Effect of remote ischemic postconditioning in inflammatory changes of the lung parenchyma of rats submitted to ischemia and reperfusion

Objective

To assess the effects of postconditioning remote in ischemia-reperfusion injury in rat lungs.

Methods

Wistar rats (n=24) divided into 3 groups: GA (I/R) n=8, GB (R-Po) n=8, CG (control) n=8, underwent ischemia for 30 minutes artery occlusion abdominal aorta, followed by reperfusion for 60 minutes. Resected lungs and performed histological analysis and classification of morphological findings in accordance with the degree of tissue injury. Statistical analysis of the mean rating of the degree of tissue injury.

Results

GA (3.6), GB (1.3) and CG (1.0). (GA GB X P<0.05).

Conclusion

The remote postconditioning was able to minimize the inflammatory lesion of the lung parenchyma of rats undergoing ischemia and reperfusion process.     

舒芬太尼后处理对二尖瓣置换患者心肌缺血/再灌注损伤的影响

目的 评价主动脉根部灌注舒芬太尼对体外循环(cardiopulmonary bypass,CPB)下二尖瓣置换患者心肌缺血/再灌注(ischemia/reperfusion,I/R)损伤的影响.方法 择期拟行二尖瓣置换术的风湿性心脏病患者60例,年龄18岁～65岁,美国麻醉医师协会(ASA)分级Ⅱ或Ⅲ级,心功能分级I或Ⅱ级,采用随机数字表法分为2组(每组30例):舒芬太尼后处理组(S组)和对照组(C组).S组在主动脉开放前5 min经主动脉根部一次性给予舒芬太尼0.2 μg/kg,C组给予同等容积的生理盐水.于麻醉诱导前(基础状态),主动脉开放后4、8、24 h和48 h,采集右颈内静脉血样,测定心肌肌钙蛋白Ⅰ(cardiac troponin Ⅰ,cTnⅠ)的浓度和肌酸激酶同工酶(creatine kinase-MB,CK-MB)的活性.记录两组患者血流动力学变化及术后呼吸机辅助时间、重症监护室(intensive care unit,ICU)停留时间、术后住院时间以及术后24 h心肌收缩评分等指标.结果 两组患者的平均动脉压(mean artery pressure,MAP)、心率(heart rate,HR)、中心静脉压(central venous pressure,CVP)、心排血量(cardiac output,CO)和每搏量(stroke volume,Sv)比较,差异无统计学意义(P＞0.05).S组主动脉开放后4、8h时cTnⅠ [(0.50±0.09)、(0.39±0.08) μg/L]浓度及CK-MB[(63±7)、(61±7) U/L]活性较C组[(0.70±0.11)、(0.50±0.10) μg/L,(83±10)、(75±7) U/L]明显降低(P＜0.05).S组术后呼吸辅助时间[(12±4)h]、ICU停留时间[(34±11) h]和术后住院时间[(10±3)d]较C组[(14±4)h、(44±14)h、(13±4)d]明显缩短(P＜0.05),且术后24 h心肌收缩评分[(7.6±2.8)μg·kg-1·min-1]也较C组[(10.3±3.9) μg· kg-1· min-1]明显降低(P＜0.05).结论 主动脉根部灌注舒芬太尼可减轻CPB下二尖瓣置换患者心肌I/R损伤,其机制有待进一步探讨.     

利多卡因后处理对大鼠肺缺血／再灌注损伤的影响

目的研究利多卡因后处理对大鼠肺缺血／再灌注损伤（lung ischemia／reperfusion injury,LI／RI）的作用并探讨其可能的机制。方法80只SD大鼠按随机数字表法分为4组,每组20只：假手术组（Sham组）、缺血,再灌注组[（ischemia／reperfusion,VR）组]、单纯缺血后处理组[（ischemic preconditioning,IPC）组]、利多卡因后处理组（Lidocaine组）。采用夹闭左肺门45min、然后复灌2h的方法建立在体肺棵模型。Lidocaine组再灌注即刻开始以4mg·kg-1·h-1泵入利多卡因,持续再灌注2h。观察肺组织病理学改变,检测支气管肺泡灌洗液（bronchoalveolar lavage fluid,BALF）中肺表面活性蛋白A（pulmonary surfatcantassociated proteinA,SP-A）、肺组织SP-AmRNA和SP-A的浓度。结果肺组织病理学观察发现Lidocaine组的肺水肿和白细胞渗出较I／R组明显减轻。再灌注后Lidocaine组与IPC组BALF中SP-A的浓度分别为（8．68±0．41）和（6．56±0．38）,明显高于I／R组（4．42±0．21）,差异有统计学意义（P〈0．05）;肺组织SP-AmRNA的浓度分别为（1．49±0．12）和（1．26±0．10）,明显高于I／R组（1．05扣．11）,差异有统计学意义（P〈0．05）;肺组织SP-A的浓度分别为（72．5±2．9）和（41．3±3．1）,明显高于I／R组（26．8±2．3）,差异有统计学意义（P〈0．05）;Lidocaine组与IPC组比较,BALF中SP-A、肺组织SP-AmRNA和SP-A的浓度明显升高,差异有统计学意义（P〈0．05）。结论利多卡因后处理可使大鼠I／R肺中SP-A的表达上调、分泌增加,可减轻肺水肿,且效果优于单纯IPC,对在体大鼠LI／RI有保护作用。     

迷走神经电刺激后处理对大鼠心肌缺血/再灌注损伤的影响

目的 评价迷走神经电刺激后处理对大鼠心肌缺血/再灌注损伤的影响.方法 雄性SD大鼠40只,体重250 g～350 g,采用计算机产生的随机数平均分为4组(每组10只):假手术组(S组)、缺血/再灌注组(IR组)、缺血预处理组(IPC组)和迷走神经电刺激后处理组(POES组).除S组外,其余各组均结扎冠状动脉左前降支30...     

芬太尼后处理、肢体远隔缺血后处理和缺血后处理对大鼠心肌缺血/再灌注初期室性心律失常的影响

目的 对比观察芬太尼后处理、远隔缺血后处理和缺血后处理3种干预措施抑制大鼠心肌缺血/再灌注初期室性心律失常作用的差别.方法 将73只成年雄性SD大鼠(体重250 g～350 g)麻醉后按随机数字表法随机分为9组:空白对照组(S组,n=5);对照组(C组,n=7);芬太尼后处理组(F组,n=9);肢体远隔缺血后处理组(R组,n=9);缺血后处理组(P组,n=8);联合应用芬太尼后处理和肢体远隔缺血后处理组(F-R组,n=9);联合应用芬太尼后处理和缺血后处理组(F-P组,n=8);联合应用肢体远隔缺血后处理和缺血后处理组(R-P组,n=9);联合应用芬太尼后处理、肢体远隔缺血后处理和缺血后处理组(F-R-P组,n=9).所有大鼠开胸后采用丝线套扎其冠状动脉左前降支(left anterior descending coronary artery,LAD)做成活结.除S组之外,所有大鼠接受局部心肌缺血30 min和再灌注60 min的处理.C组不采用任何干预措施;F组、F-R组、F-P组和F-R-P组在LAD结扎15 min时缓慢静脉注射芬太尼30 μg/kg;R组、F-R组、R-P组和F-R-P组在LAD结扎15 min时结扎大鼠双下肢造成肢体缺血10 min后恢复双下肢血流灌注;P组、F-P组、R-P组和F-R-P组开放实施再灌注的初期连续实施3个循环的开放LAD 20 s/阻断LAD 20 s的缺血后处理.记录缺血期和再灌期前30 min内的心律失常评分(AS评分)以及室性心动过速(ventricular tachycardia,VT)和心室纤颤(ventricular fibrillation,VF)的发生率和持续时间.结果 缺血期VT和VF的发生率、VT或VF的持续时间以及AS评分在C组、F组、R组、P组、F-R组、F-P组、R-P组和F-R-P组无统计学差异.C组、F组、R组、P组、F-R组、F-P组、R-P组和F-R-P组再灌注初期AS评分的中位数分别为4、2、2、1、2、1、1和2.与C组比较,其余各组再灌注初期室性心律失常发生显著减少;再灌注初期的VT持续时间和AS在F组和R组之间无统计学差异,但F-R组再灌注初期的VT持续时间则显著降低.与F组和R组比较,P组、F-R组、F-P组、R-P组和F-R-P组再灌注初期的VT持续时间和室性心律失常评分显著减低. 结论 与芬太尼后处理和远隔缺血后处理比较,缺血后处理可更有效抑制再灌注初期室性心律失常的发生.联合应用芬太尼后处理和远隔缺血后处理后,抑制心肌再灌注初期室性心律失常的作用相对增强.     

Very short cycles of postconditioning have no protective effect against reperfusion injury. Experimental study in rats

Introduction

Ischemic postconditioning has been recognized as effective in the prevention of reperfusion injury in situations of ischemia and reperfusion in various organs and tissues. However, it remains unclear what would be the best way to accomplish it, since studies show great variation in the method of their application.

Objective

To assess the protective effect of ischemic postconditioning on ischemia and reperfusion in rats undergoing five alternating cycles of reperfusion and ischemia of 30 seconds each one.

Methods

We studied 25 Wistar rats distributed in three groups: group A (10 rats), which underwent mesenteric ischemia (30 minutes) and reperfusion (60 minutes); Group B (10 rats), undergoing ischemia (30 minutes) and reperfusion (60 minutes), intercalated by postconditioning (5 alternating cycles of reperfusion and ischemia of 30 seconds each one); and group C - SHAM (5 rats), undergoing only laparotomy and manipulation of mesenteric artery. All animals underwent resection of an ileum segment for histological analysis.

Results

The mean lesions degree according to Chiu et al. were: group A, 2.77, group B, 2.67 and group C, 0.12. There was no difference between groups A and B (P>0.05).

Conclusion

Ischemic postconditioning was not able to minimize or prevent the intestinal tissue injury in rats undergoing ischemia and reperfusion process when used five cycles lasting 30 seconds each one.     

缺血后处理对缺血再灌注大鼠肝细胞即刻早期基因c-fos和c-jun表达的影响

目的 观察缺血后处理对大鼠肝脏缺血再灌注损伤的影响。方法 120只Wistar大鼠随机分为缺血再灌注组（IRI），缺血后处理组（IPO）和假手术组（S），于复灌后0，0．5，1，2，4，8，12，24h取材，应用RT-PCR法检测各组c-fos，c-jun mRNA的表达。结果 （1）在IRI组再灌注后0．5～2h，c-fos和c—jun的表达均增高，1h达高峰；4h后仅c-jun有持续较高的表达，c—fos的表达开始下降；（2）IPO组各时点c-fos mRNA的表达均较IRI组低，但无统计学差异（P〉0．05）；（3）与IRI组相比，IPO组c-jun mRNA在0．5，1h和2h组明显降低（P〈0．05）。结论 缺血后处理能有效地保护肝脏免受缺血再灌注造成的损伤，这种保护效应的机制可能与影响即早基因的转录有关。     

核因子-κB/I-κB传导通路在肝脏缺血再灌注损伤中的作用

目的 探讨核因子(NF)—κB／Ⅰ—κB传导通路在肝脏缺血再灌注损伤中的作用。方法 采用阻断大鼠部分肝血供的缺血再灌注损伤模型，左半肝缺血90min，再灌注分0、1、2、4h等时点。用凝胶滞留电泳方法测定NF—κB的结合活性；应用逆转录—聚合酶链反应(RT—PCR)测定肝组织中肿瘤坏死因子—α(TNF—α)、细胞间粘附因子—1(ICAM—1)mRNA的表达量。结果 肝脏缺血再灌注损伤时NF—κB与其特异性调控序列的结合活性增高且具有时相性。再灌注1～2h NF—κB结合活性增高，4h后开始降低。肝组织中TNF—α、ICAM—1 mRNA表达在再灌注2h后升高。讨论 肝脏缺血再灌注损伤时，NF—κB激活并进入细胞核内，与一些炎症因子基因启动子区特异序列结合，上调TNF—α、ICAM—1 mRNA表达，从而引起肝脏缺血再灌注损伤。     

舒芬太尼后处理对犬心肌缺血/再灌注Bcl-2、Bax的影响及其与JAK2-STAT3信号通路的关系

目的 研究舒芬太尼后处理对心肌缺血/再灌注损伤(ischemiia/reperfusion injury,I/RI)细胞凋亡的影响以及与信号通路JAK2-STAT3的关系.方法 健康杂种家犬24只,体重10 kg～15 kg,按随机数字表法分为4组(每组6只):假手术组(Sham组,只穿线,不结扎),心肌缺血/再灌注(ischemia/reperfusion,I/R)组,舒芬太尼后处理组(SPO组,于再灌注前5min静脉注射舒芬太尼0.6 μg/kg),舒芬太尼后处理+AG490组(SPO+AG490组,于再灌注前5 min静脉注射l mg/kg AG490,特异性的JAK2抑制剂),除Sham组外,所有犬心脏都经历30 min缺血和120 min再灌注.再灌注120 min时,取各组缺血区心肌组织,采用末端脱氧核苷酸转移酶介导的dUTP原位切口末端标记(terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling,TUNEL)法测定心肌细胞的凋亡情况,免疫组化法测定各组Bcl-2、Bax以及磷酸化STAT3 (p-ATAT3)蛋白的表达,并计算Bcl-2和Bax表达的比值(Bcl-2/Bax).结果 再灌注120 min时,可在I/R组缺血区心肌组织中检测到大量凋亡心肌细胞(63.9±4.0)％,而舒芬太尼后处理显著降低心肌细胞凋亡指数(30.7±1.5)％;与Sham组比较,I/R组、SPO组和SPO+AG490组Bcl-2与Bax表达上调,I/R组Bcl-2/Bax比值降低,SPO组Bcl-2/Bax比值升高;舒芬太尼后处理使p-STAT3表达明显增加,特异性的阻断剂AG490抑制了舒芬太尼后处理对心肌I/RI凋亡的作用,即抑制p-STAT3表达的增加. 结论 舒芬太尼后处理对心肌I/RI细胞凋亡有一定的抑制作用,通过激活JAK2-STAT3信号转导通路上调Bcl-2蛋白和下调Bax蛋白来发挥作用.     

细胞凋亡抑制参与联合应用吗啡和肢体远隔缺血后处理的心肌保护作用

目的 探讨抗细胞凋亡在联合应用吗啡和肢体远隔缺血后处理(remote ischemic postconditioning,RIP)心肌保护中的作用. 方法 采用大鼠在体心肌缺血/再灌注损伤(ischemia/reperfusion injury,I/RI)模型,根据随机数字表法将60只SD大鼠分为4组(每组15只):缺血/再灌注(ischemia/reperfusion,I/R)组(I/R组)、肢体RIP组(RIP组)、吗啡后处理组(M组)以及联合应用吗啡和肢体RIP组(M+RIP组).再灌注末留取缺血中心区、缺血边缘区和非缺血区心肌组织标本,应用Tunel染色法检测心肌细胞凋亡指数(apoptotic index,AI),应用实时定量PCR技术检测心肌细胞凋亡相关基因Bcl-2 mRNA和Bax mRNA表达,光学和电子显微镜观察缺血中心区心肌细胞形态. 结果 I/R组、RIP组、M组和M+RIP组缺血中心区心肌细胞AI分别为(49.1±4.9)％、(34.2±2.9)％、(39.7±3.2)％和(29.0±4.9)％,缺血边缘区心肌细胞AI分别为(12.7±2.2)％、(8.2±1.6)％、(10.4±2.7)％和(5.9±1.4)％.在缺血中心区和缺血边缘区,M+RIP组心肌细胞AI较I/R组和M组明显降低(P＜0.05),M+RIP组的Bcl-2 mRNA表达较I/R组、RIP组和M组明显增强(P＜0.05),而M+RIP组的Bax mRNA表达则较I/R组、RIP组和M组明显降低(P＜0.05),M+RIP组的Bcl-2/Bax较I/R组、RIP组和M组明显升高(P＜0.05).光学和电子显微镜检查显示,M+RIP组的心肌形态和线粒体结构明显改善. 结论 Bcl-2相关信号通路的细胞凋亡抑制是联合应用吗啡和肢体RIP的心肌保护作用机制之一.     

Ischemic QRS prolongation as a predictor of ventricular fibrillation in a canine model

Abstract

Objectives. An acute coronary occlusion and its possible subsequent complications is one of the most common causes of death. One such complication is ventricular fibrillation (VF) due to myocardial ischemia. The severity of ischemia is related to the amount of coronary arterial collateral flow. In dog studies collateral flow has also been shown to be associated with QRS prolongation. The aim of this study was to investigate whether ischemic QRS prolongation (IQP) is associated with impending VF in an experimental acute ischemia dog model. Methods. Degree of IQP and occurrence of VF were measured in dogs (n?=?21) during coronary occlusion for 15?min and also during subsequent reperfusion (experiments conducted in 1984). Results. There was a significant difference in absolute IQP between dogs which developed VF during reperfusion (47?±?29?ms, mean?±?SD) and those which did not (12?±?10?ms; p?=?.001). Conclusions. IQP during acute coronary occlusion is associated with reperfusion VF in an experimental dog model and might therefore be a potential predictor of malignant arrhythmias in patients with acute coronary syndrome.     

肝移植缺血再灌注损伤的比较蛋白质组学研究

目的 研究肝移植手术中供体肝组织缺血一再灌注损伤的蛋白质变化规律.方法 2009年3月,对3例肝移植供肝于3个时间点切取肝组织标本进行对照研究:(1)新鲜的供肝组织;(2)经过缺血降温保存后修整完毕,但未经血管吻合的肝脏组织；(3)复流后的供肝组织.通过2DE-MALDI-TOF和质谱技术,对上述3个时间点的蛋白表达作出比较.结果 本研究共分离出1580个蛋白点,其中与缺血再灌注损伤有关的蛋白19个.结合19个蛋白质的功能,对这些蛋白质的变化特征进一步分析.结论 我们发现了与肝移植手术中供肝缺血性损伤和再灌注损伤相关的蛋白质,并首次揭示了这些蛋白质在不同损伤阶段独立的变化规律.     

肾脏缺血再灌注损伤过程中天然免疫分子高迁移率族蛋白B1释放变化

目的 观察高迁移率族蛋白B1(HMGB1)在小鼠肾脏缺血再灌注损伤(IRI)中的表达变化.方法 建立小鼠IRI模型,再灌注0、3、6 h或24 h后取外周血及左肾,测定血肌酐(Cr)和尿素氮(BUN)水平,免疫组织化学及Western blot检测肾组织全蛋白和胞质蛋白HMGB1的表达,并观察病理学变化(HE)及细胞凋亡.结果与假手术组比较,再灌注0 h时小鼠血清Cr和BUN无明显升高,而再灌注3、6、24 h后呈阶梯性显著性升高.假手术组肾组织HMGB1几乎均表达于细胞核内,而肾脏缺血损伤后HMGB1即开始在(主要是肾小管上皮细胞)胞质或胞外表达,且HMGB1在细胞核外的表达量在再灌注3 h时最强,之后缓慢减弱,而24 h内细胞总蛋白HMGB1表达量未见明显变化.再灌注0、24 h病理损伤渐进性加重,而凋亡细胞显著性增加.结论 HMGB1在肾IRI早期表达总量恒定而表达部位发生改变,且表达部位的改变先于肾功能的变化,HMGB1可能作为重要早期炎症因子在IRI启动中发挥作用.     

UTI和丹参在鼠肝脏缺血再灌注中对肝窦内皮细胞损伤保护效应的实验研究

目的：探讨UTI和丹参在肝脏缺血再灌注中对肝窦内皮细胞损伤的保护作用。方法：将大鼠肝脏缺血再灌注模型30只大鼠分为5组，A组为空白对照组（n=3），B组为缺血再灌注组（n=7），C组为UTI组（n=6），D组为丹参组（n=6），E组为UTI＋丹参组（n=8）。除A组外，在缺血30min再灌注120min后分别取血检测AST、ALT、LDH、HA及ET，并取肝组织行光镜和电镜观察。结果：C组、D组较B组各指标明显下降（P〈0．01），E组各指标较C组或D组均有下降，（P〈0．05）。光镜和电镜观察形态学损伤程度，B组最重，C组、D组次之，E组最轻。结论：UTI、丹参在缺血再灌注中能有效减轻对肝窦内皮细胞的损伤，二药合用有协同作用。     

乌司他丁对失血性休克大鼠肝脏缺血再灌注损伤保护作用的研究

目的：探讨乌司他丁对失血性休克大鼠肝脏缺血再灌注损伤的保护作用及机制。方法：24只雄性Wista大鼠随机分为假手术组、生理盐水治疗组、乌司他丁治疗组,每组8只。建立大鼠失血性休克模型。乌司他丁治疗组,予以乌司他丁25000U·kg-1加入2mL生理盐水静脉推注,并完成液体复苏;生理盐水治疗组予以2mL生理盐水静脉推注,并完成复苏;假手术组,除不放血和输液外,其他处理与模型相同。观察3h后处死大鼠,取血液离心分离血浆检测肝功能指标、血清肿瘤坏死因子（TNF-α）;取肝右叶2块肝组织,1块用于肝组织病理改变和肝细胞凋亡观察;1块用于肝组织匀浆,离心取上清液进行肝组织MDA、SOD、髓过氧化物酶（MPO）检测。结果：失血性休克大鼠肝脏再灌注3h后,生理盐水治疗组肝组织发生了严重缺血再灌注损伤,肝细胞水样变,肝窦淤血变窄,间质大量炎性细胞浸润,而乌司他丁治疗组仅有轻度再灌注损伤。乌司他丁治疗组肝细胞凋亡、肝功能指标ALT、AST、血清TNF-α水平、肝组织MDA含量、MPO活性较生理盐水治疗组均有不同程度的减少（P〈0.05）,SOD活性较生理盐水治疗组升高（P〈0.05）。结论：乌司他丁对大鼠失血性休克再灌注后肝脏损伤具有保护作用,其机制可能与抑制中性粒细胞浸润、抑制氧自由基的形成、抗肝细胞凋亡相关。     

Ischemic preconditioning of small bowel mitigates the late phase of reperfusion injury: heme oxygenase mediates cytoprotection

Background

Ischemia and reperfusion (IR) injury of the intestine is a major cause of morbidity and mortality following small bowel transplantation. The current study evaluates the effect of ischemic preconditioning (IPC) on the intestinal microcirculation in the late phase of IR injury of the intestine.

Methods

Sixty rats were randomly allocated to 5 study groups (n = 12 per group): (1) sham, (2) IR (3) IPC, (4) pyrrolidine dithiocarbamate (PDTC) (HO-1 inducer), and (5) zinc protoporhyrin (ZnPP) (HO-1 inhibitor). Mucosal perfusion and leukocyte-endothelial interactions were measured with the aid of an intravital microscope. At the end of the experiments, blood samples for lactate dehydrogenase (LDH) levels and biopsies of ileum for histologic evaluation were obtained.

Results

IPC significantly improved the mucosal perfusion and decreased the leukocyte-endothelial interactions. Histologic examination showed that ileal mucosa was significantly less injured in the IPC and PDTC groups as compared with the IR group.

Conclusions

IPC protects the intestine from late reperfusion injury. HO-1 is involved in this protection. These findings may be of significant importance in clinical small bowel transplantation.     

Effect of Shenfu injection on nuclear factor-kB during myocardial ischemia/reperfusion injury in rats

Objective: To investigate effects of Shenfu injection on the concentrations of plasma tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), activity of Nuclear Factor kappa B (NF-κB) and heart tissue ultrastructure during myocardial ischemia/reperfusion (I/R) injury in rats and its potential mechanism.Methods: Myocardial ischemia/reperfusion (I/R) was produced by ligation and release of the left anterior descending coronary artery. Ischemia lasted for 30 min and reperfusion for 60 min. Twenty-four healthy male SD rats weighing 230-280 g were randomly divided into three groups (n=8, each): Group I (Sham-operation group); Group II (I/R group); Group III (Shenfu group), in which Shenfu injection (10 ml/kg) was intraperitoneally injected 30 min before ischemia in animals with I/R. The plasma concentrations of IL-6 and TNF-α were measured by ELISA, and the heart was harvested for determination of NF-κB levels by Ecl-western blot analysis. Electron microscopy was used to study its ultrastructure.Results: After reperfusion, NF-κB binding activity in myocardial nuclei and the plasma concentrations of IL-6 and TNF-α were significantly increased in Group II, compared with Group I (P<0.01), and they were markedly reduced in Group III, compared with Group II (P<0.01). In addition, electron microscopic examination showed more serious injury of the myocardium ultrastructure in Group II, while in Group III the myocardial ultrastructure was similar to normal state.Conclusions: Shenfu injection inhibits NF-κB activity in I/R myocardium and leads to down-regulation of proinflammatory cytokine expression, which might be one of the molecular mechanisms of Shenfu injection in cardioprotection.     

Myocardial tissue pCO2 and calcium content during ventricular fibrillation and reperfusion periods

Forty-one patients who underwent cardiac surgery under conditions of systemic hypothermia and intermittent cold crystalloid potassium cardioplegia were studied, in order to elucidate the effects of ventricular fibrillation and reperfusion on the myocardium, by using the intramyocardial pCO₂ and temperature sensor. All patients were assigned to 2 groups, namely; group A (21 cases), in which the time between the aorta declamping and defibrillation was under 10 minutes, and group B (20 cases) in which the time was over 10 minutes. In both groups A and B, myocardial pCO₂ increased at the rate of 3.58±1.70 and 2.16±0.62 mmHg/min (p<0.05) after aorta declamping, respectively and the myocardial pCO₂ decreased at the rate of 5.59±0.60 and 4.18±0.76 mmHg/min (p<0.05) after defibrillation, respectively. In group A, the myocardial calcium content, pre-CPB (cardio pulmonary bypass) was 10.98±1.62 nmol/mg/dry weight and at the time of aorta declamping it was 15.90±1.81 nmol/mg/dry weight (p<0.05). In group B, the myocardial calcium content, pre-CPB, was 14.62±2.15 nmol/mg/dry weight and at the time of aorta declamping it was 18.23±4.36 nmol/mg/dry weight (p<0.05). At both three and dix hours after the operation, the left ventricular work index per minute (LVWI) in group A showed better cardiac pump function than that in group B. We therefore conclude that when reperfusion is encountered, acidosis can be minimized by prompt defibrillation.     

艾司洛尔在体外循环主动脉开放后顽固性室颤中的应用

目的 评价艾司洛尔应用于体外循环主动脉开放后顽固性室颤的临床效果.方法 主动脉开放后出现顽固性室颤的瓣膜置换术患者40例,数字表法随机分为艾司洛尔组和对照组,每组20例.两组患者按照1 mg/kg分别静脉推注艾司洛尔(10 mg/ml)或利多卡因(10 mg/ml),2 min后继续除颤.2次除颤后仍不能复跳者,采取临床其他常月方法处理,直至心脏复跳.记录开放前主动脉阻断时间、肛温、平均动脉压、血乳酸值、血钾值、pH值;给予艾司洛尔或等浓度利多卡因后记录干预后除颤次数、复跳5 min后心律、心率,停机后记录体外循环时间及正性肌力药物用量.结果 两组相比较,艾司洛尔组除颤成功率高,复跳5 min后心率低,体外循环时间短,正性肌力药物用量少,差异均有统计学意义(P＜0.05).结论体外循环升主动脉开放后复跳困难的患者,给予艾司洛尔可明显减少除颤次数,提高除颤成功率.同时还可以改善复跳后心脏功能,减少正性肌力药物依赖,缩短体外循环时间.