Blood hibernation: a novel strategy to inhibit systemic inflammation and coagulation induced by cardiopulmonary bypass

Background Inflammation and coagulation are two intimately cross-linked defense mechanisms of most, if not all organisms to injuries. During cardiopulmonary bypass (CPB), these two process-is are activated and interact with each other through several common pathways, which may result in subsequent organ dysfunction. In the present study, we hypothesized that the addition of nitric oxide, prostaglandin E1 (PGE1), and aprotinin to the systemic circulation, hereby referred to as blood hibernation, would attenuate the inflammation and coagulation induced by CPB. Methods Thirty adult mongrel dogs were equally divided into five groups, anesthetized and placed on hypothermic CPB (32 C). Each group received respectively the following treatments: (1) inhalation of 40 ppm nitric oxide; (2) intravenous infusion of 20 ng·kg-1·min-1 of PGE1; (3) 80 000 kallikrein inhibitor units (KIU)/kg of aprotinin; (4) the combination of all three agents (blood hibernation group); and (5) no treatment (control group) during CPB. Activation of leukocyte, platelet, endothelial cell, and formation of thrombin were assessed after CPB.Results As compared with the other four groups, leukocyte counts were higher, while plasma elastase, interleukin-8, CD11b mRNA expression, myeloperoxidase activities and lung tissue leukocyte counts were lower in the blood hibernation group (P<0.05 versus other four groups after CPB). Plasma prothrombin fragment (PTF)1+2, and platelet activation factors were lower, while platelet counts were higher in the blood hibernation group (P<0.05 versus other four groups at 6 and 12 hours after CPB). Electron microscopy showed endothelial pseudopods protrusion, with cell adherence in all four groups except the blood hibernation group where endothelial cells remained intact.Conclusion Blood hibernation, effected by the addition of nitric oxide, PGE1 and aprotinin to the circulating blood during extra-corporeal circulation, was observed to attenuate the inflammation and coagulation induced by cardiopulmonary bypass, most likely by inhibiting the important common intermediates between the two cross-linked processes.     

Blood hibernation: a novel strategy to inhibit systemic inflammation and coagulation induced by cardiopulmonary bypass

Background Inflammation and coagulation are two intimately cross-linked defense mechanisms of most, if not all organisms to injuries. During cardiopulmonary bypass (CPB), these two process-is are activated and interact with each other through several common pathways, which may result in subsequent organ dysfunction. In the present study, we hypothesized that the addition of nitric oxide, prostaglandin E1 (PGE1), and aprotinin to the systemic circulation, hereby referred to as blood hibernation, would attenuate the inflammation and coagulation induced by CPB. Methods Thirty adult mongrel dogs were equally divided into five groups, anesthetized and placed on hypothermic CPB (32 C). Each group received respectively the following treatments: (1) inhalation of 40 ppm nitric oxide; (2) intravenous infusion of 20 ng·kg-1·min-1 of PGE1; (3) 80 000 kallikrein inhibitor units (KIU)/kg of aprotinin; (4) the combination of all three agents (blood hibernation group); and (5) no treatment (control group) during CPB. Activation of leukocyte, platelet, endothelial cell, and formation of thrombin were assessed after CPB.Results As compared with the other four groups, leukocyte counts were higher, while plasma elastase, interleukin-8, CD11b mRNA expression, myeloperoxidase activities and lung tissue leukocyte counts were lower in the blood hibernation group (P<0.05 versus other four groups after CPB). Plasma prothrombin fragment (PTF)1+2, and platelet activation factors were lower, while platelet counts were higher in the blood hibernation group (P<0.05 versus other four groups at 6 and 12 hours after CPB). Electron microscopy showed endothelial pseudopods protrusion, with cell adherence in all four groups except the blood hibernation group where endothelial cells remained intact.Conclusion Blood hibernation, effected by the addition of nitric oxide, PGE1 and aprotinin to the circulating blood during extra-corporeal circulation, was observed to attenuate the inflammation and coagulation induced by cardiopulmonary bypass, most likely by inhibiting the important common intermediates between the two cross-linked processes.     

Changes in phospholipase D activity of leukocytes during human systemic inflammatory response syndrome induced by cardiopulmonary bypass

Objective To investigate the fluctuations in arterial leukocyte phospholipase D (PLD) activity during the perioperative period of open heart surgery under cardiopulmonary bypass (CPB), and the relationship between PLD activity and systemic inflammatory response induced by CPB. Methods Arterial blood was obtained from 26 patients undergoing open heart surgery at 8 different time points during the perioperative period, from which leukocytes were isolated for determination of PLD activity, CD11b expression and myeloperoxidase (MPO) activity. Plasma IL-6, IL-8 and C-reactive protein were also determined. The 26 cases were retrospectively divided into 3 groups according to perfusion time in order to detect the possible influences of CPB on PLD activity and IL-6 and IL-8 levels.Results When the ascending aorta was declamped, average arterial leukocyte PLD activity was 0.305±0.132 nmol choline·min-1·mg-1, 5.0 times higher of the pre-CPB value, and remained (5.4 times higher of the pre-CPB level) at 72 hours after CPB. Leukocyte CD11b expression and plasma IL-6 and IL-8 levels increased significantly at the end of CPB, while MPO activity and C-reactive protein concentration reached their peaks at 1 and 24 hours, respectively, after CPB. At the end of CPB, the arterial leukocyte PLD activity of patients whose CPB duration was longer than 90 minutes were 1.82- and 1.74-fold that of the other two groups with CPB lasting between 90 and 60 minutes and less than 60 minutes. Conclusions Arterial leukocyte PLD activity rises significantly in CPB and its elevation is earlier and more persistent than other inflammation-related indicators tested; longer CPB duration leads to higher leukocyte PLD activity at the end of CPB. These results imply that PLD could be a new target for prevention of systemic inflammatory response induced by CPB.     

乌司他丁对体外循环手术患者脑炎性反应的影响

目的：探讨乌司他丁对体外循环心脏手术患者脑炎性反应的影响。方法：选择24例择期行心脏瓣膜置换术患者,随机分为乌司他丁组(U组)和对照组(Ｃ组),每组12例。U组患者给予乌司他丁2.4×104U／kg,其中1.2×104U／kg于麻醉诱导后静脉注射,0.6×104U／kg加于体外循环预充液中随转流进入体内,0.6×104U／kg于主动脉开放前约5min加入体外循环机内。C组患者用等量容积的生理盐水代替。于麻醉后手术前（T1）、体外循环结束后60min(T2)、体外循环结束后6h（T3）同时抽取动脉血与颈静脉球血,测定肿瘤坏死因子α(TNFα),白细胞介素6,8,10（IL-6,IL-8,IL-10）,并计算颈静脉球血与动脉血各细胞因子之差△TNFα,△IL-6,△IL-8,△IL-10。结果：C组T2时动脉血TNFα,IL-6,IL-8,IL-10及△TNFα,△IL-8,△IL-10显著升高(P<0. 01),T3时TNFα,IL-6,IL-8,IL-10及△TNFα,△IL-6,△IL-10明显升高(P<0. 01),△IL-8亦升高(P<0. 05); U组T2时IL-6,IL-8,IL-10显著升高(P<0.01),TNFα,△TNFα,△IL-10亦升高(P<0.05),T3时IL-6,IL-8,IL-10,△TNFα,△IL-8显著升高(P<0.01),△IL-6,△IL-10亦升高(P<0.05)。T2时U组动脉血TNFα,IL-6及△TNFα,△IL-8低于C组(P<0.05),动脉血IL-8显著低于C组(P<0.01);T3时U组动脉血TNFα及△IL-6低于C组(P<0.05),U组动脉血IL-6,IL-8显著低于C组(P<0.01),动脉血IL-10与△IL-10高于C组(P<0.05)。结论：乌司他丁可以减轻体外循环手术患者全身和脑局部的炎性反应。     

体外循环下心瓣膜置换术患者血小板及凝血功能的变化及普鲁泊福对其的影响

目的:观察体外循环(CPB)下心脏瓣膜置换手术中患者血小板与凝血功能的变化及普鲁泊福对其的影响.方法:ASAⅡ～Ⅲ级择期心脏瓣膜置换手术患者30例,随机分为对照组(n=15)和普鲁泊福组(n=15).对照组应用咪达唑仑0.05 mg/kg、芬太尼0.01 mg/kg、维库溴铵0.1～0.2 mg/kg行麻醉诱导,术中以0.5%～1.5%异氟烷及芬太尼、哌库溴铵维持麻醉;普鲁泊福组应用咪达唑仑0.05 mg/kg、芬太尼0.005～0.01 mg/kg、普鲁泊福1.5 mg/kg、维库溴铵0.1～0.2 mg/kg行麻醉诱导,术中以静注普鲁泊福4～5 mg/(kg·h)、芬太尼、哌库溴铵和0.5%～1.0%异氟烷维持麻醉.采用Sonoclot凝血与血小板功能分析仪分别测定麻醉前、诱导后5 min、CPB转流前、CPB结束后10 min、手术结束时5个时间点全血激活凝固时间(SonACT)、凝血速率、血小板功能(PF)、凝血达到高峰时间(TP),同时观察血小板(PLT)计数、血浆凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)的变化.结果:与麻醉前相比,诱导后和转流前2组SonACT、PF、凝血速率、TP及常规凝血试验各项指标均无显著差异;CPB结束后10 min和手术结束时2组PF显著降低(P<0.01),SonACT、凝血速率、TP、PT、APTT明显延长(P<0.01),PLT计数明显减少(P<0.01);2组间各个时间点的指标相比较无显著差异.结论:CPB是影响心脏瓣膜置换手术中血小板及凝血功能的主要因素;诱导剂量1.5 mg/kg及术中持续静脉输注浓度为4～5 mg/(kg·h)的普鲁泊福对血小板功能无明显影响.     

乌司他丁对体外循环冠脉搭桥手术围术期炎症反应的影响

目的:探讨乌司他丁对体外循环冠脉搭桥手术(CABG)围术期炎症反应的影响.方法:择期行CABG患者40例,随机分为对照组(C组,n=20)和乌司他丁组(U组,n=20).U组于体外循环(CPB)前静脉滴注乌司他丁1.5×10~4 U/kg,C组于相同时间静脉滴注生理盐水.分别于麻醉诱导前(T1)、CPB1h(T2)、CPB后1h(T3)、CPB后24 h(T4)检测血浆肿瘤坏死因子(TNF-α)、白细胞介素(IL)-6、IL-10和中性粒细胞弹性蛋白酶(NE)的浓度.比较两组患者手术后的恢复情况.结果:与T1相比,2组患者在T2,T3,T4时点TNF-α,IL-6,IL-10及NE的浓度均明显升高((P<0.05);U组在T2,T3,T4的TNF-α,IL-6及NE浓度均明显低于C组(P<0.05),而IL-10的浓度明显高于C组(P<0.05).U组患者术后肺、肾及脑功能明显优于C组(P<0.05),心、肝功能及ICU停留时间无明显差异(P>0.05).结论:乌司他丁能够减轻体外循环冠脉搭桥手术围术期炎症反应,减少术后并发症.     

不同麻醉药对体外循环细胞因子的影响

目的　观察不同麻醉药对体外循环 (CPB)炎性反应的影响。方法　 45例先天性心脏病房、室间隔缺损患者 ,按麻醉维持不同随机分为 3组 :芬太尼组 (Fen组 )主要用芬太尼维持 ;异氟醚组 (Iso组 )以吸入体积分数为 1 0 %～ 1 5 %异氟醚为主 ;异丙酚组 (Pro组 )主要用异丙酚维持。分别于以下 5个时点采集动脉血 ,麻醉诱导后 (T1)、切皮前 (T2 )、升主动脉开放后(T3 )、CPB术后 2h(T4)、CPB术后 2 4h(T5 ) ,用放射免疫法测定肿瘤坏死因子 -α(TNF -α)、白介素 - 6(IL - 6)。结果　Iso组切皮前 (T2 )TNF -α明显下降 ,从 0 94μg/L降至 0 3 8μg/L ,有极显著性差异 (P <0 0 1) ;T2～T4的值明显低于其他两组(P <0 0 5 )。各组TNF -α、IL - 6在CPB中及术后均较切皮前 (T2 )升高 (P <0 0 5或P <0 0 1)。三组间各时间点IL - 6的差异无显著性 (P >0 0 5 )。结论　CPB过程中及术后血浆TNF -α、IL - 6均有不同程度升高 ,最高值在CPB术后 2h出现 ,于术后 2 4h降低 ,但仍高于术前水平。异氟醚对TNF -α的释放虽有一定的抑制作用 ,但并不能改变CPB手术对TNF -α的影响 ;而异氟醚、芬太尼和异丙酚对IL - 6的影响无显著性差异     

Effects of beating-heart and arrested heart intracardiac procedure on the inflammation induced by cardiopulmonary bypass

Objective：To evaluate the effects of beating-heart and arrested heart intracardiac procedure on the expression of tumor necrosis factor alpha （TNF-α mRNA in myocardium. Methods： Thirty congenital ventricular septal defect （VSD） patients aged from 5 to 10 years old were randomly divided into 2 groups equally. Group A underwent traditional arrested heart intracardiac procedures ; group B underwent beating-heart procedures. Specimens of myocardium were obtained at the onset （baseline） and the end of cardiopulmonary bypass （CPB） for the determination of TNF a mRNA. Concentration of TNF-α was respectively measured after anesthetic induction （T1）, 20 min after the beginning of CPB （T2）, at the end of CPB （T3） and 6, 12, 24 h after CPB （T4-6） in all patierits： After separating polymorphonuclear leucocyte （PMN）, we distilled nuclear protein and mensurated the activation of nuclear factor-κB （NF-κB） by elec-trophoretic mobility shift assay （EMSA）. Results ：Compared with baseline, the expression of TNF-κ mRNA significantly increased in both groups （P〈0. 05）. TNF-α mRNA level of group A was significantly higher than that of group B at the end of CPB （P〈0.05）. The plasma concentration of TNF-α and neutrophil NF-κB activity in group A was significantly higher than that of group B at T,4-6（P〈0.05）. Conclusion：Compared with traditional arrested CPB, beating heart intracadiac procedure can effectively reduce the expression and release of TNF-α; it will benefit the protection of pediatric myocardial during CPB.     

两种核心体温监测方法对心脏直视手术体外循环时间及凝血功能的影响

目的 探讨两种核心体温监测方法对心脏直视手术体外循环时间及凝血功能的影响,为心脏直视手术核心体温监测提供参考.方法 将2016年6-12月该院的心脏直视手术患者140例分为对照组(n=70)和观察组(n=70),其中对照组监测膀胱温和鼻咽温,观察组监测直肠温和鼻咽温,记录手术中体外循环降温时间、阻断升主动脉时间、复温时间、体外循环总时间;两组患者均在术前1d及术毕抽血监测凝血功能,包括凝血酶时间(TT)、凝血酶原时间(PT)、活化部分凝血活酶时间(APTT).结果 对照组在降温时间、复温时间及体外循环总时间上均多于观察组,差异有统计学意义(P<0.01).术前两组患者的凝血功能指标(TT、PT、APTT)比较,差异无统计学意义(P>0.05);术毕两组患者的凝血功能指标(TT、PT、APTT)比较,差异有统计学意义(P<0.01),观察组凝血功能各指标优于对照组.结论 用直肠温监测体外循环下心脏直视手术患者的核心体温优于膀胱温,可以缩短体外循环时间,改善凝血功能.     

盐酸戊乙奎醚对风湿性心脏病患者体外循环炎症反应的影响

目的研究盐酸戊乙奎醚对风湿性心脏病患者体外循环（ECC）炎症反应的影响。方法选择184例择期行ECC瓣膜置换术的患者,随机分为盐酸戊乙奎醚组（P组）和生理盐水组（c组）,分别于麻醉诱导前（T0）、ECC30 min（T1）、主动脉开放10min（T2）、ECC结束后2h（T3）抽取动脉血,测定血浆白介素（IL）-6,肿瘤坏死因子（TNF）-α的浓度,并观察术后肺炎发生率、全身炎症反应综合征（SIRS）发生率、有无谵妄等临床指标。结果组内比较,P组和C组在他、T3时,IL-6浓度均高于T0、T1（P〈0．05）;P组TNF-a浓度在T3时低于T1和T2。组间比较,在T2、T3时,P组IL-6浓度低于C组（P〈0．05）;TNF-a浓度各时间点差异无统计学意义（P〉0．05）。肺炎发生率和SIRS发生率P组均低于C组（P〈0．05）。结论应用盐酸戊乙奎醚能一定程度上抑制细胞因子的释放,副作用少,对ECC术后SIRS和肺部并发症有-定的防治作用。     

抑肽酶对常温体外循环中TNF-α、IL-6及IL-8的影响

目的 :探讨抑肽酶对常温体外循环术中、术后炎性反应的抑制作用。方法 :4 0例常温体外循环下行心脏直视手术的风湿性心瓣膜病患者随机分为 2组。试验组 2 0例 ,于转机前加入抑肽酶 5万kIU·kg-1,对照组 2 0例未用抑肽酶。分别于麻醉前、主动脉阻断 10min、停机后 10min、术后 2 4h及术后 4 8h采取动脉血标本 ,酶标放免法分别测定血浆IL 6、IL 8及TNF α水平。结果 :2组麻醉前各因子血浆水平差异无统计学意义 (P >0 .5 ) ,对照组各因子在体外循环后各时点均升高 (P <0 .0 1) ,术后 4 8h恢复至基础值 ,而试验组各时间点各因子水平也升高(P <0 .0 5或P <0 .0 1) ,但均较对照组低 (P <0 .0 5或P <0 .0 1)。试验组与对照组相比 ,围手术期输血量及术后胸腔引流量明显减少 (P <0 .0 5 )。结论 :抑肽酶可减轻常温体外循环术中、术后患者全身炎性反应综合征 ,减少术后渗血及围手术期输血量     

体外循环心脏手术患者围术期血糖及乳酸变化

目的回顾性分析体外循环(cardiopulmonary bypass,CPB)下心脏手术患者围术期血糖和血乳酸的变化趋势。方法选取2013年1月至12月期间在首都医科大学宣武医院行体外循环心脏手术的成年患者58例,根据术前是否合并糖尿病分非糖尿病组和糖尿病组,根据体外循环时间分为CPB时间小于2 h组(A组)和大于2 h组(B组)。观察围术期血糖值和乳酸值的变化趋势,并对相关临床资料进行分析。结果 58例患者体外循环时间59~315 min,平均(126.07±50.74)min,阻断时间35~161 min,平均(67.61±22.95)min,自动复跳率52%,术中血糖及血乳酸从麻醉诱导后呈逐渐升高趋势,Pearson检验示两者之间呈正相关(r=0.939,P=0.018),手术结束时血糖升至最高随后逐渐下降。结论体外循环对合并糖尿病患者围术期血糖的影响更明显,控制围术期血糖有助于降低血乳酸。提高CPB的管理水平,有利于术中及术后血糖及乳酸值的改善,从而降低术后相关合并症,改善预后。     

改良兔体外循环急性肺损伤模型的建立

目的 探讨改良经主动脉、右心房插管,自体血预充的兔体外循环(CPB)急性肺损伤模型,及外周血肿瘤坏死因子α水平变化.方法 随机选择10只健康成年雄性新西兰兔建立体外循环模型.待心脏复跳稳定,终止体外循环后,兔存活4 h即判定为模型制作成功.监测生命体征,分别记录在麻醉后(T1)、在体外循环转流前(T2),阻断主肺动脉后15 min时(T3),主肺动脉的重新开放灌流后(T4),体外循环结束后1 h(T5)、4 h(T6)的生命体征值,与T2、T4、T6时刻采集动脉血进行血气分析,采用酶联免疫吸附(ELISA)法检测T2、T5、T6时刻外周血中肿瘤坏死因子α(TNF-α)水平.结果 通过对10只兔的实验,成功改良了兔CPB急性肺损伤模型.术中平均动脉压维持55 mmHg以上,体外转流前后红细胞压积显著下降(T230.18±2.88%,T417.73±1.95%,P<0.05),血浆乳酸Lac浓度逐步升高,开放主肺动脉时明显增加(T23.65±1.13 mmol/L,T49.36±1.28 mmol/L,P<0.05).T6氧合指数(PaO2/FiO2)比T2显著下降(T2468.36±56.28 mmHg,T6281.64±55.76 mmHg,P<0.05),血清中TNF-α水平显著升高(P<0.05),肺间质水肿显著,炎性细胞浸润增加.结论 本实验改良的兔CPB急性肺损伤模型稳定可靠,可为研究体外循环引起的急性肺损伤提供稳定可靠的研究基础.     

儿童低温体外循环围术期内皮细胞凝血及纤溶活性变化

目的 探讨儿童低温体外循环围术期内皮细胞凝血及纤溶活性变化。方法 选择20例先天性心脏病缺损患儿，于肝素化后体外循环前、转流30min、开放主动脉5min、停机、停机后4h、术后第1日晨取静脉血测循环内皮细胞（CEC）数，同时用酶联免疫法测定血浆中血管性假血友病因子（vWF）浓度、组织型纤溶酶原激活剂（t-PA）及纤溶酶原激活剂抑制物－1（PAI－1）活性，并测定血不同时间的CEC数。结果 体外循环期间及体外循环结束后各时相点CEC数、vWF浓度均较体外循环前显著增加（P＜0．05）；体外循环期间t－PA活性显著升高（P＜0．05），停机后t－PA活性逐渐下降，术后第1日t－PA活性与转流前无显著差异（P＞0．05）；转流后PAI－1活性显著下降（P＜0．05），停机后PAI－1活性显著升高（P＜0．05）。结论 低温体外循环可致血管内皮细胞激活或损伤，并致凝血及纤溶功能紊乱。     

乌司他丁对体外循环心脏病人血浆TNF-a,IL-6和IL-8的影响

目的通过观察体外循环(CPB)中预充乌司他丁对CPB心脏病血浆TNF-a,IL-6和IL-8的影响.方法选择40例主动脉阻断时间在30 min以上的心脏直视手术患者,随机分为实验组20例对照组20例.实验组在常规CPB预充液中加入乌司他丁1.5万U/kg,对照组用生理盐水.分别在手术开始前,CPB结束后即刻,CPB结束后3,6及24 h抽取桡动脉血,采用ELISA法测定血浆肿瘤坏死因子、白介素-6(IL-6)、白介素-8(IL-8)的浓度.结果实验组患者TNF-a,IL-6和IL-8以CPB结束后即刻0,3和6 h血浆浓度明显低于对照组(P＜0.01),IL-6和IL-8在CPB结束后24h也低于对照组(P＜0.05).结论乌司他丁可明显减少CPB术后TNF-a,IL-6和IL-8的释放,可减轻CPB术后全身炎症反应.     

心肺转流术对血糖,胰岛素水平的影响

目的：观察心内直视手术时的体外循环对血糖,胰岛素水平的影响。方法：２８例心脏病手术患者分别于麻醉前,ＣＰＢ前,ＣＰＢ１０ｍｉｎ,ＣＰＢ３０ｍｉｎ,心脏复跳后５ｍｉｎ,ＣＰＢ结束时抽取血标本测定血糖,胰岛素含量。结果;血糖和胰岛素浓度在ＣＰＢ期和ＣＰＢ结束时显著高于ＣＰＢ前,麻醉前ＣＰＢ前比较无明显变化。结论：ＣＰＢ期胰岛期水平增加,但组织对胰岛素的敏感性降低,对葡萄糖的利用率下降,机体发生胰岛纱耐     

还原型谷胱甘肽对体外循环期细胞因子IL-8和IL-6的影响

目的观察还原型谷胱甘肽对体外循环(CPB)期间白细胞介素-8(IL-8)和白细胞介素-6(IL-6)的影响。方法选择30例施行心脏手术患者,随机分成实验组和对照组(每组15例)。实验组患者于手术开始时分别予还原型谷胱甘肽(35 mg/kg)溶于100 ml生理盐水静滴,对照组予生理盐水静滴。于CPB前(T1)、CPB 30 min(T2)、CPB停机(T3)、停机后2 h(T4)四个时点采血,采用放射免疫法测定两组血清中IL-8和IL-6的浓度。结果实验组IL-8、IL-6血清浓度较对照组降低,差异有统计学意义(P<0.05)。结论还原型谷胱甘肽能减少CPB期间IL-8和IL-6的释放,减轻全身炎性反应的程度。     

川芎嗪对体外循环下炎症反应和心肌缺血-再灌注损伤的保护作用

目的 探讨不同剂量川芎嗪对体外循环(CPB)所致炎症反应和心肌缺血-再灌注损伤(MIRI)的保护作用.方法 60例先天性房间隔或(和)室间隔缺损患者随机分为对照组(A组)、盐酸川芎嗪3 mg/kg组(B组)、9 mg/kg组(C组)、12mg/kg组(D组).分别于诱导后(T0)、转机后15 min(T1)、停机后2 h(T2)、停机后6 h(T3)、手术后24 h(T4)抽取静脉血测量血清中肿瘤坏死因子(TNF)、心肌肌钙蛋白Ⅰ(cTnI)的浓度,并观察血流动力学指标.结果 TNF的含量B、C、D组T2与A组相比有统计学差异,但是C、D两组的差异更加显著;整体上,C、D两组较A、B两组显著降低.cTnI的含量:A组cTnI的峰值出现在T4,C组T2、T3、T4与T1无统计学差异;C组T4时与A组相比具有显著差异;整体上,C组较A组降低.各组血流动力学指标无差异.结论 川芎嗪对体外循环(CPB)所致炎症反应和心肌缺血-再灌注损伤(MIRI)有保护作用,以9mg/kg作用较为显著.     

N-乙酰半胱氨酸对体外循环大鼠肠损伤的影响

目的观察N-乙酰半胱氨酸（NAC）对体外循环（CPB）大鼠肠损伤的影响。方法成年雄性SD大鼠32只,随机均分为假手
术组（S组）、NAC对照组（N组）、CPB组（C组）、CPB+NAC治疗组（NC组）,每组8只。S组和N组仅置管和肝素化,不进行CPB,
C组和NC组进行CPB 1 h,然后观察2 h。N组和NC组在术前3天每天腹腔注射0.5 g/kg NAC,且NC 组在预充液中加入NAC
100 mg/kg,然后以20 mg/（kg·h）速度输注直到停转流,C组仅给予等量的生理盐水。CPB后2 h取小肠标本和血标本,观察肠组
织病理学改变,检测肠组织丙二醛（MDA）水平和超氧化物歧化酶（SOD）、谷胱甘肽（GSH）和谷胱甘肽过氧化物酶（GSH-Px）活
性和肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6及血清二胺氧化酶（DAO）水平。结果CPB后2 h,肠组织出现明显的损伤性改
变和氧化应激损伤;而NAC处理可以显著减轻小肠粘膜损伤,降低MDA和DAO,上调SOD、GSH和GSH-Px等抗氧化酶的活
性和降低TNF-α、IL-6水平。结论围术期使用NAC能够减轻CPB诱发的氧化应激和炎症反应的程度,对CPB诱发的肠损伤具
有一定的保护作用。
     

Resection of tracheal tumor under cardiopulmonary bypass: a case report

A nesthesia for low tracheal tumor surgery presents many challenges: conventional anesthetic techniques would be catastrophic if one attempts to insert a tracheal tube which may cause a complete obstruction of the airway;