骨髓间充质干细胞对烟雾吸入性损伤兔早期炎症因子分泌的影响

目的 探讨骨髓间充质干细胞(MSCs)对烟雾吸入性损伤早期外周血及肺组织中肿瘤坏死因子-α(TNF-α)、白细胞介素(IL-1β、IL-6、IL-10)分泌的影响.方法 全骨髓培养法体外培养兔MSCs,用流式细胞术鉴定.将56只健康新西兰大耳白兔按随机数字表法分为正常对照组(C组,n=8)、烟雾吸入性损伤组(S组,n=24)、烟雾吸入性损伤+MSCs移植组(M组,n=24),后两组再分为伤后2、4、6 h亚组,每组8只.采用酶联免疫吸附法(ELISA)检测血浆及肺组织匀浆液中促炎因子TNF-α、IL-1β、IL-6及抗炎因子IL-10的含量.结果 与C组比较,S组各时间点血浆促炎、抗炎因子均显著升高;各时间点肺组织促炎因子显著升高,抗炎因子无明显变化.与S组比较,M组各时间点血浆促炎因子显著下降,抗炎因子显著升高[6 h时TNF-α(μg/L):1.7±1.7比4.1±1.6,IL-1β(ng/L):9.9±1.7比21.2±2.6,IL-6(μg/L):1.0±0.3比1.3±0.2,IL-10(ng/L):15.2±4.4比7.9±3.5,均P＜0.05];各时间点肺组织促炎因子显著降低,而抗炎因子仅在4 h、6 h显著升高[6 h时TNF-α(ng/L):503.0±156.4比587.7±171.2,IL-1β(ng/L):0.4±0.2比0.6±0.2,IL-6(ng/L):155.2±13.7比350.2±20.3,IL-10(ng/L):23.3±5.4比11.0±5.6,均P＜0.05].结论 MSCs移植能降低烟雾吸入性损伤早期促炎因子水平,升高抗炎因子水平,改善全身炎症反应,对烟雾吸入性损伤肺组织具有一定的保护作用.

Abstract：

Objective To explore the effect of bone marrow mesenchymal stem cells (MSCs) engraftment on secretion of tumor necrosis factor-α (TNF-α), interleukins (IL-1β, IL-6, IL-10) in peripheral blood and lung homogenates in the early stages of smoke inhalation injury. Methods MSCs were proliferated by the method of whole marrow culture and identified by flow cytometry. Fifty-six healthy New Zealand rabbits were randomly divided into control group (C group, n=8), smoke inhalation injury group (S group, n=24)and smoke inhalation injury+MSCs engraftment group (M group, n=24). The latter two groups were subdivided into 2, 4, 6 hours after injury subgroups, with 8 rabbits in each group. The levels of TNF-α,IL-1β, IL-6 and IL-10 in peripheral blood and lung homogenates were measured by enzyme-linked immunosorbent assay (ELISA). Results Compared with C group, concent of pro-inflammatory and anti-inflammatory cytokines in peripheral blood at each time point in S group were increased significantly.The concent of pro-inflammatory cytokines in lung homogenate at each time point in S group was significantly higher than thoae in C group, and that of anti-inflammatory cytokines showed no significant changes.Compared with the S group, concent of pro-inflammatory cytokines in peripheral blood in M group was decreased significantly, and that of anti-inflammatory cytokines was increased significantly [6 hours TNF-α(μg/L):1.7±1.7 vs. 4.1±1.6, IL-1β (ng/L): 9.9±1.7 vs. 21.2±2.6, IL-6 (μg/L): 1.0±0.3 vs.1.3 ± 0. 2, IL-10 (ng/L): 15. 2 ± 4. 4 vs. 7. 9 ± 3.5, all P＜0.05]. Concent of pro-inflammatory cytokines at each time point in M group was decreased significantly when compared with S group in lung homogenate,while only anti-inflammatory cytokine at 4 hours and 6 hours was increased significantly [6 hours TNF-α (ng/L): 503. 0±156. 4 vs. 587.7±171.2, IL-1β (ng/L): 0.4±0.2 vs. 0.6±0.2, IL-6 (ng/L): 155.2±13.7 vs. 350.2±20.3, IL-10 (ng/L): 23.3±5.4 vs. 11.0±5.6, all P＜0.05]. Conclusion MSCs engraftment could decrease pro-inflammatory cytokines and increase anti-inflammatory cytokines in the early stages of smoke inhalation injury, thus amelioratea inflammatory reaponse, which confers protective effect on smoke inhalation injury.     

膜攻击复合物C5b-9对创伤失血性休克大鼠肝损害的影响研究

目的 观察大鼠创伤失血性休克时肝脏是否受膜攻击复合物攻击,以及膜攻击复合物是否对肝脏细胞凋亡产生影响.方法 雄性Wistar大鼠50只,按随机数字表法均分为正常组及模型1、3、6、24 h组5组.采用骨折后经颈动脉放血至血压40 mm Hg(1 mm Hg=0.133 kPa)制备创伤失血性休克模型.取血浆,采用酶联免疫吸附法(ELISA)检测膜攻击复合物C5b-9浓度,采用速率法测定丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)浓度;取肝脏组织,采用免疫组化法检测C5b-9阳性表达,用原位末端缺刻标记法(TUNEL)检测肝细胞凋亡,苏木素-伊红(HE)染色,光镜下观察病理改变.结果 正常组血中能检测到少量的C5b-9;模型1、3、6 h组血中C5b-9浓度(ng/L)较正常组显著升高(272.91±9.56、192.01±9.04、156.78±8.37比25.98±5.87,均P＜0.05).模型3 h组血ALT(U/L)、模型1 h组血AST(U/L)即显著上升(92.90±8.83、264.83±31.14),24 h达高峰(184.30±12.98、647.36±60.02),与正常组(38.75±5.40、66.69±19.95)比较差异均有统计学意义(均P＜0.05).正常组及模型1 h、6 h组肝脏未发现C5b-9阳性表达;模型3 h组门管区大量肝脏实质细胞存在C5b-9(个)沉积(22.60±1.06),模型24 h组C5b-9沉积明显减少(2.20±0.60,P＜0.05).正常组未检测到凋亡细胞;模型1、6、24 h组发现散在凋亡细胞(个:1.20±0.25、5.60±0.37、1.60±0.26),模型3 h组中央静脉周围凋亡细胞明显增加,出现凋亡高峰(20.60±0.47),与其余各组比较差异均有统计学意义(均P＜0.05).模型组可见肝细胞水肿变性、肝细胞膜完整性破坏,细胞溶解,以24 h病理损害最重.结论 创伤失血性休克时大鼠肝脏受到膜攻击复合物C5b-9的攻击,并且肝脏C5b-9的表达高峰与凋亡高峰在同一时间点出现,但并不是同一部位;模型3 h后血中低水平的C5b-9提示预后极差.

Abstract：

Objective To observe whether the membrane attack complex C5b-9 would accumulate in the rats' liver after receiving the assault of traumatic hemorrhagic shock, and whether the membrane attack complex deals an impact on liver apoptosis. Methods Fifty male healthy Wistar rats were randomly divided into five groups: normal group, 1, 3, 6, 24-hour model groups. The model of traumatic hemorrhagic shock was reproduced by withdrawal of blood from carotid artery after a bone fracture till the blood pressure lowered to 40 mm Hg(1 mm Hg= 0. 133 kPa). Plasma membrane attack complex C5b-9 concentration was assayed using enzyme linked immunoadsorbent assay. Alanine aminotransferase(ALT)and aspartate aminotransferase(AST)in blood was determined by Rate method. Immunohistochemistry was used to detect C5b-9 deposition in the liver. Apoptosis of liver cells was then detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)assay. The pathological changes in paraffin sections stained with hematoxylin-eosin(HE)were observed under light microscope. Results A small amount of C5b-9 in plasma was found in normal group, and the values(ng/L)of 1, 3, 6-hour models were significantly higher than those of the normal group(272. 91±9.56, 192. 01±9. 04, 156. 78±8. 37 vs. 25. 98±5.87, all P＜0. 05). ALT(U/L)in 3-hour model group and AST(U/L)in 1-hour model group were increased significantly(92.90 ± 8. 83, 264.83 ± 31.4), peaked at 24 hours(184.30 ± 12. 98, 647.36 ± 60. 02), and there was significant difference compared with normal group(38. 75±5.40, 66. 69± 19.95, all P＜0. 05). In the normal group and the 1-hour and 6-hour model groups, no C5b-9 was found in liver, but in the 3-hour model group a large number of liver parenchymal cells in the portal area were found to contain C5b-9 (22. 60± 1.06), however the number decreased significantly in the 24-hour model(2. 20±0. 60, P＜0. 05).In normal group there was no apoptotic cell, and in 1, 6, 24-hour model groups there were scattered apoptotic cells(1. 20±0. 25, 5. 60±0. 37, 1. 60±0. 26). In the 3-hour model group apoptosis of hepatic cells around the central vein was increased to the peak(20. 60 ± 0. 47), and there was significant difference compared with other groups(all P＜0. 05). In the model groups the liver cells became edematous, and the integrity of the membrane was lost, and some cells were even lysed. The pathological damage is most serious in 24-hour model group. Conclusion The membrane attack complex C5b-9 insulted the rats' liver after a traumatic hemorrhagic shock, and apoptosis of hepatic cells and the content of C5b-9 peaked in 3-hour model, though they do not occur in the same site. A low level of C5b-9 in blood 3 hours after shock predict a poor prognosis.     

胸部爆震伤致兔急性呼吸窘迫综合征模型的建立及相关因素分析

目的 构建室内胸部爆震伤致兔急性呼吸窘迫综合征(ARDS)模型并分析其发生机制及早期死亡原因,为研究肺爆震伤早期预警体系和治疗方法提供依据.方法 按照不同炸药量和致伤距离所产生的压强,将60只新西兰大白兔按随机数字表法分为5个致伤组和1个无致伤对照组.伤后观察存活率和组织病理学,并监测病理生理学指标、肺含水量.结果 冲击波压强低于1 210.5 mm Hg(1 mm Hg=0.133 kPa,A、B组)时,肺损伤较轻,表现为点状肺挫伤,肺简明损伤评定分级法(ALS)均在2级内,动物伤后24 h内全部恢复,长期存活无并发症.冲击波压强高于2 036.1 mm Hg(D、E组)时,肺损伤过重,表现为广泛的肺挫伤、肺门撕裂伤和肺内大血肿,AIS均大于5级,动物于伤后1 h内全部死亡.冲击波压强为1 917.3 mm Hg(C组)时,肺表现为广泛而恒定的挫伤,累及4个肺叶以上,AIS 4～5级,伤后6 h内出现动脉氧分压下降;肺组织可见肺泡壁水肿,部分肺泡壁断裂,肺泡融合;肺泡内充满大量炎性细胞,偶见透明膜形成.与对照组比较,C组兔致伤6 h肺湿/干重比值即显著升高(6.46±0.24比3.98±0.19,P＜0.01),血浆及支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)即明显升高[血浆TNF-α(ng/L):328.89±6.26比62.12±2.98,BALF TNF-α(ng/L):164.87±4.59比29.51±1.12;血浆IL-6(ng/L):128.51±4.13比19.32±1.53,BALF IL-6(ng/L):94.97±1.14比22.72±0.19,均P＜0.05].结论 在1 917.3 mm Hg爆炸压强的密闭环境下,冲击伤可诱导兔发生ARDS;TNF-α及IL-6参与爆震伤致ARDS的形成与发展;特定环境下,肺脏破裂致气胸为早期死亡原因,而冲击波致循环系统功能紊乱也是引起早期死亡的重要原因.

Abstract：

Objective To reproduce acute respiratory distress syndrome (ARDS) model in rabbit induced by chest blast injury and to analyze the pathogenesis and causes of early death in order to provide the basis for the early diagnosis of lung blast injury and its early-warning system to facilitate an early treatment.Methods Sixty healthy New Zealand white rabbits were divided into six groups according to the different explosion distance with the random number table method. The survival rate and its resulting pathological changes were observed and patho-physiological indexes and lung fluid content were determined at sequential time points post-explosion. Results Shock wave pressure less than 1 210. 5 mm Hg (1 mm Hg=0. 133 kPa,group A, B) resulted in limited injury to the lung within grade-2 as assessed with the abbreviated injury scale (AIS). The rabbits in these groups recovered soon and survived without any complication. Shock pressure higher than 2 036. 1 mm Hg (group D, E) caused severe injuries to the lung, including deep laceration, disruption of lung hilus and large hematoma in the lung, and the injury severity of lungs was assessed above grade-5 as assessed with AIS. All rabbits died within 1 hour post-explosion. The groups described above failed to meet the demand of an ARDS model for the present study. Shock wave pressure at 1 917. 3 mm Hg (group C) produced extensive contusion from grade-4 to grade-5 as assessed with AIS. The rabbits survived in poor general condition, and arterial partial pressure of oxygen (PaO2) lowered within 6 hours. Pathological examination showed extensive and constant multi-focal bleeding involving more than four lobes. The alveolar wall was edematous, with partial rupture and alveolar fusion in lung tissues was observed in the group C. Alveoli were filled with inflammatory cells, and hyaline membrane was formed occasionally. Compared with control group, the wet to dry weight ratio (W/D) in lungs increased obviously (6.46±0. 24 vs. 3. 98±0. 19, P＜ 0. 01) in group C within 6 hours postinjury. The contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in plasma and bronchoalveolar lavage fluid (BALF) were also increased distinctly compared with the control group [TNF-α (ng/L) in plasma: 328. 89± 6.26 vs.62.12±2. 98, TNF-α (ng/L) in BALF: 164.87±4.59 vs. 29. 51±1.12; IL-6 (ng/L) in plasma: 128. 51±4.13 vs. 19.32±1.53: IL-6 (ng/L) in BALF: 94.97±1.14 vs. 22.72±0. 19, all P＜0. 05]. Conclusion In an airtight environment, rabbit ARDS model can be reproduced successfully by blast injury with 1 917.3 mm Hg explosion pressure; TNF-α and IL-6 are involved in the pathogenesis and development of ARDS in blast injury. Pneumothorax as a result of lung rupture is the chief reason for early death and dysfunction of circulatory system is also an important reason in producing early death.     

危重症应激性高血糖患者炎症反应与胰岛素组分关系的研究

目的 研究应激性高血糖(SHG)患者炎症反应与胰岛素组分的关系,探讨炎症反应对胰岛素抵抗及胰岛β细胞分泌功能的影响.方法 选择SHG患者45例,根据其临床炎症反应状态分为应激期和应激消除期,并选择25例健康体检者作为对照;分别测定血中肿瘤坏死因子-α(TNF-α)、血糖、胰岛素组分[包括胰岛素原(PI)、免疫反应性胰岛素(IRI)、真胰岛素(TI)、C-肽(C-P)]浓度及功能指标[包括胰岛素抵抗指数(HOMA-IR)、胰岛β细胞功能指数(HOMA-β)]水平,比较组间血糖、TNF-α、胰岛素组分及功能指标,并进行TNF-α与血糖、胰岛素组分及功能指标的相关性分析.结果 ①SHG应激期、应激消除期及健康对照组TI水平比较差异无统计学意义[3.68(1.57,7.70)、3.42(2.41,7.40)、1.46(0.35,4.90)mU/L,均P＞0.05],应激期血糖[(10.04±2.43)mmol/L]、TNF-α[13.70(11.77,20.00)ng/L]、PI[6.20(3.22,9.27)pmol/L]、IRI[13.45(9.88,19.88)mU/L]及C-P[3.01(2.37,4.00)μg/L]水平均明显高于应激消除期[血糖:(6.09±0.84)mmol/L,TNF-α:11.58(8.80,13.22)ng/L,PI:1.54(0.36,11.82)pmol/L,IRI:10.80(5.35,12.60)mU/L,C-P:2.42(1.17,3.56)μg/L]和健康对照组[血糖:(4.87±0.56)mmol/L,TNF-α:9.27(7.48,12.16)ng/L,PI:2.20(1.88,4.54)pmol/L,IRI:5.50(4.00,8.00)mU/L,C-P:1.15(0.87,1.76)μg/L,P＜0.05或P＜0.01].②SHG应激期HOMA-IR[5.17(3.41,11.51)]明显高于应激消除期[3.24(1.51,6.95)]及健康对照组[1.14(0.81,1.79),P＜0.05和P＜0.01];应激期HOMA-β[10.80(3.72,31.40)]明显低于应激消除期[28.42(6.46,125.01)]及健康对照组[21.94(7.77,62.01),P＜0.01和P＜0.05].③SHG患者TNF-α与PI、IRI、C-P及HOMA-IR呈正相关(r1=0.292,r2=0.344,r3=0.397,r4=0.324,P＜0.05或P＜0.01);与HOMA-β呈负相关(r=-0.235,P＜0.05).结论 危重症SHG患者炎症反应越重,胰岛素组分PI、IRI、C-P升高越明显,而TI相对分泌不足;炎症反应可影响危重症SHG患者胰岛素抵抗和胰岛β细胞分泌功能.

Abstract：

Objective To observe the relationship between inflammatory response and the constituents of islet β cell secretion during stress hyperglycemia(SHG)in critically ill patients, in order to study the impact of inflammatory response on insulin resistance and the secretion function of islet β cells.Methods According to the state of inflammatory response, 45 critical patients with SHG were divided into two groups: stress and the convalescence period. Twenty-five healthy individuals were enrolled as control group. The blood levels of tumour necrosis factor-α(TNF-α), blood glucose(BG), and insulin components including proinsulin(PI), immunoreactive insulin(IRI), true insulin(TI), C-peptide(C-P)were measured respectively. The levels of BG, TNF-α, insulin components, insulin resistance index (HOMA-IR) and the secretion index(HOMA-β)were compared among groups. The relationship between TNF-α and BG, insulin components, HOMA-IR, HOMA-β were analyzed. Results ①There was no difference in concentrations of TI among stress period, convalescence stage and control group[3.68(1.57, 7. 70), 3. 42(2.41, 7.40),1.46(0. 35, 4.90)mU/L, all P＞0. 05], whereas the concentration of BG[(10. 04 ± 2. 43)mmol/L],TNF-α[13. 70(11.77, 20.00)ng/L], PI[6. 20(3. 22, 9.27)pmol/L], IRI[13.45(9. 88, 19. 88)mU/L]and C-P[3. 01(2. 37, 4. 00)μg/L]in stress period were significantly higher than those in the convalescence stage[BG:(6. 09±0. 84)mmol/L, TNF-α: 11.58(8. 80, 13. 22)ng/L, PI: 1.54(0. 36, 11.82)pmol/L,IRI: 10.80(5.35, 12.60)mU/L, C-P: 2.42(1.17, 3.56)μg/L]and control group[BG:(4.87±0.56)mmol/L,TNF-α: 9.27(7.48, 12.16)ng/L, PI: 2.20(1.88, 4.54)pmol/L, IRI: 5.50(4.00,8.00)mU/L, C-P: 1.15(0.87, 1.76)μg/L, P＜0.05 or P＜0.01]. ②The HOMA-IR[5.17(3.41,11.51)]in stress period was significantly higher than that in the convalescence[3.24(1.51, 6. 95)]and control group[l. 14(0. 81, 1.79), P＜0. 05 and P＜0. 01]. The HOMA-β[10. 80(3. 72, 31.40)]of islet βcell in stress period was significantly lower than that in the convalescence[28.42(6. 46, 125.01)]and control group[21.94(7. 77, 62. 01), P＜0. 01 and P＜0. 05]. ③There were positive correlations between the concentration of TNF-α and PI, IRI, C-P and HOMA-IR(r1 = 0. 292, r2 = 0. 344, r3 = 0. 397, r4 = 0. 324,P＜ 0. 05 or P ＜ 0. 01). There were negative correlation between concentration of TNF-α and HOMA-β(r=-0. 235, P＜0. 05). Conclusion The severer the inflammatory response, the higher PI, IRI and C-P,while the secretion of TI is relatively deficient. Inflammatory response could affect insulin resistance and the secretion function of islet β cell during SHG in critically ill patients.     

亚低温对急性肺损伤大鼠肺泡表面活性蛋白A含量的影响

目的 探讨亚低温对内毒素脂多糖(LPS)诱导急性肺损伤(ALI)大鼠肺泡表面活性蛋白A(SP-A)含量的影响.方法 按随机数字表法将40只雄性Wistar大鼠分组.采用气管内滴入LPS制备ALI动物模型;对照组气管内只滴人生理盐水.模型组和对照组分别于术后1 h和8 h处死8只大鼠;亚低温组于滴入LPS 1 h后将体温降低并维持在32.5～33.0℃,8 h后处死8只大鼠.各组分别于术前及术后1 h、8 h测定动脉血气,并计算氧合指数(PaO2/FiO2);采用酶联免疫吸附法检测支气管肺泡灌洗液(BALF)中SP-A含量;光镜下观察肺组织形态结构的变化.结果 气管内滴入LPS 1 h后,大鼠PaO2/FiO2均达到ALI的诊断标准.与对照1 h组比较,模型1 h组BALF中SP-A含量(μg/L)明显降低(53.27±1.95比74.81±6.55,P＜0.01);模型8 h组和亚低温8 h组SP-A含量(4.35±2.76和51.36±2.33)均较对照8 h组(70.81±5.01)明显降低,但亚低温8 h组SP-A含量较模型8 h组明显增高(均P＜0.01).光镜下观察,对照1 h和8 h组肺泡结构基本正常;模型8 h组肺组织炎症反应最重;模型1 h组和亚低温8 h组肺组织炎症反应较模型8 h组有所减轻.结论 亚低温能延缓内毒素诱导的ALI大鼠早期肺泡内SP-A含量下降的程度,在一定程度上可减轻肺损伤.

Abstract：

Objective To investigate the effect of hypothermia (HT) on the concentration of surfactant protein A (SP-A) during lipopolysaccharide (LPS) induced acute lung injury (ALI) in rats.Methods Forty male Wistar rats were randomly divided into three groups. The ALI model was reproduced by LPS intratracheal instillation; only saline was instilled intratracheally for control group. Rats in both model group and control group were sacrificed respectively at 1 hour and 8 hours (each n= 8). In HT group the body temperature was lowered to 32. 5 - 33.0 ℃ 1 hour after LPS instillation, and 8 rats were sacrificed st 8 hours. The arterial blood gas was determined in all the groups before and 1 hour and 8 hours after instillation of saline or LPS, and the oxygenation index (PaO2/FiO2) was calculated. The concentration of SP-A in bronchoalveolar lavage fluid (BALF) was determined by enzyme linked immunosorbent assay. The morphological changes in lung tissue of rats were observed under light microscope. Results At 1 hour after intratracheal instillation of LPS, the PaO2/FiO2 of each group reached the diagnostic criterion of ALI.Compared with control 1-hour group, the SP-A (μg/L) in BALF of model 1-hour group was decreased (53. 27±1.95 vs. 74. 81±6. 55, P＜0. 01); the SP-A in model 8-hour group and HT 8-hour group (4.35±2. 76 and 51.36±2. 33) was both obviously decreased compared with control 8-hour group (70. 81±-5. 01,both P＜0. 01). Compared with model 8-hour group, the SP-A of HT 8-hour group was obviously increased (P＜0. 01). Results of light microscopic examination, it was revealed that the alveolar structure of control 1-hour group and control 8-hour group was almost normal. Inflammatory response in lung tissues in model 8-hour group was found to be most serious; compared with model 8-hour group, inflammatory response in lung tissues in model 1-hour group and HT 8-hour group was reduced in certain degree. Conclusion A certain extent of HT may reduce lung injury of early endotoxin-induced ALI rats by delaying lowering of alveolar SP-A levels.     

p38MAPK和COX-2mRNA在创伤后多器官功能障碍综合征患者外周血中的表达

目的 探讨创伤后多功能障碍综合征(multiple organ dysfunction syndrome,MODS)患者外周血单核细胞(peripheral blood mononuclear cells,PBMCs)环氧化酶-2(cyclooxygenase-2,COX-2)与p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38MAPK)mRNA的表达以及与MODS病情变化的关系.方法 选择符合1995年中华医学会急诊分会危重病专业组制定的MODS病情分期诊断标准和1991年Knaus提出急性生理和慢性健康评分Ⅲ(APACHE Ⅲ)的患者40例,其中男22例,女18例;与患者年龄、性别相匹配的健康对照组40名.用酶联免疫吸附试验法(ELISA)检测PBMCs培养上清液COX-2与p38MAPK含量;用逆转录-聚合酶链反应(RT-PCR)法检测PBMCs中COX-2与p38MAPK的mRNA表达.并分析它们的表达与APACHEⅢ评分的相关性.结果 MODS组患者PBMCs的COX-2与p38MAPK含量及两者的mRNA表达均显著高于健康对照组(均P<0.05);MODS死亡患者PBMCs的COX-2与p38MAPK含量及两者的mRNA表达与存活患者比较,差异具有统计学意义(均P<0.05);相关分析显示,PBMCs培养上清液中COX-2与p38MAPK含量呈正相关(r=0.614 7,P<0.01);患者 PBMCs的COX-2和p38MAPK mRNA表达与APACHEⅢ评分呈正相关(r1=0.500 9,P1<0.05,r2=0.531 6,P2<0.05).结论 COX-2与p38MAPK参与了MODS的发病过程,而且可作为判断MODS预后的辅助指标.

Abstract：

Objective To explore the expression of COX-2 and p38MAPK in patients with trauma MODS. Methods Forty MODS patients were evaluated. The levels of peripheral blood mononuclear cells COX-2 and p38MAPK in MODS patients and 40 normal controls was detected by enzyme linked immunosor-bent assay (ELISA). RT-PCR was used to measure the COX-2 mRNA and p38MAPK mRNA expression of in PBMCs. ANOV and correlation analysis were used in statistical analysis. Results The levels of COX-2 and p38MAPK of PBMCs and the mRNA expression in MODS group were higher than in control group (all P <0.05). The levels of COX-2 and p38MAPK of PBMCs and the mRNA expression in dead group were higher than in survival group( all P <0.05). The levels of COX-2 and p38MAPK of PBMCs were positively correlated, (r =0.6 147, P<0.01). The expression of COX-2 mRNA, p38MAPK mRNA of PBMCs and APACHE I scoring were positively correlated (r1 =0.5 009, P1 <0.05,r2 =0. 5 316, P2 <0. 05). Conclusions COX-2 and p38MAPK of PBMCs take part in the onset of MODS, and may service as index to judge the prognosis of MODS.     

食管鳞状细胞癌患者血清T辅助细胞类细胞因子的表达及其临床意义

目的 探讨食管癌患者血清T辅助细胞(Th1、Th2)类细胞因子的表达及其临床意义.方法 采用双抗体酶联免疫吸附法(ELISA)检测45例食管鳞状细胞癌患者及30名健康体检者外周血Th1[干扰素(INF)-γ、白细胞介素(IL)-2]、Th2类(IL-4)细胞因子的含量.结果 食管癌患者Th1类细胞因子INF-γ、IL-2表达含量较健康对照组降低[(11.51±2.15)、(16.31±2.27)ng/L,t=18.24,P＜0.01);(10.20±2.10)、(16.92±2.41)ng/L,t=15.31,P＜0.05];Th2类细胞因子(IL-4)较健康对照组升高[(5.30 -0.11)、(2.23±0.29)ng/L,t=5.79,P＜0.05],且其表达趋势与肿瘤的TNM分期有关.结论 食管癌患者体内存在Th1/Th2漂移现象.该现象可能与肿瘤细胞发生免疫逃逸有关.

Abstract：

Objective To study the expression of Th1 and Th2 types cytokines in patients with esophageal squamous cell carcinoma and the clinical significance. Methods The expressions of Th1 ( INF-γ、IL-2) and Th2 (IL-4) types cytokines in cultured peripheral blood mononuclear cells (PBMC) from 30 healthy controls and 45 esophageal squamous cell carcinoma patients were determined by Enzyme-linked immunosorbent assay (ELISA). Results Compared with the control group, the expressions of Th1 type cytokines, IL-2 and INF-γwere significantly lower in the cultured PBMCs from the cancer patients (tINF-γ= 18. 24 ,tIL-2 = 15.31 ,Ps ＜0. 01 ) ,while the expression of Th2 type cytokines,IL-4 was significantly higher in the cultured PBMCs from the cancer patients ( tIL-4 = 5.79, P ＜ 0. 05 ). The expression changes of the cytokines showed a correlation with TNM (tumou-node-metastasis) stage of the tumor. Conclusion The Th1/Th2 shift existed in patients with esophageal squamous cell carcinoma and it might be one of the underline mechanisms of tumor immune escape.     

Effects of bone marrow mesenchymal stem cells on the expressions of inflammatory factors in rats with multiple organ dysfunction syndrome北大核心CSCD

Objective: To investigate the effects of bone marrow mesenchymal stem cells (BMSC) on the expression of inflammatory factors in rats with multiple organ dysfunction syndrome (MODS). Methods: BMSC extracted from the 4-week-old Sprague-Dawley (SD) rats was cultivated and identified in vitro, then the 4th passage of which was used in the experimental study. Sixty SD rats were randomly(random number) divided into three groups (n=20 in each group): Sham group (SG), MODS group (MG) and BMSC group (BG). Rats in the MG was injected by 1 mg/kg lipopolysaccaride (LPS) via great saphenous vein, rats in the SG injected with the same volume sterile phosphate buffer saline and rats in the BG infused by l×106/cells BMSCs through the tail vein at 2 h after LPS injection. The survival rate, tissue pathological changes of the lung, liver and heart by hematoxylin and eosin (HE) staining, organ dysfunction measurement by blood gas analysis and biochemical indicators as well as the related inflammatory factors by protein microarray and enzyme linked immunosorbent assay (ELISA), were detected 72 h post operation. Multi-group quantitative data was analyzed by one way ANOVA, paired-comparisons by LSD-t test and the comparisons of survival curves in the three groups by Log-rank test. The value of P<0.05 was considered statistically significant. Results: The survival rate in SG, MG and BG was 100%, 60% and 80%, respectively. The survival curves showed that the survival rate of SG was higher than the MG and BG (SG vs. MG, χ2=9.798, F=0.001 7; SG vs. BG, χ2=4.333, P=0.037 4), but there was no significant difference comparing the BG to the MG (χ2=2.408, P=0.120 7). The tissue congestion and edema, and inflammatory cells infiltration in the lung, liver, and heart of the MG were observed by HE staining, while these changes reduced in the BG. Compared with the SG, the levels of pH and PaCO2 and lactic acid (Lac) increased significantly (all P<0.01), the level of total bilirubin (TB) significantly increased [(0.801±0.501)U/L vs. (2.533±0.382)U/L, P=0.003], while the albumin(ALB) level decreased significantly[(35.471±4.015)U/L vs. (23.202±4.872)U[L, P<0.01], and creatine kinase (CK) level increased significantly in MG [(315.670±41.402) vs. (708.250±219.201), P=0.042]. After BMSC treatment, the organ function improved significantly (all P<0.05). Gamma interferon (IFN-γ) and monocyte chemotactic protein 1 (MCP-1) were the differential expression factors in protein chips. The results of ELISA were similar to the protein chips: compared with the SG, IFN-γ and MCP-1 expressions in the MG increased significantly (F<0.01). Compared with MG, the expressions of IFN-γ and MCP-1 decreased significantly in the BG (P<0.01). Conclusion: BMSC administration could modulate the inflammatory response of MODS rats by inhibiting the levels of IFN-γ and MCP-1, and improve the organ function and the survival rate. © 2018 Chinese Medical Association. All rights reserved.     

高浓度氧对未成年大鼠肺部炎症反应的影响

目的 探讨高浓度氧对未成年大鼠肺部炎症反应的影响.方法 将40只出生21 d的SD大鼠按随机数字表法分为空气对照组及高氧暴露12、24、48、72 h组,每组8只,分别将大鼠置于空气和常压高氧箱(氧含量达92%～94%)中.于相应时间点采用放血法处死大鼠后取肺组织,并行支气管肺泡灌洗.采用硫代巴比妥酸法和比色法分别测定肺组织丙二醛(MDA)含量及髓过氧化物酶(MPO)活性;采用酶联免疫吸附法(ELISA)检测支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和IL-10含量;观察肺组织病理改变,并进行肺损伤评分.结果 与空气对照组比较,高氧暴露12 h肺组织MDA含量(mmol/g)即显著升高(2.24±0.43比1.57±0.31),MPO活性(U/g)于高氧暴露24 h显著升高(1.24±0.25比0.69±0.22),并均随高氧暴露时间延长逐渐增加(P<0.05或P<0.01).BALF中TNF-α、IL-6和IL-10含量于高氧暴露24 h时较空气对照组显著增加[TNF-α(ng/L):135.2±44.0比94.5±22.3,IL-6(ng/L):73.1±14.2比55.7±17.3,IL-10(ng/L):67.9±21.7比48.2±7.6,P<0.05或P<0.01];但高氧暴露48 h时较24 h时显著降低(48 h时BALF中TNF-α、IL-6、IL-10分别为105.4±17.0,54.3±17.4,50.9±6.9,均P<0.05).高氧暴露12 h时肺损伤评分(分)即较空气对照组显著升高(4.5±1.4比1.3±0.5),并随高氧暴露时间延长进一步升高(P<0.05或P<0.01).结论 高浓度氧可引起未成年大鼠肺部炎症损伤;炎症细胞因子的出现高峰均在高氧暴露24 h.     

产兔与非孕兔休克复苏后肺损伤的比较研究

目的 探讨产兔和非孕兔失血性休克复苏后急性肺损伤的差异.方法 将18只新西兰兔按随机数字表法分为产兔组和非孕兔组,每组9只.采用颈动脉放血致失血性休克1h,乳酸林格液复苏持续3h建立失血性休克复苏模型.分别于产前期、产后期(休克前期,0h)、休克期末(1 h)、复苏期间(2.5 h)以及复苏期末(4 h)5个时间点采血测定肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10);复苏期持续3h后处死动物,取肺组织检测丙二醛(MDA)、超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)、干/湿重比值(D/W),以及核转录因子-κB(NF-κB)活性和细胞间黏附分子-1(ICAM-1)mRNA表达.结果 产兔产前期血清TNF-α(ng/L)、IL-10(ng/L)含量与非孕兔差异无统计学意义(TNF-α:87.6±6.8比83.2±5.3;IL-10:44.9±3.9比42.7±3.4,均P＞0.05);休克前期TNF-α水平显著增高(102.5±8.1比87.6±6.8,P＜0.05).产兔与非孕兔休克1h后TNF-α、IL-10均升高;各复苏时期产兔TNF-α水平明显高于非孕兔(1 h:230.0±14.9比202.0±10.1,2.5 h:290.0±18.6比236.0±14.4,4 h:265.0±15.9比217.0±12.8,均P＜0.05),而IL-10水平明显低于非孕兔(1 h:104.3±6.9比135.0±7.8,2.5 h:146.8±9.4比178.3±11.7,4 h:126.0±7.9比165.8±9.6,均P＜0.05).休克复苏后产兔肺组织MDA、MPO、D/W比值、NF-κB活性和ICAM-1 mRNA表达均显著高于非孕兔[MDA(nmol/mg):52.6±5.9比39.4±4.7,MPO(U/mg):4.62±0.85比3.26±0.62,D/W比值:0.186±0.025比0.143±0.016,NF-κB(A值):0.89±0.27比0.46±0.15,ICAM-1mRNA:4.6±1.2比2.5±0.7,均P＜0.05];而SOD(U/mg)水平较低(47.8±6.7比63.5±8.2,P＜0.05).结论 分娩可致产兔血清炎症因子TNF-α显著升高,失血性休克复苏后产兔出现肺组织炎症损伤较非孕兔更为严重,炎症因子的差异可能是导致休克复苏后炎症应答差异的原因之一.     

高压氧对油酸诱导大鼠急性肺损伤作用的实验研究

目的 探讨高压氧(HBO)对油酸(OA)诱导大鼠急性肺损伤(ALI)的干预作用.方法 80只SD大鼠按随机数字表法分为4组.OA组30只,经鼠尾静脉注射OA 0.15 ml/kg制备ALI模型,分别于制模后4 h、3 d、7 d各随机活杀10只;OA+HBO组20只,在HBO治疗箱给予2.5 atm(1 atm=101.325 kPa)下单次治疗90 min,分别于HBO治疗后3 d、7 d各随机活杀10只;单纯HBO干预组20只,分别于HBO治疗后3 d、7 d各随机活杀10只;另设正常对照组10只.取腹主动脉血进行血气分析,测定血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、IL-6;取左肺标本,观察大体形态改变及镜下病理学改变;取右肺,测定湿/干重(W/D)比值.结果 OA组4 h后动脉血氧分压(PaO2,mm Hg,1 mm Hg=0.133 kPa)由107.70±5.37降至57.40±2.63;肉眼可见肺脏明显淤血、水肿;光镜下肺泡正常结构消失,间质水肿增宽,大量炎性细胞浸润,毛细血管明显扩张、透明膜形成;W/D比值较正常对照组明显增加(6.94±0.44比4.59±0.44,P<0.05),血清TNF-α、IL-1β、IL-6水平升高[TNF-α(μg/L):18.52±1.20比5.27±0.61,IL-1β(μg/L):13.73±1.37比6.13±1.51,IL-6(μg/L):14.51±1.21比11.14±0.89].经HBO治疗3 d、7 d时PaO2(mm Hg,3 d:79.20±1.68比59.00±2.70,7 d:94.30±3.77比74.00±3.85)、肺W/D比值(3 d:7.43±0.73比9.82±0.99,7 d:6.75±1.14比8.77±1.60)均较OA组同期有不同程度改善(P<0.05或P<0.01).治疗3 d后HBO有降低血清中IL-1β(μg/L)的作用(6.46±1.99比9.09±1.09,P<0.05).结论 HBO治疗有改善ALI大鼠氧合,促进肺水吸收、抑制部分炎症介质产生的作用.     

血管紧张素Ⅱ对急性肺损伤大鼠肺水通道蛋白1表达的影响

目的 观察血管紧张素Ⅱ(AngⅡ)对急性肺损伤(ALI)大鼠肺水通道蛋白1(AQP1)表达的影响及在肺水肿形成中的作用.方法 按随机数字表法将40只SD大鼠分为假手术组、模型组、AngⅡ受体阻滞剂预处理组及治疗组,每组10只.采用失血性休克-内毒素二次打击建立大鼠ALI模型.预处理组静脉注射脂多糖(LPS)前30 min注射AngⅡ受体阻滞剂30 μg/kg,注射LPS后30 min注射30 μg/kg生理盐水;治疗组注射LPS前30 min注射30 μg/kg生理盐水,注射LPS后30 min再注射AngⅡ受体阻滞剂30 μg/kg;模型组注射LPS前、后均给予30 μg/kg生理盐水.制模后6 h处死大鼠,取下腔静脉血,用放射免疫法测定血清肿瘤坏死因子-α(TNF-α)水平;取肺组织,计算湿/干重(W/D)比值,用放射免疫法测定肺组织AngⅡ表达,用逆转录-聚合酶链反应测定AQP1 mRNA表达.结果 与假手术组相比,ALI大鼠血清TNF-α水平及肺组织W/D比值、AngⅡ表达明显增加,AQP1 mRNA表达明显减少.预处理组及治疗组血清TNF-α水平(μg/L)较模型组明显减少(4.79±0.24、5.55±0.36比6.34±0.31,均P<0.05),肺组织W/D比值减小(4.34±0.23、4.85±0.20比5.41±0.26,均P<0.05),AQP1 mRNA表达明显增加(0.854±0.067、0.727±0.081比0.358±0.071,均P<0.05);而AngⅡ表达(ng/g)有所降低(172.19±15.82、202.82±20.47比245.88±26.31),但差异无统计学意义(均P>0.05).AQP1 mRNA表达与AngⅡ表达和肺组织W/D比值均呈负相关(r1=-0.782,r2=-0.726,均P<0.05).结论 ALI时AngⅡ可能直接或通过炎症介质下调肺脏AQP1 mRNA表达,为肺水肿形成的机制之一.     

卡巴胆碱对脓毒症大鼠内脏组织缺血引起脂质过氧化损伤的作用研究

目的 探讨卡巴胆碱(CAR)对脓毒症大鼠脏器组织灌流和脂质过氧化损伤的影响.方法 雄性SD大鼠64只,采用盲肠结扎穿孔术(CLP)制备大鼠脓毒症模型.随机分为CAR处理组和CLP组,每组32只,术后即刻两组分别静脉注射CAR 10 μg/kg或等量生理盐水.每组16只用于观察12 h和24 h死亡率;其余16只于CLP后18 h测定平均动脉压(MAP)和肝、肾、空肠组织血流量;取血测定血浆丙氨酸转氨酶(ALT)和肌酐(Cr)水平;后处死动物,测定空肠组织二胺氧化酶(DAO)活性及肝、肾、空肠组织黄嘌呤氧化酶(XOD)活性、丙二醛(MDA)含量和组织含水量.结果 CAR组12 h和24 h死亡率分别为25.0%(4/16)和50.0%(8/16),显著低于CLP组[37.5%(6/16),75.0%(12/16),P均<0.05].CLP后18 h,两组MAP差异无统计学意义(P>0.05);CAR组肝、肾、空肠组织血流量均明显大于CLP组(P均<0.05),肾和空肠组织XOD活性、MDA含量及组织含水量显著低于CLP组(P均<0.05);脏器功能指标[ALT;(64.3±8.3)U/L,Cr:(96.4±7.0)μmol/L,DAO;(0.20±0.04)U/L]的改善程度也均显著优于CLP组EALT:(81.5±7.9)U/L,Cr:(117.1±6.7)μmol/L,DAO;(0.12±0.03)U/L,P均<0.053.结论 CAR能改善脓毒症大鼠内脏灌流、抑制氧自由基生成,减轻组织水肿和脏器功能损害.     

急性呼吸窘迫综合征大鼠多器官中Gq/11蛋白表达的变化及意义

目的 探讨急性呼吸窘迫综合征(ARDS)大鼠肺、脑、心、肾、肝、小肠中Gq/11蛋白表达及作用.方法 40只Wistar大鼠按随机数字表法分为5组,每组8只.由大鼠尾静脉注射油酸(OA)0.2 ml/kg复制ARDS模型,对照组从尾静脉注射等量生理盐水.模型组分别于制模后30、60、90和120 min检测血浆和各器官中乳酸脱氢酶(LDH)、丙二醛(MDA)、血管紧张素转换酶(ACE);蛋白质免疫印迹法(Western blotting)检测各器官中Gq/11蛋白α活性亚基Gαq/11蛋白表达.结果 与对照组相比,LDH活性于30 min后在血浆和心呈进行性升高[血浆(kU/L):9.69±1.66比6.27±1.70,心(kU/g):0.81±0.12比0.59±0.09],60 min后在肺、脑、肾、小肠呈进行性升高[肺(kU/g):1.15±0.19比0.87±0.11,脑(kU/g):2.27±0.37比1.53±0.61,肾(kU/g):1.13±0.26比0.64±0.09,小肠(kU/g):0.72±0.10比0.60±0.13],90 min后在肝(kU/g)呈进行性升高(0.50±0.14比0.39±0.05,P<0.05或P<0.01);MDA含量于30 min后在心(μmol/g)呈进行性升高(2.20±0.47比1.45±0.27),60 min后在血浆、肺、肾呈进行性升高[血浆(μmol/L):3.10±0.58比2.33±0.35,肺(μmol/g):5.56±1.30比2.05±0.52,肾(μmol/g):1.61±0.27比0.98±0.42],90 min后在脑、肝、小肠呈进行性升高[脑(μmol/g):6.78±1.38比5.83±1.58,肝(μmol/g):2.58±0.68比2.11±0.42,小肠(μmol/g):2.14±0.51比0.81±0.26,P<0.05或P<0.01];ACE活性于60 min后在血浆和肺呈进行性降低[血浆(μmol·min-1·L-1):15.47±1.68比19.87±3.11,肺(μmol·min-1·g-1):20.61±1.81比26.26±1.93],在肾(μmol·min-1·g-1)呈进行性升高(15.92±1.20比13.67±2.26),90 min后在小肠(μmol·min-1·g-1)呈进行性升高(4.42±0.34比3.29±0.24,均P<0.01);Gαq/11蛋白表达于30 min后在肺、小肠呈进行性升高[肺:(119.24±2.38)%比(100.00±18.74)%,小肠:(138.91±23.03)%比(100.00±19.43)%],60 min后在脑、心、肾呈进行性升高[脑:(141.85±33.82)%比(100.00±16.81)%,心:(124.72±24.05)%比(100.00±16.04)%,肾:(123.98±25.74)%比(100.00±8.50)%],90 min后在肝呈进行性升高[(134.34±19.14)%比(100.00±13.04)%,P<0.05或P<0.01].Gαq/11蛋白表达与各器官中LDH的变化呈正相关(r=0.584,P<0.05).结论 ARDS过程中肺、脑、心、肾、肝、小肠中Gq/11蛋白表达有不同程度上调,引发肌醇磷脂信号转导通路活性异常,参与了各器官的损伤发生.     

重症肺炎患者核转录因子-κB DNA结合活性变化及血必净注射液的干预作用

目的 探讨核转录因子-κB(NF-κB)在重症肺炎发病机制中的作用及血必净注射液的干预效应.方法 重症肺炎患者30例,按随机数字表法分为常规治疗组14例,血必净干预治疗组16例,后者在常规治疗基础上加血必净注射液100 ml静脉滴注,每日1次,连用7 d;两组于治疗前及治疗3 d、7 d测定外周血单核细胞NF-κB DNA结合活性、炎症介质及凝血指标水平,同时行急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分.并以10例健康体检者作为健康对照组.结果 两组重症肺炎患者NF-κB DNA结合活性及肿瘤坏死因子-α(TNF-α)、降钙素原(PCT)、C-反应蛋白(CRP)、纤维蛋白原(Fib)、D-二聚体含量均明显高于健康对照组,凝血酶原时间(PT)、凝血酶时间(TT)短于健康对照组(P<0.05或P<0.01).与常规治疗组比较,干预治疗组治疗7 d NF-κB DNA结合活性(灰度值)显著降低(66.60±36.23比79.90±39.11),TNF-α(ng/L,25.81±11.67比33.78±13.36)、PCT(μg/L,1.91±1.09比2.96±1.80)、CRP(mg/L,20.01±7.21比26.59±10.66)、Fib(g/L,4.02±1.26比5.09±1.43)、D-二聚体(mg/L,0.24±0.06比0.31±0.11)均明显下降,治疗3 d时TT(s)即明显延长(15.68±1.89比14.65±1.33),7 d时APACHEⅡ评分(分,15.81±3.47比17.93±3.05)明显下降(均P<0.05).治疗前及治疗3 d、7 d NF-κB DNA结合活性分别与TNF-α含量(r1=0.373,r2=0.362,r3=0.419)、PCT含量(r1=0.800,r2=0.716,r3=0.920)、CRP含量(r1=0.368,r2=0.441,r3=0.366)呈正相关(均P<0.05).结论 重症肺炎患者NF-κB活化,凝血功能紊乱,NF-κB参与调控炎症反应;血必净注射液可减轻重症肺炎的全身炎症反应,可能与其抑制NF-κB活化及抗凝机制有关.     

CA-1500全自动血凝仪的分析性能评价

目的对CA-1500全自动血凝仪的分析性能进行评价,判断其分析性能是否满足临床要求。方法按照美国临床实验室标准化委员会（NCCLS）EP5-A标准,应用定值质控品,评价CA-1500全自动血凝仪凝血酶原时间（PT）、活化部分凝血活酶时间（APTT）、凝血酶时间（TT）、纤维蛋白原（FIb）、出凝血10凝血因子Ⅶ活性水平（FⅧ：C）、抗凝血酶Ⅲ（AT-Ⅲ）及D-二聚体（D-dimer）的准确度、批内精密度和日间精密度、线性范围,以及检测下限、携带污染率、仪器抗干扰能力。结果PT、APTT、TT、FIb、FⅧ：C、AT-Ⅲ及D-dimer的批内精密度均小于1/4总允许误差（TEa）,日间精密度低于1/3;检验结果的准确度符合要求;Fib、FⅧ：C、AT-Ⅲ、D-dimer检测的线性良好;检测下限、携带污染率和抗干扰能力均符合临床要求。结论CA-1500全自动血凝仪的分析性能符合临床要求,可用于临床病人标本的检测。     

孕妇高凝状态Pre—DIC／DIC相关检测指标的探讨

目的探讨孕妇高凝状态Pre-DIC／DIC相关检测指标的临床意义。方法应用Clauss法、凝固法、免疫散射比浊法、发色底物法，分别检测孕妇与健康非孕育龄妇女的Fib、Ⅶ、Ⅷ、Ⅹ、AT—Ⅲ和D—D水平并结合DIC病例进行临床分析。结果孕妇组（n=40）Fib为（4．41±0．72）g／L；Ⅶ（160．30±29．17）％；Ⅷ（143．87±50．30）％；Ⅹ（120．17±18．47）％；AT—Ⅲ（81．28±10．86）％；D—D为（1．56±0．98）mg／L。对照组（n=20）：Fib为（3．05±0．60）g／L；Ⅶ（97．80±11．93）％；Ⅷ（112．00±25．69）％；Ⅹ（93．20±9．31）％；AT—Ⅲ（105．00±7．84）％；D—D为（0．23±0．08）mg／L。孕妇组各项指标与对照组比较差异显著（P〈0．01；P〈0．05）。6例产前孕妇Pre—DIC相关指标检测结果，4例PT在正常参考范围内（11．5～14．5s），2例分别为10．8、16．9s；6例APTT均在正常参考范围内（28．0～43．5s）；4例Fib分别为5．16、5．13、5．10、5．70g／L，2例分别为3．95、2．86g／L；D-D均〉5．00mg／L。10例DIC产妇PT均延长，平均33．98s（15～120s）；APTY平均78．19S（31．6—180S），其中4例在正常参考范围内，分别为40．0、41．0、33．9、31．6s；Fib均〈1．48g/L；D—D平均18．39mg/L（6．24～49．6mg／L）。结论Fib与D—D为孕妇高凝状态Pre-DIC／DIC检测的敏感、实用指标；PT、APTT仅能作DIC检测指标。