不同深低温停循环方法对脑组织S-100蛋白表达的影响

目的观察不同深低温停循环方法对脑组织S—100蛋白表达及组织结构的影响。方法将18只实验犬随机分为3组，深低温停循环（deep hypothermic circulatory arrest，DHCA组）组，深低温停循环结合逆行脑灌注（retrograde cerebral perfusion，RCP，DHCA＋RCP组）组，深低温停循环结合顺行性间断脑灌注（intermittent antegrade cerebral perfusion，IACP，DHCA＋IACP组）组。3组犬体外循环开始后将鼻咽温降至18℃，随后停循环90min，开放循环后复温至36℃，随后停机。在停循环前、停循环后45min、90min及开放循环后15min和30min由颈静脉插管留取血液标本进行S-100蛋白含量测定。手术结束时取脑海马组织作透射电子显微镜检查，观察脑组织及神经细胞超微结构的变化。结果3组犬在停循环前颈静脉血S-100蛋白含量差异无统计学意义（P〉0．05），停循环后DHCA组和DHCA＋RCP组S-100蛋白含量较停循环前显著升高（P〈0．01），DHCA＋IACP组S-100蛋白含量停循环前后无显著变化。结论DHCA时间较长时，脑组织会发生缺血缺氧性损伤；RCP对脑组织有一定的保护作用，但易发生脑组织及神经细胞水肿；IACP的脑保护效果较为理想。     

深低温停循环后梯度灌注复温的脑保护作用

目的 探讨深低温停循环(deep hypothermia circulatory arrest,DHCA)后应用梯度灌注复温,调整脑组织血流-温度-代谢平衡,籍以优化体外循环复温过程中的神经保护策略.方法 3～4周龄上海白猪12只,雌雄不拘,体质量(9.78 ±0.93)kg.通过简单随机分为实验组和对照组,每组6只,建立微创的乳猪DHCA灌注模型(肛温18℃).实验组DHCA停循环90 min,术后复温策略为梯度灌注复温,肛温每升高5℃,维持平台温度15 min;对照组DHCA停循环90 min后常规复温.以肛温33℃为目标恢复温度.两组均采用pH稳态方法管理血气,分别于转流开始后10 min,复温开始后15、30和45 min采样,监测肛温、心率、心电图、血气分析、颈动脉血流量、颈静脉谷氨酸/天冬氨酸浓度,术后1h取实验动物脑组织,对海马CA1区进行组织学评估,并应用免疫组化方法测定脑组织内的损伤敏感因子、NF-κB组分p50蛋白的表达.结果 实验组的复温时间为(67.3 ±7.8) min,对照组的复温时间为(41.8±3.6) min(P ＜0.05).复温后15 min时,实验组和对照组脑血流量的差异无统计学意义.升温30 min和45 min时,实验组的脑血流量显著低于对照组(P＜0.05).高压液相色谱( HPLC)分析显示,升温30 min和45 min时对照组颈静脉谷氨酸浓度高于实验组,仅在升温45 min时,对照组的颈静脉天冬氨酸的浓度高于实验组.组织学评估显示梯度复温组海马CA1区椎体细胞层损失较少,免疫组化分析示实验组和对照组NF-κB的表达差异无统计学意义.结论 深低温停循环后,梯度灌注复温有一定的神经保护作用,其神经保护效应可能与保持复温阶段脑部血流-代谢-温度平衡有关.     

深低温停循环中不同脑灌注方式皮层超氧化物歧化酶、丙二醛及超微结构的变化

目的观察不同脑灌注方法对深低温停循环（DHCA）中脑皮质超氧化物歧化酶（SOD）、丙二醛（MDA）及超微结构的影响，比较不同灌注方式的脑保护效果。方法健康成年杂种犬15条，随机分为3组。Ⅰ组单纯行DHCA为对照，Ⅱ组DHCA＋逆行脑灌注（RCP），Ⅲ组DHCA＋选择性顺行脑灌注脑保护（SACP）。转流降温至鼻咽部温18℃时停循环90min，然后复温再灌注90min。结果停循环期皮层SOD活性下降而MDA含量上升，复温再灌注时变化更明显，各时间点差异有统计学意义（P〈0．05）。增加或下降程度以Ⅰ组最为明显，Ⅱ组次之，Ⅲ组最小。Ⅱ、Ⅲ组与Ⅰ组比较SOD、MDA变化明显减轻（P〈0．01），Ⅱ、Ⅲ组间亦差异有统计学意义（P〈0．05），与电镜观察结果一致。结论深低温停循环期间SACP有明显脑保护作用，RCP亦可减轻DHCA中脑损害。     

深低温停循环经右锁骨下动脉持续脑灌注与经上腔静脉逆行脑灌注的比较

目的比较深低温停循环(DHCA)时经右锁骨下动脉持续脑灌注(RSA)和经上腔静脉逆行脑灌注(SVC)对脑组织的保护效果。方法将36只杂种猫随机分为6组(n=6)建立体外循环(CPB)。1组DHCA45min,无脑灌注;2组DHCA45min,经上腔静脉逆行脑灌注;3组DHCA45min,经右锁骨下动脉持续脑灌注;4组DHCA90min,无脑灌注;5组DHCA90min,经上腔静脉逆行脑灌注;6组DHCA90min,经右锁骨下动脉持续脑灌注。检测各组脑组织超微结构、颈静脉血乳酸含量、脑组织ATP含量和一氧化氮合成酶(NOS)活性。结果DHCA时间相同时,SVC组和RSA组脑组织光镜及电镜下缺血、缺氧改变明显轻于无脑灌注组,颈静脉血乳酸含量和脑组织NOS活性均显著低于无脑灌注组(P<0.05),脑组织ATP含量显著高于无脑灌注组(P<0.05)。DHCA45min后,SVC组和RSA组比较各指标差异无统计学意义。DHCA90min后,RSA组脑组织超微结构缺血、缺氧改变轻于SVC组。且RSA组脑组织ATP含量[(2.02±0.19)μmol/g]显著高于SVC组[(1.72±0.21)μmol/g,P<0.05]。结论长时间深低温停循环时经右锁骨下动脉持续脑灌注比经上腔静脉逆行脑灌注更有利于保护脑组织的氧供需平衡。     

不同脑灌注方法对深低温停循环脑组织温度、温差的影响

目的比较不同脑灌注方法对深低温停循环(DHCA)中脑组织温度、温差的影响,以及与自由基及脑皮质超微结构改变的关系,评价不同灌注方式的脑保护效果。方法健康成年杂种犬15只,随机分为3组(n=5)。Ⅰ组单纯行DHCA,Ⅱ组DHCA RCP,Ⅲ组DHCA 选择性顺行脑灌注(SACP)。转流降温至鼻咽部温18℃时停循环,期间Ⅱ、Ⅲ组分别行逆行脑灌注(RCP)及SACP,90 min后复温,再灌注90 min。结果停循环后犬脑组织温度缓慢上升,脑皮质温度(BCT)及脑深部温度(BBT)在不同时间点间差异有统计学意义(P<0.01);3组之间BCT、BBT亦有明显差异(P<0.01),停循环时间与不同脑灌注方式之间存在交互效应。停循环过程中及复温后各组脑皮质-深部温差(Dc-bT)、SOD活性及MDA含量均有明显差异(P<0.05),Ⅰ组复温30 min时Dc-bT最大,Ⅲ组停循环前Dc-bT最小。Ⅲ组脑超微结构改变轻于Ⅰ、Ⅱ组。结论DHCA中存在脑组织自然复温及较明显的脑皮质-深部温差。RCP有利于维持脑部低温,但不能有效降低脑皮质-深部温差。SACP可保持脑温低温,有效减小脑皮质-深部温差,脑保护效果优于RCP和DHCA。     

深低温停循环大鼠脑保护模型的建立

目的 建立一种新的深低温停循环(DHCA)大鼠脑保护模型.方法雄性SD大鼠30只,随机分为3组,即颈动脉阻断DHCA组(A组)、颈内动脉引流DHCA组(B组)和假手术组(C组).于深低温停循环后60 min时监测脑电图变化,停循环60 min后恢复循环并升温.所有大鼠于术后24 h处死,并取脑组织测脑含水量.结果 B组大鼠α波相对功率值明显低于A组(P＜0.01),而且两组大鼠α波相对功率值均明显低于C组(P＜0.01);B组大鼠θ波相对功率值明显低于A组和C组(P＜0.01),而后两组大鼠θ波相对功率差异无统计学意义.脑含水率结果 显示B组大鼠脑含水量高于A组(P＜0.05).结论 颈内动脉引流DHCA模型较颈动脉阻断DHCA模型脑缺血更完全,是一种较为理想的DHCA大鼠脑保护模型.     

DeBakeyⅠ型主动脉夹层术中双侧脑灌注脑保护的体会

目的 总结DeBakeyⅠ型主动脉夹层在深低温停循环选择性脑保护下行全弓置换＋支架象鼻术的体外循环及双侧脑保护经验.方法 350例DeBakeyⅠ型主动脉夹层患者,当鼻温降至20℃,肛温〈23℃时暂停下半身体外循环,经头臂动脉、左颈总动脉插入Y形双侧脑灌注管行脑灌注.然后完成支架象鼻、弓部置换术.恢复下半身体外循环,缓慢复温,复温至鼻咽温32℃以上,心脏复跳,辅助循环至停机.结果 体外循环时间（156.24±42.25）min;心肌阻断时间（90.82±17.73）min;脑灌注时间（35.78±10.49）min,停循环时间（19.22±9.56）min;死亡11例,死亡率3.13%.结论 DeBakeyⅠ型主动脉夹层在深低温停循环手术,行双侧顺性脑灌注,能提供满意的脑保护效果,安全、可靠、有效,术后并发症少.     

深低温停循环下兔脑内兴奋性氨基酸的早期变化与脑损伤研究

目的　探讨体外循环(CPB)和深低温停循环(DHCA)下脑内兴奋性氨基酸(EAA )早期变化规律,及其“兴奋毒性”作用在脑损伤中的作用。方法　建立应用脑微透析技术的兔CPB和DHCA模型。利用高效液相的电化学检测方法,测定兔脑海马CA1区脑细胞间液中EAA的连续性变化。术后利用透射电子显微镜给予组织学损伤评分。结果　谷氨酸在CPB组各阶段变化差异无统计学意义(P >0 .0 5 ) ;DHCA组在恢复循环早期明显升高(P <0 .0 5 ) ,升高程度DHCA组明显高于CPB组(P <0 .0 1)。天冬氨酸在DHCA组恢复灌注3 0～60min阶段明显升高(P <0 .0 1) ,但与CPB组的组间对照差异无统计学意义(P >0 .0 5 )。透射电镜发现两组脑细胞超微结构均明显损伤,DHCA组损伤重于C组(P <0 .0 5 )。结论　“兴奋毒性”作用与中低温CPB造成的脑损伤无关。DHCA可使再灌注早期兴奋性氨基酸升高,并导致脑损伤加重     

支架"象鼻"术治疗DeBakey Ⅰ型主动脉夹层动脉瘤

目的 探讨支架"象鼻"手术治疗DeBakey Ⅰ型主动脉夹层动脉瘤(AD)的方法和效果.方法 12例DeBakey Ⅰ型AD患者,平均年龄48.1岁.采用深低温停循环(DHCA),右腋动脉顺行灌注(SCP)脑保护,实施支架"象鼻"手术(即升主动脉和全弓置换及降主动脉腔内支架植入).结果 术后死亡1例,手术死亡率8.3%.术中体外循环时间(163.2±17.7)min,停循环时间(41.6±12.3)min.随访3～6个月,无死亡病例.结论 支架"象鼻"手术简单,停循环时间短,治疗DeBakey I型夹层主动脉瘤安全、有效.     

猪主动脉手术选择性脑灌注期间脑血流的变化

目的 观察猪主动脉手术不同阶段脑血流流量、血流分布,以及氧代谢变化状况.方法 18～22 kg雌性小型猪8只,通过右房静脉引流,右侧颈动脉和升主动脉插入动脉灌注管建立单泵双管灌注模型,降温至20℃时停止升主动脉灌注,实施右侧选择性脑灌注,60 min后恢复循环,静脉氧饱和度达到95％以上时开始复温,膀胱温度达到36C停止体外循环转流.整个过程中使用TRANSONIC超声血流仪监测动脉插管内灌注流量,记录灌注压力,使用近红外分光光度仪监测脑氧饱和度( rSO2)动态变化,不同时间点监测血气分析和生化检查.结果 观察期间右侧股动脉压力维持(60±20) mmHg.总的血液灌注流量(85.30±6.81) ml·kg-1·min-1,其中右侧脑灌注流量( 14.42±1.76) ml·kg-1·min-1,占全部灌注流量(16.72±2.77)％.停循环选择性脑灌注期间,脑灌注流量(15.11±0.44) ml·kg-1 · min-1.实验不同阶段静脉氧饱和度波动于0.40 ～0.99(0.83 ±0.13),rSO2 0.56～0.79(0.67±0.06).停循环后血糖[(8.18±3.34) mmol/L]和乳酸浓度[(9.30±2.31) mmol/L]较停循环前明显升高(P＜0.05).结论 可以连续性观测主动脉手术体外循环转流以及停循环期间的全身以及脑部血流分布、氧代谢的小型猪动物模型,是进行主动脉弓部心血管外科研究的良好模型.     

深低温停循环逆行脑灌注脑组织自由基变化的实验研究

研究深低温停循环（ＤＨＣＡ）与逆行脑灌注（ＲＣＰ）时脑组织自由基的变化。健康杂种犬１４只，随机等分为ＤＨＣＡ组和ＲＣＰ组，在停循环前（Ａ点）、ＤＨＣＡ／ＲＣＰ３０分（Ｂ点）、ＤＨＣＡ／ＲＣＰ６０分（Ｃ点）ＤＨＣＡ／ＲＣＰ９０分（Ｄ眯）和复温再灌注３０分（Ｅ点）取脑皮层ｌｇ，检测丙二醛（ＭＤＡ）和超氧化物歧化酶（ＳＯＤ）水平。结果见两组在Ａ点ＭＤＡ和ＳＯＤ无差别。在Ｂ、Ｃ、Ｄ、Ｅ点，ＤＨＣＡ组ＭＤＡ     

脑红蛋白在内毒素脑损伤大鼠模型中的表达变化

目的 了解内毒素脑损伤大鼠额叶皮质、脑脊液(CSF)和血清中脑红蛋白(Ngb)的表达变化并分析其意义.方法 选用SD大鼠70只,随机分为对照组10只和内毒素干预组60只.内毒素干预组大鼠于脑池内注射0.1 mg/kg LPS,对照组注入等体积等渗盐水.内毒素干预组大鼠于注射后3、6、12、24、48、72 h收集血清和CSF,并处死大鼠留取额叶皮质,每时相点10只大鼠.应用酶联免疫吸附测定(ELISA)法和蛋白质印迹法测定Ngb含量,干燥法测定额叶皮质含水量;并对各样本中Ngb含量与额叶皮质含水量行相关性分析.采用生物素-链霉亲和素-辣根过氧化物酶(SP)法检测Ngb在额叶皮质中的表达.对照组大鼠亦进行上述检测.结果 ELISA结果 显示,内毒素干预组大鼠注射后各时相点额叶皮质、CSF、血清中Ngb含量高于对照组,其中48 h达峰值[分别为(35.4±3.9)、(22.7±3.1)、(14.4±2.8)ng/mL,P<0.01].蛋白质印迹法显示,各组均表达相对分子质量约为17×103的Ngb蛋白,Ngb表达变化与ELISA检测结果 相似.注射后6～72 h,内毒素干预组大鼠额叶皮质含水量明显高于对照组(P<0.01),其中48 h达峰值(83.3±1.9)%.内毒素干预组大鼠各时相点血清、CSF、额叶皮质Ngb含量与额叶皮质含水量4项指标两两比较,均呈正相关(γ为0.631～0.719,P<0.01).SP法显示.Ngb免疫反应阳性细胞主要位于神经元的细胞质.结论 LPS所致脑损伤中Ngb表达的上调与LPS的注入时间相关.     

Metabolism of Ca2+ in myocytes and peroxidation products in ischemia-reperfusion injury under extracorporeal circulation]

The metabolism of calcium ion (Ca2+) in myocytes in ischemia-reperfusion injury under extracorporeal circulation (ECC) was studied by cytochemistry and electron microscopy. Ten mongrel dogs were under ECC with aortic cross-clamping for 120 minutes. A cold GIK crystalloid cardioplegic solution was infused via the aortic root intermittently during ischemia, and the myocardial temperature was maintained at 5-10 degrees C with ice slush. The morphological changes of Ca(2+)-ATPase activity in myocytes were estimated using the "lead citrate method". The activities of mitochondria, which had been temporarily decreased just before reperfusion, increased immediately after reperfusion and decreased again 60 minutes later. Electromicroscopy revealed swelling of mitochondria and laceration of myofibrils as well as intracellular edema 60 minutes after reperfusion. Immediately after reperfusion and 60 minutes later, creatine phosphokinase iso-enzyme (CK-MB) release in coronary sinus blood was significantly (p < 0.01) greater than that before the start of ECC. Anaerobic metabolism immediately after reperfusion was more active than that before aortic cross-clamping, as demonstrated by changes in excess lactate (delta XL) and redox potential (delta Eh) of lactate and pyruvate (delta XL, p < 0.05; delta Eh, p < 0.01). Thus, in ischemia-reperfusion injury, alterations of Ca(2+)-ATPase activity of mitochondria reflect the functional and morphological viability of the myocardium. Immediately and 60 minutes after reperfusion, the level of thiobarbituric acid was significantly (p < 0.01) higher and the level of alpha-tocopherol was significantly (p < 0.01) less than respective levels before the start of ECC.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of low-flow cardiopulmonary bypass and circulatory arrest on brain oxygen and metabolism

BACKGROUND: In the neonatal brain we measured oxygen (Bo(2)), extracellular striatal dopamine (DA), and striatal tissue levels of ortho-tyrosine (o-tyr) during low-flow cardiopulmonary bypass (LFCPB) or deep hypothermic circulatory arrest (DHCA) and the post-bypass recovery period. METHODS: Newborn piglets were assigned to sham (n = 6), LFCPB (n = 8), or DHCA (n = 6) groups. Animals were cooled to 18 degrees C and underwent DHCA or LFCPB (20 mL x kg(-1) x min(-1)) for 90 minutes. The Bo(2) was measured by quenching the phosphorescence, DA by microdialysis, and hydroxyl radicals by o-tyr levels. The results are presented as the mean +/- SD (p < 0.05 was significant). RESULTS: Baseline Bo(2) was between 45 to 60 mm Hg. At the end of LFCPB, Bo(2) was 10.5 +/- 1.2 mm Hg. By 5 and 30 minutes of arrest during DHCA, Bo(2) fell to 4.2 +/- 2.5 mm Hg and 1.4 +/- 0.7 mm Hg, respectively. Compared with control, extracellular DA did not change during LFCPB. During DHCA extracellular levels of DA increased, by 750-fold from baseline at 45 minutes and to a maximum of 53000-fold at 75 minutes. After 2 hours of recovery from DHCA, the o-tyr within the striatum increased about sixfold as compared with control. There was no change in o-tyr measured after LFCPB. CONCLUSIONS: In DHCA, but not LFCPB, levels of DA and o-tyr increased considerably in the striatum of piglets, a finding that may indicate the exhaustion of cellular energy levels and contribute substantially to cellular injury.     

肠缺血/再灌注损伤时中性粒细胞呼吸爆发活性的变化

目的:研究肠缺血/再灌注(I/R)时中性粒细胞(PMN)呼吸爆发活性的变化.方法:30只成年雄性Wistar大鼠,按照随机数字表法分为假手术,缺血45 min,缺血45 min再灌注60min、120min、360min等5组.阻断肠系膜上动脉血流45min后复流,复制I/R模型:假手术组只进行同样的手术操作但不阻断肠系膜上动脉血流.在各时间点分别取门静脉血测定白细胞计数,并分离PMN进行化学发光(CL)测定.结果:肠I/R损伤过程中,缺血组与假手术组比较,PMN的CL峰值无明显差异(P＞0.05),再灌注组PMN的CL峰值均明显升高(P＜0.01).肠缺血组白细胞数量较假手术组降低,再灌注后开始回升,再灌注360 min时白细胞计数最高.PMN化学发光峰值变化和血白细胞计数的变化趋势呈显著正相关(r=0.748,P＜0.05).结论:肠I/R损伤可激活循环中的PMN,使血中的PMN数量增加,PMN的呼吸爆发化学发光活性明显升高,可能是引起全身炎症反应和器官损害的因素之一.     

Ulinastatin attenuates reperfusion injury in the isolated blood-perfused rabbit heart

BACKGROUND: Ventricular dysfunction after long cardioplegic arrest has been observed in cardiac operations. Urinary trypsin inhibitor, also called ulinastatin, may attenuate myocardial ischemia-reperfusion injury. The present study was designed to determine the protective efficacy of ulinastatin in blood-perfused parabiotic isolated rabbit hearts as a surgically relevant model with long (4-hour) cardioplegic arrest. METHODS: Each isolated rabbit heart, with a latex balloon inserted in the left ventricle, was parabiotically blood-perfused using a modified Langendorff column. The left ventricular developed pressure, rate of pressure development, and coronary flow with a left ventricular end-diastolic pressure of 10 mm Hg were measured before ischemia and 15, 30, 45, and 60 minutes after reperfusion began (control, n = 10). Ulinastatin (15,000 U/kg) was administered to the support animal just before reperfusion began (group U-1, n = 10) or at the beginning of the extracorporeal circulation and readministered before reperfusion (group U-2, n = 10). The endothelium of the coronary artery was observed by scanning electron microscopy to evaluate the extent of endothelial ischemia-reperfusion injury. RESULTS: Ulinastatin enhanced the recovery of developed pressure in both the U-1 (p<0.05) and U-2 (p < 0.01) groups compared with the control group. Although ulinastatin given just before reperfusion (group U-1) did not enhance the recovery of the rate of pressure development or the coronary flow compared with the control, earlier administration did improve the recovery of the rate of pressure development compared with the control (U-2, p<0.05), and there was improvement of the recovery of coronary flow after 60 minutes of reperfusion (U-2, p<0.05). Scanning electron microscopy showed that ulinastatin had ameliorated coronary endothelial damage. CONCLUSIONS: Ulinastatin improved functional recovery after long cardioplegic arrest and reduced coronary endothelial injury. Administration of ulinastatin at the beginning of cardiopulmonary bypass and just before reperfusion may be useful clinically in cases requiring prolonged aortic cross-clamping.     

L-Arginine transport is augmented through up-regulation of tubular CAT-2 mRNA in ischemic acute renal failure in rats

BACKGROUND: Ischemic acute renal failure (iARF) is associated with increased nitric oxide (NO) production during the reperfusion period, as endothelial nitric oxide synthase (eNOS) is maximally activated, and renal tubular inducible NOS (iNOS) is stimulated. Increased NO production leads to augmented tubular injury, probably through the formation of peroxynitrite. l-Arginine (l-Arg), the only precursor for NO, is transported into cells by cationic amino acid transporters, CAT-1 and CAT-2. We hypothesized that the increased NO production observed in iARF may result from increased l-Arg uptake, which would be reflected in the augmented expression of l-Arg transporter(s). METHODS: Ischemic acute renal failure was induced in rats by right nephrectomy + left renal artery clamping for 60 minutes. l-Arg uptake was examined in freshly harvested glomeruli and tubuli from control, sham operated, and animals subjected to 15, 30, and 60 minutes, and 24 hours of reperfusion, following 60 minutes of ischemia. Using RT-PCR, renal tissues were examined further for the expression of iNOS, CAT-1, CAT-2, arginase I and arginase II. RESULTS: Tubular expression of iNOS mRNA was initiated by ischemia, continued to increase after 60 minutes of reperfusion, and decreased after 24 hours. l-Arg transport into glomeruli was similar in all experimental groups. l-Arg uptake into tubuli was markedly augmented following the 60-minute reperfusion, while it moderately increased after 24 hours of reperfusion. This was accompanied by a parallel, preferential increase in tubular CAT-2 mRNA expression at 60 minutes of reperfusion. CAT-1 mRNA expression was unchanged, as detected by RT-PCR. In addition, the expression of arginase II and arginase I mRNA was attenuated by 30 minutes and one hour of reperfusion, and returned to baseline values after 24 hours of reperfusion. CONCLUSIONS: Ischemic ARF is associated with augmented tubular CAT-2 mRNA expression, which leads to enhanced l-Arg transport and increased NO production. This may contribute to the renal injury exhibited in iARF.     

Utility of near-infrared spectroscopic measurements during deep hypothermic circulatory arrest

BACKGROUND: Near-infrared spectroscopy (NIRS) is used to monitor cerebral oxygenation during cardiac surgery. However, interpretation of the signals is controversial. The aim of the study was to determine which NIRS variable best correlated with brain damage as assessed by animal behavior and neurohistologic score and to compare the accuracy of NIRS and magnetic resonance spectroscopy (MRS) in predicting brain injury. METHODS: Forty 5-week-old piglets underwent 60 minutes of deep hypothermic circulatory arrest (DHCA) at 15 degrees C. Changes in brain adenosine triphosphate (ATP), phosphocreatine (PCr), and intracellular pH (pHi) were determined by MRS and correlated to changes in oxygenated hemoglobin (HbO2), deoxygenated hemoglobin (Hb), and oxidized cytochrome a,a3 (CytOx) NIRS signals. Brains were fixed on day 4 and examined using a neurohistologic score. RESULTS: Reductions in CytOx and HbO2 values were correlated closely with decreases in ATP, PCr, and pHi. The changes in CytOx and PCr showed the strongest correlation (r = 0.623). Maximal CytOx reduction during DHCA of more than -25 microM * differential pathlength factor (DPF) predicted brain damage with a sensitivity of 100% and a specificity of 75%. The histologic score was also correlated with a decrease in ATP (r = -0.52 for CytOx; r = -0.32 for ATP); HbO2, PCr, and pHi showed no correlations. CONCLUSIONS: Reduction in CytOx correlates with decreased brain energy state and predicts histologic brain injury after DHCA with a high sensitivity. These data suggest that the level of CytOx could be a very important predictor of brain damage during DHCA.     

ICAM-1mRNA在大鼠缺血/再灌注肝脏组织中的表达

目的探讨肝脏缺血/再灌注损伤过程中,肝脏组织中ICAM-1mRNA的表达规律及其意义。方法应用RT-PCR技术,观察缺血时间分别为15min、30min及45min的三组大鼠肝脏于再灌注60min时ICAM-1mRNA的表达情况。结果三组肝脏缺血前及缺血末组织内仅有少量ICAM-1mRNA表达于肝细胞,但于再灌注60min时,ICAM-1mRNA表达程度则显著增强,且缺血时间越长的肝脏,其表达强度越高。结论肝脏的缺血能明显诱导再灌注期间肝细胞表达ICAM-1mRNA,增强肝窦内皮细胞的粘附力,进而引发一系列病理生理改变。     

大鼠肝脏缺血再灌注过程中信号转导与转录激活子1的表达变化及其意义

目的 观察JAK-STAT信号通路蛋白STAT1和半胱氨酸天冬氨酸蛋白酶(Caspase)-3在大鼠肝脏缺血再灌注不同时限的表达及丹参对两者表达的影响.方法 将80只SD大鼠随机分为正常组、假手术组、缺血再灌注组和丹参组,建立肝缺血再灌注模型,采用免疫组织化学方法 检测STAT1及Caspase-3在肝缺血45 min再灌注0、3、12、24、72 h时的表达.结果 STAT1、Caspase-3在正常及假手术组中未见明显表达.缺血再灌注组STATI在再灌注0 h即有表达(PU=10.29±0.92),再灌注12～24 h表达最明显(PU=38.73±1.59～38.90±2.29),Caspase-3在再灌注0 h亦有表达(PU=8.18±0.95),峰值出现在再灌注24 h(PU=38.06±2.85).丹参组STAT1在各时限点均较同期缺血再灌注组低(P＜0.05),除再灌注72h外丹参组Caspase-3在各时限点均较同期缺血再灌注组低(P＜0.05).结论 STAT1在大鼠肝缺血再灌注损伤中被激活,丹参可能通过抑制STAT1的表达减轻缺血再灌注对肝的损伤.