大鼠烫伤后不同时间切痂骨骼肌解偶联蛋白2、3 mRNA表达水平的改变

目的观察烫伤大鼠伤后不同时间切痂其骨骼肌解偶联蛋白(UCP)2、UCP3 mRNA表达水平的异同. 方法选用120只雄性Wistar大鼠,其中8只作为正常对照组;余下112只造成30%TBSAⅢ度烫伤后分成4组A组不切痂,分别于伤后8、24、96、120、168 h处死;B组伤后8 h切痂,于伤后24、96、120、168 h处死;C组伤后24 h切痂,伤后96、120、168 h处死;D组伤后96 h切痂,伤后120、168 h处死.测定各组大鼠各时相点的血清瘦素、肿瘤坏死因子(TNF)α含量以及腓肠肌UCP2、UCP3 mRNA表达水平. 结果 (1)血清瘦素水平A组大鼠伤后24～168 h均低于正常对照组(P<0.01),B、C、D组伤后120 h和(或)168 h均高于A组(P<0.01).(2)血清TNF-α水平A组伤后各时相点均高于正常对照组(P<0.01),B组伤后各时相点均低于A组(P<0.05或0.01).C组伤后168 h低于A组(P<0.05).(3)腓肠肌UCP2 mRNA的表达量A组大鼠在烫伤后8 h即已明显升高(P<0.01),24 h到达高峰,以后逐渐下降.B、C组伤后168 h时分别为0.32±0.20、0.35±0.15,明显低于同时相点A组 0.71±0.12(P<0.05).各组腓肠肌UCP3 mRNA表达的变化趋势与UCP2类似. 结论大鼠严重烫伤后UCP2、UCP3 mRNA表达上调可能是代谢率升高的重要因素之一,休克期切痂可降低这一表达,降低代谢率.     

犬烟雾吸入性损伤早期肺洗出液灌注大鼠肺所致损伤的研究

目的　研究犬烟雾吸入性损伤早期肺洗出液的生物学活性。　方法　获取犬急性烟雾吸入性损伤早期肺洗出液及正常犬肺洗出液。将Wistar大鼠随机分为A(2 8只 )、B(2 9只 )、C(37只 )组 ,每组各取 7只不作处理作为正常对照 ,其余大鼠肺部作如下处理 :A组注入等渗盐水 ,B组注入正常犬肺洗出液 ,C组注入致伤犬肺洗出液。处死各组中正常对照大鼠 ,并于灌注后 4、12、2 4h处死灌注大鼠 ,观察各组大鼠处死前的存活情况、处死后双肺大体变化及组织病理学改变。检测肺组织匀浆中 6 酮 前列腺素F1α/血栓素B2 (PGF1α/TXB2 )、肿瘤坏死因子α(TNF α)、髓过氧化物酶 (MPO)含量及肺毛细血管通透性。　结果　A、B组大鼠处死前均存活 ,C组大鼠非处死死亡 9只。犬吸入性损伤早期肺洗出液可引起大鼠肺产生类似于烟雾吸入性损伤样的病理变化。A、B组大鼠灌注后肺组织PGF1α/TXB2 均有升高倾向 ;C组大鼠灌注后PGF1α/TXB2 逐渐降低 (P <0.0 1),A、B组灌注后肺组织TNF α、MPO含量均无明显变化 (P >0.0 5 ),C组灌注后 4h肺组织TNF α、MPO含量显著增加 ,分别为 (1.0 2± 0 .0 4 )ng/ml、(1.0 1± 0.0 9)U/g肺组织湿重 ,随后下降 (P <0.0 5～ 0.0 1)。肺灌注后4hC组大鼠肺组织毛细血管通透性高于A、B组 (P <0.0 1)。结论　犬     

舒芬太尼靶控输注诱导时脑电双频指数及血流动力学的变化(前瞻性随机对照研究)

目的观察不同剂量舒芬太尼复合丙泊酚靶控输注全麻诱导时脑电双频指数及血流力学的变化,探讨适用于短小腹腔镜手术的舒芬太尼诱导剂量。方法60例ASAⅠ～Ⅱ级择期全麻下行腹腔镜手术,按靶控输注舒芬太尼的效应室浓度不同随机分为3组,即A组(0.4ng/ml),B组(0.6ng/ml)和C组(1.2ng/ml)组,每组20例。丙泊酚血浆靶浓度均为3μg/ml,与舒芬太尼同时靶控输注,直至气管插管后5min停止输注。记录麻醉诱导气管插管过程中不同时点的脑电双频指数(bispectral index,BIS)、平均动脉压(mean arterial pressure,MAP)、心率(heart rate,HR)、丙泊酚和舒芬太尼用量、预计苏醒时间。结果气管插管后C组BIS值明显低于A组和B组(插管后5min BIS值C组为39.8±5.2,A组为45.0±6.2,B组为43.7±6.0;qC-A=8.114,P=0.007;qC-B=4.687,P=0.037)。A组插管后3min MAP(79.8±9.3)mm Hg显著高于插管前即刻(72.1±7.9)mm Hg(q=8.042,P=0.007),HR(80±11)次/min亦显著高于插管前即刻(72±11)次/min(q=5.138,P=0.029)。B组仅在插管后1min MAP(84.7±8.7)mm Hg显著高于插管前即刻(71.2±6.3)mm Hg(q=31.546,P=0.000),B组插管后1min HR(81±10)次/min亦显著高于插管前即刻(71±10)次/min(q=16.433,P=0.000)。C组仅插管后1min MAP(79.5±9.8)mm Hg显著高于插管前(71.1±6.6)mm Hg(q=9.480,P=0.004),HR各时点无显著变化(P>0.05)。丙泊酚用量各组相似,舒芬太尼总量C组(73.9±13.6)μg显著高于A组(24.3±4.9)μg和B组(35.4±8.1)μg(qC-A=237.924,P=0.000;qC-B=119.385,P=0.000)。预计苏醒时间A组16min和B组28min短于C组54min。结论与丙泊酚复合靶控输注用于全麻诱导时,舒芬太尼呈剂量依赖性地降低BIS并抑制血流力学反应。舒芬太尼效应室靶浓度0.6ng/ml复合丙泊酚血浆靶浓度3μg/ml靶控输注适用于短小腹腔镜手术的全麻诱导。     

肺纤维化对大鼠阴茎勃起功能的影响

目的:研究肺纤维化对大鼠勃起功能的影响及其机制。方法:12周雄性SD大鼠40只,随机分为4组:正常对照4周组(A组)、6周组(B组)和肺纤维化大鼠4周组(C组)、6周组(D组)各10只,分别用生理盐水(A、B组)及博莱霉素(5 mg/kg)气管内注入,饲养4周(A、C组)、6周(B、D组)后,测定大鼠血清睾酮、动脉血气分析、阴茎海绵体内压/平均颈动脉压(ICP/MAP),取阴茎标本测定NOS活性及cGMP含量,实时荧光PCR检测eNOS、iNOS和nNOS的mRNA在阴茎海绵体的表达,W estern印迹检测阴茎海绵体eNOS蛋白的表达。结果:电刺激的3 V,5 V C组ICP/MAP×100(16.37±2.19,27.19±3.18)较A组(30.78±2.66,50.09±6.97)显著降低(P<0.05),D组ICP/MAP×100,3 V,5 V(10.17±1.31,17.40±1.74)较B组(31.45±3.07,51.23±7.23)显著降低(P<0.05),D组ICP/MAP×100值较C组显著降低(P<0.05)。C组PaO2(75.50±13.87)mmHg较A组(103.80±6.88)mmHg显著降低(P<0.05),D组PaO2(83.60±5.50)mmHg较B组(102.70±5.77)mHg显著降低(P<0.05)。C组血清睾酮水平(391.1±264.7)ng/d l较A组(175.9±53.0)ng/d l显著升高(P<0.05),D组血清睾酮水平(745.4±408.8)ng/d l较B组(177.8±52.3)ng/d l显著升高(P<0.05),同时D组血清睾酮水平较C组显著升高(P<0.05)。C组NOS活性及cGMP含量[(1.50±0.14)U/mg prot,(35.69±3.64)pmol/mg]较A组[(2.66±0.39)U/mg prot,(51.10±7.22)pmol/mg]显著降低(P<0.05),D组NOS活性及cGMP含量[(1.40±0.20)U/mg prot,(34.55±4.30 pmol/mg)]较B组[(2.75±0.36)U/mg prot,(52.15±6.86)pmol/mg]显著降低(P<0.05),C组与D组比较NOS活性及cGMP含量无显著性差异(P>0.05)。C组eNOS蛋白表达量(0.79±0.01)较A组(0.87±0.01)显著降低(P<0.01),D组eNOS蛋白表达量(0.71±0.02)较B组(0.88±0.01)显著降低(P<0.05),D组较C组eNOS蛋白表达量显著降低(P<0.05)。C组eNOS mRNA表达量(4.46±0.92)较A组(2.61±0.68)显著升高(P<0.05),D组eNOS mRNA(2.79±0.60)表达量与B组(2.69±0.65)无显著性差异(P>0.05),nNOS及iNOS的mRNA表达量在A、B组与C、D组间均无显著性差异(P>0.05)。结论:肺纤维化可通过抑制阴茎海绵体eNOS蛋白的表达、降低总NOS活性及cGMP含量等机制抑制阴茎勃起功能。     

犬单侧肺重度吸入性损伤模型的建立

目的　建立犬单侧肺重度烟雾吸入性损伤模型,观察伤后24h内犬肺组织的变化。　方法　将25只雄性犬随机分为3组:单肺组10只,插入气管导管至左支气管,双肺分离通气,制作单侧肺重度烟雾吸入性损伤模型;双肺组8只,建立普通双肺吸入性损伤模型;对照组7只,不灌烟,其他操作均与单肺组相同。观察3组犬在伤后24h内的存活情况、血流动力学及血气分析指标、肺组织的病理及生理变化。　结果　单肺组和对照组犬伤后24h内全部存活,血流动力学指标稳定, 无全身缺氧表现。双肺组犬伤后24h内死亡5只,存活犬出现呼吸、循环衰竭。单肺组犬伤后24h动脉血氧分压为(65±5)mmHg(1mmHg=0. 133kPa)、混合静脉血氧饱和度0. 64±0. 04,低于对照组而高于双肺组;单肺组犬伤肺的病理形态与传统模型有相似特征并表现出高度的一致性,对侧肺亦出现轻度损伤性病理变化。　结论　本文建立的犬单侧肺重度吸入性损伤模型稳定、可靠,对研究吸入性损伤有重要价值。     

参附注射液对兔脊髓缺血损伤保护作用的量效关系研究

目的探讨参附注射液对脊髓缺血性损伤保护作用的剂量效应关系。方法24只雄性新西兰大白兔,随机分为四组A组(n=6),单纯缺血再灌注组,B组(n=6)、C组(n=6)和D组(n=6)分别于缺血前30min内持续恒速静脉输入参附注射液5ml·kg-1、10ml·kg-1、20ml·kg-1;采用肾下主动脉阻断法造成脊髓缺血(20min);术后观察神经功能变化并记录再灌注1h、4h、8h、12h、24h和48h神经功能评分,再灌注48h处死动物后取脊髓(L5～7)标本行病理学观察。结果术后神经功能评分除再灌注1hD组与A组之间无显著性差异,其余各时间点B组、C组和D组均明显高于A组(P<0．05),B组、C组和D组间则无显著性差异(P>0．05),且48h时各组神经功能评分分别为A组0．5±0．8、B组3．2±0．9(P<0．001)、C组3．0±1．0,(P<0．001)和D组2．7±0．8(P<0．05);再灌注48h脊髓前角正常运动神经元计数B组(78±25,P<0．001)、C组(41±23,P<0．05)和D组(42±27,P<0．05)均高于A(8±7)组,B组与C组、D组间亦有显著性差异(P<0．05)。结论参附注射液对脊髓缺血性损伤有保护作用,但无明显剂量效应关系。     

局部应用胰岛素对烫伤大鼠创面愈合的影响

目的观察局部应用小剂量胰岛素对烫伤大鼠创面愈合的影响,探讨其可能的作用机制.方法制作深Ⅱ度烫伤大鼠模型.部分大鼠创面下浸润注射0.1、1.0 U胰岛素,分别设为B、C组;以创面下浸润注射等渗盐水(A组)和腹部皮下注射0.1 U胰岛素(D组)的烫伤大鼠作为对照.记录各组创面愈合时间,伤后3 d起隔日计算A、B、C组的创面愈合百分率.观察各组创面愈合后的组织形态学改变,采用流式细胞仪对各组创面表皮细胞进行细胞周期分析,并测定血糖浓度的变化. 结果A、B、C、D组创面愈合时间分别为(24.57±5.19)、(18.36±4.12)、(21.46±2.97)、(24.50±1.05)d,B组较其他3组明显缩短(P<0.01).伤后5、9、11、13、15、17、19 d B组创面愈合率均明显高于A组,且伤后17 d时明显高于C组(P<0.05～0.01).组织形态学观察可见A组表皮层薄,钉脚数量少,真皮层内多见纤维细胞;B、C组表皮层增厚,钉脚数量多,真皮层内多见成纤维细胞.B组伤后4 d S期细胞比例明显高于A组(P<0.01);B组伤后4、5 d G2-M期细胞比例均明显高于A、C组(P<0.05～0.01).烫伤后24 h A组血糖波动在3.42～4.62 mmol/L;B组血糖变化规律与A组相似;C、D组注射后1 h血糖明显降低(P<0.01),注射后4 h逐渐恢复正常.结论局部应用小剂量胰岛素能明显地促进烫伤大鼠创面愈合,胰岛素可加速修复细胞的增殖分裂可能是其作用机制之一.     

关节镜下同种异体组织重建膝关节前后交叉韧带的临床研究

目的　评价关节镜下同种异体组织重建膝关节前后交叉韧带 (ACL ,PCL)的疗效。方法　回顾调查了 36例孤立性交叉韧带损伤病人 ,将其分为 2组 ,A组 :ACL损伤 2 8例 ;B组 :PCL损伤 8例。分别应用同种异体B -PT -B、半腱与股薄肌腱、胫后肌腱、跟腱 -骨和四头肌腱 -骨重建 ,平均随访 2 1 5个月。结果　Lysholm评分 :A组术前平均 6 3± 5 6 ;术后 90±5 5 ;B组术前平均 6 1± 7 6 ,术后 88± 6 0 ;两组手术前后差异显著 (P <0 0 1) ;IKDC评分 :A组A级 2例 (7% ) ,B级 16例 (5 7% ) ,C级 8例 (2 9% ) ,D级 2例 (7% ) ;B组A级 1例 (12 5 % ) ,B级 3例 (37 5 % ) ,C级 3例 (37 5 % ) ,D级 1例 (12 5 % )。KT2 0 0 0测定 :A组由术前胫骨前移平均 11 90± 0 2 7mm减少至术后 4 30± 1 4 2mm ;B组胫骨后移由术前平均 10 5± 2 5mm减少至术后 5 9± 1 5mm ,两组手术前后有显著差异 (P <0 0 1)。术后健患侧比较 :A组平均 2 3± 0 9mm ;B组 2 7± 1 3mm ;健患差异 :A组 <3mm2 3/ 2 8例 (82 % ) ,>5mm 3例 (11% ) ;B组 <3mm 5 / 8例 (6 2 5 % ) ,>5mm 2例 (2 5 % )。前后抽屉试验大部分平均恢复 1°以上 ,并呈现明显的硬终点。术后ROM ,A组 :正常 2 6 / 2 8例 (93% ) ,接近正常 2 / 2 8例 (7% ) ;B组 :     

乙酰半胱氨酸对脓毒症大鼠炎症介质的影响及对肝脏的保护作用

目的探讨乙酰半胱氨酸(NAC)对脓毒症大鼠肝脏损伤的保护作用。方法90只Wistar大鼠随机分为3组,每组30只。即假手术组(A组),脓毒症模型组(B组),NAC治疗组(C组)。A组除不结扎盲肠,不刺穿盲肠外,余操作同B组；B组成功后不做任何处理；C组NAC治疗组,盲肠结扎穿孔后大鼠立即经尾静脉给予NAC 150 mg/kg体重。各组大鼠在术后6、12、24 h分次处死,每次10只,取下腔静脉血检测血清中炎性细胞因子水平,并取肝组织行病理检查。结果血清ALT、AST水平B组、C组二组12 h后明显上升,ALT水平在12 h以后B组显著高于C组[(132．80±12．36)U/L比(87．40±10．22)U/L；(284．60±26．47)U/L比(156．60±13．56)U/L],AST水平24 h B组显著高于C组[(308．60±30．42)U/L比(175．60±17．67)U/L]；B组大鼠血中炎性细胞介质水平显著升高,肿瘤坏死因子(TNF)-α为165．41±20．14,325．36±42．20,578．40±61．70；白细胞介素(IL)-1β为(128．24±17．21),(298．24±32．02),(302．36±46．26)肝功能与形态出现损伤性变化；C组血中炎性介质水平明显降低,TNF-α为(142．25±18．72)、(232．32±30．24)、(342．20±44．55)ng/L；IL-1β(96．41±16．3)、(164．30±26．18)、(201．47±40．56)ng/L肝功能与形态损伤减轻。结论NAC对大鼠脓毒症有治疗作用,其机制可能是通过减少机体炎症介质的释放引起。     

严重烫伤大鼠休克期淋巴循环动力学及淋巴液中肿瘤坏死因子α和白细胞介素6、8水平的变化

目的观察严重烫伤大鼠休克期淋巴管运动变化及淋巴液中肿瘤坏死因子(TNF)α、白细胞介素(IL)6 、IL-8水平的变化. 方法将36只雄性Wistar大鼠造成30%TBSAⅢ度烫伤后,随机分为补液组(18只)和未补液组(18只);另设对照组(6只,不烫伤).用放射免疫分析法检测各组大鼠淋巴液中TNF-α、IL-6、IL-8水平,利用倒置显微镜及录像系统观察大鼠伤后6、24、48 h的肠系膜淋巴管运动变化,计算淋巴管收缩频率.经乳糜池插管收集淋巴液,计算淋巴液流速并行组织学观察. 结果伤后6 h两组烫伤大鼠TNF-α、IL-6增多,24 h达高峰,此时补液组TNF-α(1.61±0.27)μg/L,IL-6(398±67)ng/L;未补液组TNF-α(1.86±0.34)μg/L,IL-6(572±97)ng/L,两组间比较差异,有统计学意义(P<0.01),且各时相点浓度均显著高于对照组(P<0.01).伤后24 h两组烫伤大鼠IL-8浓度开始升高,直至48 h升高更明显,此时补液组为(540.29±0.32)ng/L,未补液组为(863.48±0.16)ng/L,两组间比较差异有统计学意义(P<0.01),且显著高于对照组(P<0.01).两组烫伤大鼠淋巴管收缩频率较低,尤以伤后24 h为明显(P<0.01) , 淋巴液流速各时相点均升高(P<0.01) ;镜下见小肠绒毛中央乳糜管扩张. 结论严重烫伤大鼠休克期淋巴管扩张,运动频率减少,但淋巴液流速加快,淋巴液中TNF-α、IL-6、IL-8的水平升高.液体复苏能够改善淋巴循环.     

Role of nitric oxide in treatment of acute lung injury after surgery with extracorporeal circulation

Postoperative acute lung injury (ALI) compromises oxygen transfer across alveolar-capillary membrane with consecutive hypoxia, one of its indicators being reduction of oxygenation index PaO2/FiO2 below 40 kPa (300 mm Hg). Management of ALI includes different procedures like mechanical lung ventilation (MLV), drugs and others. One of the new possibilities for treatment of ALI is nitric oxide (NO) inhalation. The aim of this prospective study was to examine the role of NO inhalation in treatment of ALI. 14 patients with ALI developed immediately after operation with extracorporeal circulation (ECC) were included in the study. Group A (n = 8) inhaled NO and group B (n = 6) did not inhale NO during treatment of ALI. All other therapeutic measures were the same in both groups. The groups were similar in relation to demographic data, type of surgery and duration of ECC. PaO2/FiO2 was calculated before operation (T1), immediately after surgery (T2) and after lung recovery, when the need for MLV stopped (T3). The duration of MLV was also registered. PaO2/FiO2 (kPa) in referent times was in group A 54.9 +/- 1.6, 33.8 +/- 1.2 and 46.2 +/- 0.8 and in group B 52.2 +/- 1.1, 33.5 +/- 1.5 and 47.3 +/- 0.9, respectively. There was a statistically significant decrease of PaO2/FiO2 in T2 and T3 vs T1 in both groups (p < 0.05), while the difference between the groups was not statistically significant. The duration of MLV (h) in group B (28.5 +/- 1.6) was statistically significantly shorter than in group A (63.1 +/- 8.7) (p < 0.01). According to the results of this study we conclude that NO inhalation during ALI after surgery with ECC significantly reduces the duration of MVL and improves pulmonary recovery.     

Immediate positive pressure ventilation with positive end-expiratory pressure (PEEP) improves survival in ovine smoke inhalation injury.

BACKGROUND: The purpose of this study was to compare the effects of immediate initiation of positive pressure ventilation (PPV) with positive end-expiratory pressure (PEEP) versus the initiation of PPV with PEEP only after hypoxemia ensued following severe smoke inhalation injury. METHODS: We prospectively evaluated chronically instrumented adult sheep treated with immediate versus delayed PPV with PEEP and compared oxygen requirements, hemodynamics, pleural fluid formation, postinjury survival, and tracheobronchial pathologic processes among groups. The immediate group (group I; smoke, n = 6; sham, n = 2) underwent tracheostomy and bilateral chest tube placement before they received inhalation injury. They were then immediately placed on PPV with PEEP (12 cm H2O). The animals in the delayed group (group D) (n = 6) were placed on PPV with PEEP when arterial hypoxemia (PaO2 < 80 mm Hg [11.2 kPa] on 0.4 FIO2) or respiratory distress developed. RESULTS: Groups were matched for smoke exposure and peak carboxyhemoglobin. Both groups developed a characteristic decrease in PaO2/FIO2 ratio. Initiation of PPV + PEEP improved PaO2 in the delayed group (69 +/- 7 to 126 +/- 21 mm Hg [9.2 +/- 0.9 to 16.7 +/- 2.8 kPa]). Pleural fluid output was greater in the immediate group compared with the delayed group (1559 +/- 415 vs. 426 +/- 236 mL). At 96 hours after injury five of six animals in the delayed group had died. In contrast, six of six animals in the immediate smoke group survived 96 hours (p < 0.05 versus delayed group). The immediate group had fewer and less extensive tracheobronchial casts at necropsy. CONCLUSIONS: Immediate PPV + PEEP did not prevent the development of hypoxia and was associated with increased pleural fluid formation. Death within 96 hours in the delayed group was the result of respiratory failure aggravated by bronchial cast formation despite vigorous pulmonary toilet. Early positive pressure ventilation with PEEP, preferably initiated immediately after the inhalation insult, significantly increases short-term survival and is associated with decreased tracheobronchial cast formation in this ovine model of severe smoke inhalation injury.     

Changes in arterial oxygen tension during and after enflurane or halothane anesthesia as well as epidural analgesia

Recovery from inhalation anesthesia is often marked by the occurrence of postoperative hypoxemia. In this study, we compared the effects of enflurane or halothane anesthesia and epidural analgesia on arterial oxygen tension during and after the operation in 60 ASA physical status 1-2 patients who underwent cholecystectomy. Anesthesia was induced with thiopental and maintained with 66% N2O and -enflurane (1.5%), -halothane (1%), or -epidural lidocaine (1% solution, 17.5 ml) in oxygen. Blood gas analysis was done before and 10, 30, 60 min after induction. PaO2 was measured on 1st and 3rd postoperative days in all patients breathing air spontaneously. PaO2 decreased during operation in all three groups of anesthesia. PaO2 values on first postoperative day were significantly lower than those before operation, and PaO2 value in enflurane group (PaO2 = 67 +/- 1 mmHg) was significantly lower than that in halothane group (PaO2 = 72 +/- 2 mmHg, P less than 0.05).     

复方红景天对大鼠高原严重烧伤后早期心肌损伤的保护作用

目的　观察高海拔 (3480m)地区大鼠 30 %TBSAⅢ度烧伤后心肌损害的程度 ,探讨使用复方红景天后对大鼠心肌损伤的作用机制。　方法　 10 4只Wistar大鼠 ,随机分为红景天组 (48只 )、盐水组 (48只 )、正常对照组 (8只 )。正常对照组大鼠不作烧伤和其他处理。红景天组伤前 1周向大鼠胃内灌注复方红景天液 4ml,2次 /d;盐水组同方法灌注等量等渗盐水。分别在伤后 3、6、12、2 4、4 8、72h(每时相点 8只大鼠 )剖腹抽血 ,检测大鼠心肌酶谱及动脉血气变化 ,再摘取大鼠心脏作病理学检查。　结果　烧伤后 3h盐水组大鼠心肌组织损害明显 ,随后逐渐减轻 ,伤后 72h接近正常对照组水平。红景天组与盐水组大鼠心肌酶谱值均明显高于正常对照组 (P <0.0 1),但红景天组则明显低于盐水组 (P <0.0 1)。血气分析 :pH值 :盐水组与红景天组均低于正常对照组 (P <0.0 5 ),红景天组伤后 12～ 2 4h高于盐水组 (P <0.0 5)。剩余碱 :盐水组与红景天组均明显低于正常对照组 (P <0.0 1)。红景天组伤后 6h后高于盐水组 (P <0.0 5～ 0.0 1)。二氧化碳分压 :盐水组与红景天组均明显低于正常对照组 (P <0.0 5～ 0.0 1),伤后 4 8h红景天组 (35 .70± 4 .2 3)mmHg(1mmHg =0.133kPa)与正常对照组 (37.5 0± 6 .5 3)mmHg比较 ,差异无显著性意义     

Echanges gazeux per- et postopératoires : hyperventilation isocapnique versus normoventilation

The effects of isocapnic hyperventilation (A) and normoventilation (B) on PaCO2, PaO2 and A-aDO2 were compared in 102 patients undergoing elective surgery, randomized into two comparable groups A and B. Cases for thoracic, high abdominal and intracranial surgery were excluded, as well as patients with clinically evident pulmonary pathology. A volumetric ventilator was used in association with three different breathing systems (A: Bain system and circle system without CO2 absorption; B: circle system with CO2 absorption). The groups were comparable, except for percentage of overweight: 75% in group A and 56% in group B. Overweight was defined as weight above the mean ideal weight of 100%, and obesity as a weight above 120% the mean ideal weight. Blood gases were sampled 1) preoperatively, 2) 15 min and 3) 60 min after the beginning of mechanical ventilation, 4) postoperatively, 90 min after extubation, without supplemental oxygen. The preoperative mean PaO2 values were 79 +/- 11.4 mmHg (A) and 82.5 +/- 13.2 mmHg (B); the PaCO2 were 37.2 +/- 3.7 mmHg (A) and 37.2 +/- 3.8 mmHg (B). During surgery, PaO2 was distinctly higher (p less than 0.01) in group A than in group B (on average 15-20 mmHg higher), indicating the favourable effect of great tidal volumes on gas exchange. Correspondingly, the A-aDO2 was less increased in group A than in group B (p less than 0.01). At 15 min, 33% of the patients were hypocapnic (PaCO2 less than 35 mmHg): one case in group A and three in group B could be classed as severe hypocapnia (PaCO2 = 25-30 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prostanoid production and pulmonary hypertension after fat embolism are not modified by methylprednisolone

Bilateral cemented arthroplasty (BCA) in anaesthetized mongrel dogs produces particulate fat and marrow embolism of the lung. Methylprednisolone sodium succinate (MPSS) has been advocated for post-traumatic fat embolism to prevent acute lung injury. We used the BCA procedure to produce acute fat and marrow embolism, and tested the efficacy of MPSS (30 mg.kg-1) in preventing physiological and pathological markers of acute lung injury. Dogs (n = 6) pre-treated with MPSS demonstrated similar acute increases in pulmonary artery pressure (PAP) within one minute of BCA (17.8 +/- 7.3 mmHg) as the untreated (control n = 7) dogs (18.6 +/- 12.6). Pulmonary vascular resistance (PVR) increased to the same degree in both groups (455 +/- 323 and 319 +/- 137 dyne.sec.cm-5) and PaO2 decreased by 18.3 +/- 6.4 mmHg in the control group as opposed to 12.4 +/- 7.7 mmHg in the MPSS group within five minutes of BCA. Circulating arterial and mixed venous plasma concentrations of thromboxane B2 (TxB2) increased within one minute of BCA in both groups with no increase in the transpulmonary gradient. Arterial plasma 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) increased (0.91 +/- 0.29 ng.ml-1 and 0.87 +/- 0.43 ng.ml-1) in both groups one minute after BCA. Mixed venous 6-keto PGF1 alpha plasma concentration also increased, but a significant transpulmonary 6-keto PGF1 alpha gradient was found.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Response to Repeated Nitric Oxide Inhalation Is Inconsistent in Patients with Acute Respiratory Distress Syndrome

Background: Nitric oxide (NO) is administered frequently in patients with acute respiratory distress syndrome (ARDS) and pulmonary hypertension. The efficacy of this therapy over several days is not well known. The authors first determined the consistency of the response to repeated administration of NO and then the baseline variables that were associated with improvement in patients with severe ARDS.

Methods: In a prospective trial, 32 mechanically ventilated patients with severe ARDS received 10 parts per million NO by inhalation. In 22 of these patients, its effect was tested repeatedly (up to four times) in several days. Improvement was defined as an increase > 10% in the ratio of pressure of oxygen in arterial blood (PaO sub 2) to the inspiratory pressure of oxygen (FIO2) from baseline. Patients showing such an improvement were maintained on NO inhalation.

Results: Twelve of the 22 patients (54%) showed a clinically significant and reproducible increase in the PaO2 /FIO2 ratio with NO, from 74 +/- 30 mmHg (mean +/- SD) to 95 +/- 41 mmHg (P <0.001). In three patients (14%), PaO2 did not improve, even with multiple exposures. In seven patients (32%), an inconsistent response was seen on different days. Mean pulmonary artery pressure decreased for the entire group from 34 +/- 10 mmHg to 29 +/- 9 mmHg (P < 0.01), but this decrease did not correlate with the increase in PaO2 in individual patients. The baseline PaO2 /FIO2 ratio and mixed venous oxygenation (PvO2) were significantly lower, and the venous admixture was greater in patients showing beneficial effects of NO inhalation on PaO2.     

骨髓间充质干细胞移植对吸入性损伤家兔炎症反应和肺损伤的影响

目的 初步了解骨髓间充质干细胞(MSC)移植对烟雾吸入性损伤兔外周血主要炎症因子和肺水质量分数以及肺组织损伤的影响. 方法 取16只成年新西兰大耳白兔制成烟雾吸入性损伤模型后,按随机数字表法分成单纯致伤组和MSC移植组(各8只).单纯致伤组伤后立即经耳缘静脉注入10 mL PBS;MSC移植组伤后立即经耳缘静脉注入10 mL PBS,内含兔第3代MSC(分离自健康幼龄新西兰大耳白兔)1×107个.另取8只成年新西兰大耳白兔作为正常对照组,不致伤,仅经耳缘静脉注入10 mL PBS.单纯致伤组和MSC移植组分别于致伤后2、4、6 h采血,以ELISA法检测血清TNF-α、IL-1β、IL-6、IL-10含量;伤后24 h,取兔肺行大体观察和组织病理学观察(左下肺),取右肺中叶组织计算肺水质量分数.正常对照组同法抽血并取肺组织进行检测.对实验数据行t检验.结果 (1)两致伤组家兔各时相点血清TNF-α含量均明显高于正常对照组(t=2.43～9.57,P＜0.05或P＜0.01).单纯致伤组各时相点血清IL-1β和IL-6含量明显高于正常对照组(t=8.49～19.80,P值均小于0.01);MSC移植组各时相点IL-1β含量与正常对照组接近(t=0.11～0.92,P值均大于0.05),IL-6含量伤后2 h与正常对照组接近(t=2.12,P＞0.05),4、6 h显著升高(t值均为2.83,P值均小于0.05).MSC移植组家兔各时相点血清TNF-α、IL-1β、IL-6明显低于单纯致伤组(t=2.35～12.45,P＜0.05或P＜0.01).(2)MSC移植组伤后2、4、6 h血清IL-10含量分别为(13.0±3.6)、(11.6±8.5)、(15.2±4.4)pg/mL,与单纯致伤组各对应时相点的含量[分别为(5.5±3.4)、(5.0±1.7)、(7.9±3.5)pg/mL]相比均显著升高(t值分别为4.28、2.15、3.67,P值均小于0.01).两致伤组亦明显高于正常对照组(t=2.46～8.14,P＜0.05或P＜0.01).(3)大体观察及组织病理学观察见,MSC移植组肺组织损伤程度较单纯致伤组明显改善.(4)伤后24 h,与正常对照组肺水质量分数(48±3)%相比,两致伤组均明显升高(t值分别为16.93、7.22,P值均小于0.01).MSC移植组肺水质量分数为(69±7)%,较单纯致伤组(87±6)%明显降低(t=5.49,P＜0.01). 结论 MSC移植能降低烟雾吸入性损伤兔外周血促炎因子水平,升高抗炎因子水平,降低肺水质量分数,改善全身炎症反应,对肺组织具有保护作用.     

Low-potassium UW solution for lung preservation. Comparison with regular UW, LPD, and Euro-Collins solutions.

University of Wisconsin solution has been used successfully in clinical kidney and liver preservation. The object of this study was to determine if low-potassium UW (LPUW) solution could be applied to pulmonary preservation. Rabbit lungs were stored after hypothermic pulmonary artery (PA) flush with four different solutions (group 1: low-potassium dextran (LPD) solution, group 2: high-potassium UW (HPUW) solution, group 3: LPUW solution, group 4: modified Euro-Collins (E-C) solution). The lungs were preserved at 10 degrees C for 30 hr and evaluated in an ex vivo ventilation/perfusion apparatus using fresh pooled venous rabbit blood. Mean PA flush pressures (MFP) during harvesting were significantly lower in groups 1 and 3 (8.1 +/- 1.0 mmHg and 7.3 +/- 0.6 mmHg, respectively; mean +/- SEM) than in groups 2 and 4 (15.5 +/- 1.7 mmHg and 12.3 +/- 0.9 mmHg, respectively). Lungs in groups 1 and 3 showed significantly higher PaO2 (103.5 +/- 8.0 mmHg and 89.3 +/- 7.2 mmHg) than groups 2 and 4 (48.3 +/- 7.7 mmHg, 66.7 +/- 4.7 mmHg). Groups 1 and 3 showed significantly lower wet/dry weight (W/D) ratios after reperfusion (6.21 +/- 0.15 and 6.39 +/- 0.23) than groups 2 and 4 (7.70 +/- 0.57 and 7.13 +/- 0.21, respectively). There were no significant differences in MFP, PaO2, PaCO2, mean pulmonary artery pressure, or W/D ratio between groups 1 and 3. These results suggest that LPUW solution may be as beneficial as LPD solution for pulmonary arterial flush and lung preservation.     

Continuous Arterial PO(2) and PCO(2) Measurements in Swine during Nitrous Oxide and Xenon Elimination: Prevention of Diffusion Hypoxia

Background: During nitrous oxide (N2 O) elimination, arterial oxygen tension (PaO(2)) decreases because of the phenomenon commonly called diffusive hypoxia. The authors questioned whether similar effects occur during xenon elimination.

Methods: Nineteen anesthetized paralyzed pigs were mechanically ventilated randomly for 30 min using inspiratory gas mixtures of 30% oxygen and either 70% N2 O or xenon. The inspiratory gas was replaced by a mixture of 70% nitrogen and 30% oxygen. PaO(2) and carbon dioxide tensions were recorded continuously using an indwelling arterial sensor.

Results: The PaO(2) decreased from 119 +/- 10 mmHg to 102 +/- 12 mmHg (mean +/- SD) during N2 O washout (P < 0.01) and from 116 +/- 9 mmHg to 110 +/- 8 mmHg during xenon elimination (P < 0.01), with a significant difference (P < 0.01) between baseline and minimum PaO(2) values (Delta PaO(2), 17 +/- 6 mmHg during N2 O washout and 6 +/- 3 mmHg during xenon washout). The PaCO(2) value also decreased (from 39.3 +/- 6.3 mmHg to 37.6 +/- 5.8 mmHg) during N2 O washout (P < 0.01) and during xenon elimination (from 35.4 +/- 1.6 mmHg to 34.9 +/- 1.6 mmHg; P < 0.01). The Delta PaCO(2) was 1.7 +/- 0.9 mmHg in the N2 O group and 0.5 +/- 0.3 mmHg in the xenon group (P < 0.01).