediate time, the treatment group 2 using Pentoxifylline at electrical burn immediate time, the control group no electricity and medicine. At 15mins before HEB and 5mins,1,2,4,8h after HEB to observe. With WX-9 microscope and its image analytical system to observe leucocyte rheological change in mesentery veinule of anterior three groups. Observing indexes: rolling leucocyte count (a/min), rolling leucocyte speed (m/s), adhesion leukocytes, leucocyte-endothelial contact time (TLECT); by enzyme-linked immunosorbent method (ELISA)to measure selectin-P、selectin-E、selectin-L of center three groups , used the LISCA Laser Doppler Hemoperfusion image instrument(LDPI) to observe skin perfusion and used WX-9 microscope to to observe adhesion leukocytes. Used flow cytometric to detect CD11 / CD expression in neutrophils of aboral three groups, by ELISA to measure sICAM - 1 content, used the LISCA Laser Doppler Hemoperfusion image instrument(LDPI) to observe skin perfusion and used WX-9 microscope to to observe adhesion leukocytes. SPSS statistics software were used in the statistic analysis of the data (P < 0.05 level for examination) .
Results:
1 The comparison of rolling leucocyte count in anterior three groups . The rolling leucocyte count of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the rolling leucocyte count in the electrical burn group 1 were significantly more than before the burn 15min, at 5min after HEB, the rolling leucocyte count was 51.40±3.20, have a trend of increase gradually 1h later after HEB. The treatment group 1 and the electrical burn group 1 have same trend, at 5min after HEB, the rolling leucocyte count in treatment group 1 was 24.60±1.88.
The rolling leucocyte count of three groups at 15min before burn intercomparison(P﹥0.05). The rolling leucocyte count of electrical burn group 1 and treatment group 1 in each phase were more than the control group 1(P﹤0.05). The treatment group 1 each phase are less than the electrical burn group 1 (P﹤0.05).
2 The comparison of rolling leucocyte speed in anterior three groups. The rolling leucocyte speed of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the rolling leucocyte speed in the electrical burn group 1 after HEB were slower significantly than before the burn 15min, at 5min after HEB, the rolling leucocyte speed was (90.29±8.72)μm/ s, have a trend of increase gradually 1h later after HEB. The treatment group 1 and the electrical burn group 1 have same trend, at 5min after HEB, the rolling leucocyte speed in treatment group 1 was (175.22±13.42)μm/ s.
The rolling leucocyte speed of three groups at 15min before burn intercomparison (P﹥0.05). The rolling leucocyte speed of electrical burn group 1 and treatment group 1 in each phase were slower than the control group 1(P﹤0.05). The treatment group 1 each phase were faster than the electrical burn group 1 (P﹤0.05).
3 The comparison of adhesion leukocytes in anterior three groups.
The adhesion leukocytes of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the adhesion leukocytes in the electrical burn group 1 after HEB were significantly more than before the burn 15min, at 5min after HEB, the adhesion leukocytes was 23.13±3.34, have a trend of increase gradually 1h later after HEB. The treatment group 1 and the electrical burn group 1 have same trend, at 5min after HEB, the adhesion leukocytes in treatment group 1 was 5.87±1.60.
The adhesion leukocytes of three groups at 15min before burn intercomparison (P﹥0.05). The adhesion leukocytes of electrical burn group 1 and treatment group 1 in each phase were more than the control group 1(P﹤0.05). The treatment group 1 each phase were less than the electrical burn group 1 (P﹤0.05).
4 The comparison of leucocyte-endothelial contact time (TLECT) in anterior three groups.
The TLECT of each phase in control group 1 after bogus HEB compared with 15min before the burn , no significant difference(P﹥0.05). But the TLECT in the electrical burn group 1 were significantly more than before the burn 15min, at 5min after HEB, the TLECT was (14.45±1.99)s/ min, have a trend of increase gradually 1h later after HEB. the treatment group 1 and the electrical burn group 1 have same trend. at 5min after HEB, the TLECT in treatment group 1 was(3. 66±0. 96)s/ min.
The TLECT of three groups at 15min before burn intercomparison (P﹥0.05). The TLECT of electrical burn group 1 and treatment group 1 in each phase were more than the control group 1(P﹤0.05). The treatment group 1 each phase were less than the electrical burn group 1 (P﹤0.05).
5 The comparison of selectin-P in center three groups.
The selectin-P of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the selectin-P in the electrical burn group 2 after HEB were significantly higher than before the burn 15min, have a trend of increase gradually. The treatment group 2 and the electrical burn group 2 have same trend.
The selectin-P of three groups at 15min before burn intercomparison (P﹥0.05). The selectin-P of electrical burn group 2 and treatment group 2 in each phase were higher than the control group 2(P﹤0.05). The treatment group 2 each phase were lower than the electrical burn group 2 (P﹤0.05).
6 The comparison of selectin-E in center three groups.
The selectin- E of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). The selectin- E in electrical burn group 2 at 5min after HEB compared with 15min before the burn , no significant difference (P﹥0.05). But 1h later after HEB, have increasing trend and higher than before the burn. The treatment group 2 and the electrical burn group 2 have same trend.
The selectin- E of three groups at 15min before burn and 5 min after HEB intercomparison (P﹥0.05). The selectin- E of electrical burn group 2 and treatment group 2 in each phase(1h later ) were higher than the control group 2(P﹤0.05). The treatment group 2 each phase(1h later ) were lower than the electrical burn group 2 (P﹤0.05).
7 The comparison of selectin-L in center three groups .
The selectin-L of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the selectin-L in the electrical burn group 2 after HEB were significantly higher than before the burn 15min, have a trend of increase gradually. The treatment group 2 and the electrical burn group 2 have same trend.
The selectin-L of three groups at 15min before burn intercomparison (P﹥0.05). The selectin-L of electrical burn group 2 and treatment group 2 in each phase were higher than the control group 2(P﹤0.05). The treatment group 2 each phase were lower than the electrical burn group 2 (P﹤0.05).
8 The comparison of adhesion leukocytes in center three group.
The adhesion leukocytes of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the adhesion leukocytes in the electrical burn group 2 after HEB were significantly more than before the burn 15min, most at 5min after HEB, the adhesion leukocytes have a trend of increase gradually 1h later after HEB. The adhesion leukocytes in the treatment group 2 after HEB were significantly more than before the burn 15min, and have a trend of increase gradually 5min later after HEB.
The adhesion leukocytes of three groups at 15min before burn intercomparison (P﹥0.05). The adhesion leukocytes of electrical burn group 2 and treatment group 2 in each phase were more than the control group 2(P﹤0.05). The treatment group 2 each phase were less than the electrical burn group 2 (P﹤0.05).
9 The comparison of chest wall skin perfusion in center three group.
The skin perfusion of each phase in control group 2 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the skin perfusion in the electrical burn group 2 after HEB were significantly less than before the burn 15min, least at 1h after HEB. The skin perfusion in the treatment group 2 after HEB were significantly less than before 15min.
The skin perfusion of three groups at 15min before burn intercomparison (P﹥0.05). The skin perfusion of electrical burn group 2 and treatment group 2 in each phase were lower than the control group 2(P﹤0.05). The treatment group 2 each phase were more than the electrical burn group 2 (P﹤0.05) .
10 The comparison of sICAM-1 in aboral three groups.
The sICAM-1 of each phase in control group 3 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the sICAM-1 in the electrical burn group 3 after HEB were significantly higher than before the burn 15min, most at 5min after HEB, the sICAM-1 have a trend of decrease gradually 1h later after HEB. The sICAM-1 in the treatment group 3 after HEB were significantly hegher than before the burn 15min.
The sICAM-1 of three groups at 15min before burn intercomparison (P﹥0.05). The sICAM-1 of electrical burn group 3 and treatment group 3 in each phase were hegher than the control group 3(P﹤0.05). The treatment group 3 each phase were less than the electrical burn group 3 (P﹤0.05). 11 The comparison of CD11b/CD18 in aboral three groups.
The CD11b/CD18 of each phase in control group 3 after bogus HEB compared with 15min before the burn , no significant difference (P﹥0.05). But the CD11b/CD18 in the electrical burn group 3 after HEB were significantly higher than before the burn 15min, most at 5min after HEB, the CD11b/CD18 have a trend of decrease gradually later. The CD11b/CD18 in the treatment group 3 after HEB were significantly hegher than before the burn 15min.
The CD11b/CD18 of three groups at 15min before burn intercomparison (P﹥0.05). The CD11b/CD18 of electrical burn group 3 and treatment group 3 in each phase were hegher than the control group 3(P﹤0.05). The treatment group 3 each phase were less than the electrical burn group 3 (P﹤0.05).
12 The adhesion leukocytes in aboral three groups and center three groups have same trend.
13 The skin perfusion in aboral three groups and center three groups have same trend.
Conclusion:
1 High-voltage electrical burns can cause leucocyte rheological abnormity change : count increase, rolling speed decrease, adhesion leukocytes increase, TLECT value extend.
2 Ulinastatin can reduce abnormity leucocyte rheological that were caused by high-voltage electrical.
3 High-voltage electrical burns can increased selectin-P, and selectin-E, and selectin-L and adhesion leukocytes in mesentery venuel, decreased chest wall skin perfusion.
4 Pentoxifylline can reduce selectin-P, and selectin-E, and selectin-L ,decrease adhesion leukocytes in mesentery venuel , increase chest wall skin perfusion.
5 High-voltage electrical burns can increase sICAM-1, and CD11b/CD18, and adhesion leukocytes and decrease chest wall skin perfusion.
6 Ulinastatin can decrease sICAM-1, and CD11b/CD18, and adhesion leukocytes and increase chest wall skin perfusion.
7 High-voltage electrical burns can cause leucocyte rheological abnormity change, selectin-P, and selectin-E, and selectin-L, and sICAM-1, and CD11b/CD18 et al play an important role in leukocyte adhesion. Ulinastatin and Pentoxifylline can reduce leucocyte rheological abnormity change.
引文
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