Effect of thyroid hormone on myocardial and cerebral ischemia reperfusion injury in valve replacement under cardiopulmonary bypass

Objective:To study the effect of thyroid hormone (euthyrox) on myocardial and cerebral ischemia reperfusion injury in valve replacement under cardiopulmonary bypass.Methods:A total of 76 patients who received valve replacement under cardiopulmonary bypass in our hospital between January 2013 and December 2016 were collected and divided into control group (n=38) and observation group (n=38) according to random number table. Observation group took euthyrox orally 1 week before surgery, control group took vitamin C tablets orally at the same point in time, and both therapies lasted for 1 week. Before taking medicine and after cardiopulmonary bypass (before end of surgery), serum levels of myocardial enzyme spectrum indexes and nerve injury indexes were compared between the two groups of patients. Results: Before taking medicine, differences in the serum levels of myocardial enzyme spectrum indexes and nerve injury indexes were not statistically significant between the two groups of patients. After cardiopulmonary bypass, serum myocardial enzyme spectrum indexes cTnT, CK-MB,α-HBD and LDH levels in observation group were lower than those in control group;serum nerve injury indexes NSE, S100B and GFAP levels were lower than those in control group while bFGF level was higher than that in control group.Conclusion: Euthyrox intervention in valve replacement under cardiopulmonary bypass can effectively reduce the myocardial and cerebral ischemia reperfusion injury.

A novel, recovery, and reproducible minimally invasive cardiopulmonary bypass model with lung injury in rats

Background Cardiopulmonary bypass （CPB） has been shown to be associated with a systemic inflammatory response leading to postoperative organ dysfunction. Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of CPB have been hampered due to the absence of a satisfactory recovery animal model. The purpose of this study was to establish a good rat model of CPB to study the pathophysiology of potential complications. Methods Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into a CPB group （n=10） and a control group （n=10）. All rats were anaesthetized and mechanically ventilated. The carotid artery and jugular vein were cannulated. The blood was drained from the right atrium via the right jugular and transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. Priming consisted of 8 ml of homologous blood and 8 ml of colloid. The surface of the hollow fiber oxygenator was 0.075 m~. CPB was conducted for 60 minutes at a flow rate of 100-120 ml. kg-1. min-1 in the CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg. Blood gas analysis, hemodynamic investigations, and lung histology were subsequently examined. Results All CPB rats recovered from the operative process without incident. Normal cardiac function after successful weaning was confirmed by electrocardiography and blood pressure measurements. Mean arterial pressure remained stable. The results of blood gas analysis at different times were within the normal range. Levels of IL-113 and TNF-a were higher in the lung tissue in the CPB group （P 〈0.005）. Histological examination revealed marked increases in interstitialcongestion, edema, and inflammation in the CPB group. Conclusion This novel, recovery, and reproducible minimally invasive CPB model may open the field for various studies on the pathophysiological process of CPB and systemic ischemia-reperfusion injury in vivo.

Ischemic postconditioning alleviates lung injury and maintains a better expression of aquaporin-1 during cardiopulmonary bypass

Background It has found that ischemic postconditioning （IPO） might decrease pulmonary ischemia/reperfusion （I/ R） injury,which is one of the main reasons of lung injury caused by cardiopulmonary bypass （CPB）.It was found that aquaporins （AQPs） play a role in the maintenance of fluid homeostasis.But it is still unclear whether IPO influences the expression of aquaporin-1 （AQP1）.This study was designed to investigate whether IPO can reduce CPB-related lung injury and affect the expression of AQP1 of lungs.Methods Twelve healthy dogs were divided into control group （C group） and ischemia postconditioning group （IPO group）.CPB procedures were implemented.Ten minutes later,the left pulmonary artery was separated and blocked.Postconditioning consisted of two cycles of 5-minute pulmonary artery reperfusion/5-minute reocclusion starting at the beginning of reperfusion.The 2×4 cm tissues of both sides of pulmonary apex,superior,middle and inferior lobe were taken before CPB （T1）,before occlusion and reopening of left pulmonary artery （T2,T3）,and 2 hours after CPB （T4）.Samples were used to evaluate lung injury degrees and to detect the expression of AQP1.At T1 and T4,blood was collected from femoral artery to calculate pulmonary function.Results At T4,each pulmonary function showed significant deterioration compared with T1.Lung injury could be found at the onset of CPB.However,the expression of AQP1 decreased and wet to dry weight ratio （W/D） increased after T2.In the left lung of C group,the worst pulmonary function and structures were detected.The slightest changes were discovered in the right lung of C group.A close relationship between W/D and lung injury score was found.The lung injury score was negatively related with the expression of AQP1.It was found that the expression of AQP1 was negatively connected with W/D.Conclusions In dog CPB models,lung injury induced by CPB was related with down regulated expression of AQP1.AQP1 is believed to be involved in the mechanisms of lung ischemia/reperfusion （I/R） injury caused by CPB.IPO increases the expression of AQP1,provides a protective effect on lung suffering from CPB,and alleviates CPB-related lung injury.

A novel, minimally invasive rat model of normothermic cardiopulmonary bypass model without blood priming

Background Cardiopulmonary bypass （CPB） has been shown to be associated with systemic inflammatory response leading to postoperative organ dysfunction. Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of CPB have been hampered due to the absence of a satisfactory recovery animal model. The purpose of this study was to establish a novel, minimally invasive rat model of normothermic CPB model without blood priming. Methods Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into CPB group （n=10） and control group （n=10）. All rats were anaesthetized and mechanically ventilated. The carotid artery and jugular vein were cannulated. The blood was drained from the right atrium via the right jugular and further transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. The volume of the priming solution, composed of 6% HES130/0.4 and 125 IU heparin, was less than 12 ml. The surface of the hollow fiber oxygenator was 0.075 m2. CPB was conducted for 60 minutes at a flow rat of 100-120 ml. kg -1. min-1 in CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg. Results All CPB processes were successfully achieved. Blood gas analysis and hemodynamic parameters of each time point were in accordance with normal ranges. The vital signs of all rats were stable. Conclusions The establishment of CPB without blood priming in rats can be achieved successfully. The nontransthoracic model should facilitate the investigation of pathophysiological processes concerning CPB-related multiple organ dysfunction and possible protective interventions. This novel, recovery, and reproducible minimally invasive CPB model may open the tield tor various studies on the pathophysiological process of CPB and systemic ischemia-reperfusion injury in vivo.

CARDIOPULMONARY BYPASS WITH AUTOLOGOUS LUNG AS SUBSTITUTE FOR ARTIFICIAL OXYGENATOR ATTENUATES INFLAMMATORY RESPONSIVE INSPIRATORY DYSFUNCTION

Objective To study if using autologous lung as a substitute of oxygenator in cardiopulmonary bypass is better than the conventional cardiopulmonary bypass with artificial oxygenator in pulmonary preservation. Methods Twelve piglets were randomly divided into two groups (n=6). The isolated lung perfusion model was established. The experimental animals underwent continuous lung perfusion for about 120 min. While the control animals underwent 90 min lung ischemia followed by 30 min reperfusion. Another 12 piglets were randomly divided into two groups (n=6). The experimental animals underwent bi-ventricular bypass with autologous lung perfusion. While control animals underwent conventional cardiopulmonary bypass with artificial oxygenator. The bypass time and aortic cross clamping time were 135 min and 60 min respectively for each animal. The lung static compliance (Cstat), alveolus-artery oxygen difference (PA-aO_ 2 ), TNF-α, IL-6 and wet to dry lung weight ratio (W/D) were measured. Histological and ultra-structural changes of the lung were also observed after bypass. Results After either isolated lung perfusion or cardiopulmonary bypass, the Cstat decreased, the PA-aO_ 2 increased and the content of TNF-α increased for both groups, but the changes of experimental group were much less than those of control group. The lower W/D ratio and mild pathological changes in experimental group than those in control group were also demonstrated. Conclusion Autologous lung is able to tolerate the nonpulsatile perfusion. It can be used as a substitute to artificial ogygenator in cardiopulmonary bypass to minimize the inflammatory pulmonary injury caused mainly by ischemic reperfusion and interaction of the blood to the non-physiological surface of artificial oxygenator.

乌司他丁在体外循环手术围手术期的保护作用研究进展

体外循环是进行心血管外科手术中的重要辅助手段,由此会导致机体各器官缺血再灌注损伤及炎症反应,增加术后并发症的发生率。乌司他丁作为一种广谱的胰蛋白酶抑制剂,其能抑制炎症介质释放,上调抗炎因子释放;抑制氧自由基生成与脂质过氧化反应,稳定溶酶体膜,减轻细胞与组织损伤,对于辅助治疗由体外循环手术引起的缺血再灌注损伤及全身炎症反应均有良好的治疗作用,并在围手术期对包括心脏、肝脏、肺脏、肾脏以及凝血、免疫等在内的多脏器多系统起保护作用。

不同剂量右美托咪定对成人体外循环心脏手术后血流动力学的影响研究

目的:探讨不同剂量右美托咪定对成人体外循环心脏手术后血流动力学的影响。方法:将2019年1月至2021年9月绵阳市中心医院收治的体外循环心脏手术后的成年患者共180例采用随机数字表法分为对照组、低剂量组和高剂量组(每组60例)。低剂量组患者给予右美托咪定0.4μg/(kg·h)泵入,高剂量组患者给予右美托咪定0.8μg/(kg·h)泵入,对照组患者给予等量0.9%氯化钠注射液泵入,其余处理方案三组一致。测量进入重症监护室(ICU)时(T_(0)),进入ICU后6 h(T_(1))、12 h(T_(2))和24 h(T_(3))的血流动力学指标和心肌酶学指标水平,记录心律失常发生率及最终点ICU停留时间。结果:低剂量组和高剂量组患者在T_(1)、T_(2)、T_(3)时的心输出量大于对照组,静脉血肌钙蛋白I、肌酸激酶同工酶及乳酸水平低于对照组,但未表现出明显剂量-效应关系。高剂量组患者较低剂量组和对照组更易出现缓慢型心律失常,但使用右美托咪定能缩短ICU停留时间。结论:使用右美托咪定可以稳定体外循环心脏手术后血流动力学,并对心肌缺血再灌注损伤起到一定的保护作用,缩短ICU停留时间,但无明显剂量-效应关系。使用高剂量的右美托咪定更易出现低血压及缓慢型心律失常。

心脏停搏液的临床应用进展

良好的心肌保护是影响心脏手术成功的关键因素之一,而心脏停搏液是心肌保护的基石,在心肌保护中扮演着重要的角色。本文将对心脏停搏液的各要素比如停搏液设计、停搏液类型、灌注方式、停搏液温度等进行综述。

Cardioprotection of Shenfu Injection(参附注射液) against Myocardial Ischemia/Reperfusion Injury in Open Heart Surgery

Objective： To investigate the protective effect of Shenfu Injection （参附注射液, SFI） against myocardium ischemia/reperfusion injury （IRI） in mitral valve replacement （MVR） with cardiopulmonary bypass （CPB）. Metheds： Forty patients undergoing selective MVR were randomly assigned to the control group and trial Groups Ⅰ, Ⅱ,Ⅲ, and Ⅳ according to the different administrations of SFI, 8 patients in each group. The changes of systolic blood pressure （SBP）, mean blood pressure （MBP）, diastolic blood pressure （DBP） in each group were monitored, respectively. The recovering percentage of spontaneous heart beat, the heart rate （HR） and cardiac rhythm as well as the abnormal duration of ECG-ST segment were recorded after the restoration of heart beat. The serum concentration of cardiac troponin Ⅰ （cTnl）, malondialdehyde （MDA） and the activity of superoxide dismutase （SOD） were determined as well. Results： （1） The SBP, MBP and DBP values, the recovering rate of spontaneous heart beat, HR, ECG-ST, atrioventricular block and ventricular arrhythmia were significantly improved in group Ⅳ compared with any other groups. （2） Compared with the control group, the postoperative serum contents of cTnl and MDA were significantly decreased, but the activity of SOD was significantly increased in group Ⅳ. Cenclusiens： SFI had a certain protective effect against myocardium IRI. Moreover, better efficacy was seen with the administration of 1.5 mL/kg SFI into CPB priming fluid and pumping 1.5 mL/kg SFI via CPB as soon as the clamped aorta was unclamped.

TBC1结构域家族成员4与心肌胰岛素抵抗的研究进展

体外循环是心血管外科开胸心内直视手术必需的重要辅助手段,而体外循环术后常见的严重并发症是心肌缺血再灌注损伤(MIRI)。MIRI的发生机制复杂,心肌胰岛素抵抗(IR)是其重要发病机制之一,其中心肌细胞葡萄糖转运蛋白4(GLUT4)的表达和转位异常是心肌IR发生的主要原因。TBC1结构域家族成员4是TBC家族蛋白的重要成员,可通过Rab蛋白调控GLUT4的囊泡转运,是磷脂酰肌醇-3-激酶/蛋白激酶B信号通路和AMP活化的蛋白激酶信号通路重要的下游靶点,与IR的发生密切相关。

右美托咪定对体外循环下心肌缺血再灌注损伤的保护效应

目的 观察右美托咪定（DEX）对体外循环下心肌缺血再灌注损伤的影响.方法 择期体外循环下行心脏二尖瓣置换术的患者60例,随机分为DEX组和对照组,各30例;DEX组恒速输注DEX 0.5 μg/（kg·h）,对照组恒速输注等量0.9%氯化钠.其余麻醉用药两组相同.两组患者分别于麻醉诱导前（T0）、主动脉开放后10 min（T1）、停机即刻（T2）、停机后4 h（T3）和术后24 h（T4）5个时点采集颈内静脉血各4 mL,测定血清一氧化氮（NO）、丙二醛（MDA）、超氧化物歧化酶（SOD） 以及心肌肌钙蛋白T（cTn-T）,肌酸激酶同工酶（CK-MB）的变化.结果 与T0时比较,两组T1～T4时血清NO及SOD活性均下降,血清MDA、cTn-T及CK-MB升高（P〈0.05）;两组之间比较,T2～T4时DEX组患者血清MDA、cTn-T和CK-MB低于对照组,SOD及NO高于对照组（P〈0.05）.结论 右美托咪定能在一定程度上减轻体外循环下的心肌缺血再灌注损伤,其机制可能与其抗氧化应激作用有关.

黄芪注射液配伍川芎嗪抗心肌缺血再灌注损伤的临床研究

目的：探讨黄芪注射液配伍川芎嗪防治体外循环心内直视手术中心肌缺血再灌注损伤（ＭＩＲＩ）的作用机理，并探讨ＭＩＲＩ的中医病机、治则。方法：风湿性心脏病瓣膜置换术和先天性心脏病室间隔修补术患者２４例，随机分为对照组、黄芪注射液组（益气组）川芎嗪组（活血组）、黄芪注射液配伍川芎嗪组（益气活血组）各６例。术中动态监测心电；分别在麻醉前（Ｔ１）、主动脉阻断１０ｍｉｎ（Ｔ２）、主动脉开放１０ｍｉｎ（Ｔ３）、３０ｍｉｎ（Ｔ４）、手术结束（约主动脉开放１８０ｍｉｎ，Ｔ５）经锁骨下中心静脉取血。测定血清谷草转氨酶（ＡＳＴ）、肌酸磷酸激酶（ＣＫ）、肌酸磷酸激酶同工酶（ＣＫ－ＭＢ）、乳酸脱氢酶（ＬＤＨ）、丙二醛（ＭＤＡ）含量、超氧化物歧化酶（ＳＯＤ）活力、一氧化氮（ＮＯ）和一氧化氮合成酶（ＮＯＳ）活性。结果：治疗各组与对照组比较，可减轻心肌酶、ＭＤＡ和ＳＯＤ变化，益气活血组最明显，与对照组比较多数有显著性差异（Ｐ＜０．０５，Ｐ＜０．０１）。益气组（Ｔ５）和益气活血组（Ｔ４、Ｔ５）ＮＯ活力高于对照组（Ｐ＜０．０５）。结论：ＭＩＲＩ中医辨证，病位在心，证属气虚血瘀，其治则是益气活血。黄芪注射液配伍川芎嗪注射液对其有良好的保护作用，优?

七氟醚后处理下调RAGE抑制犬体外循环肺缺血/再灌注损伤

目的探讨七氟醚后处理对犬体外循环肺缺血/再灌注损伤的效果及晚期糖基化终末产物受体(receptor for ad-vanced glycosylation end products,RAGE)在此过程中的作用。方法 12只健康犬依据主动脉开放后是否吸入七氟醚随机分为两组:对照组(control,n=6)在主动脉开放后常规机械通气和实验组(test,n=6)在主动脉开放后吸入1MAC七氟醚,持续10min。在开胸后即刻(T1)、主动脉开放90min实验结束前(T2)留取肺组织标本和肺静脉血标本。标检测肺组织湿干重比(wet/dry weight,W/D);比色法检测肺组织髓过氧化物酶活性(myeloperoxidase activity,MPO);光镜观察并盲法评分比较肺组织病理学变化;分别采取RT-PCR方法、Western blot检测肺组织RAGE的表达;酶联免疫吸附法检测血清白介素6(IL-6)和肿瘤坏死因子α(TNF-α)含量。结果两组相比,实验组肺组织W/D、MPO、肺损伤评分、RAGE基因表达和蛋白表达、IL-6和TNF-α含量在T2时较对照组降低(P<0.05);组内比较,所有指标实验结束时均较基础值明显升高(P<0.05)。结论七氟醚后处理对体外循环缺血/再灌注导致的肺损伤具有一定的保护作用,可能与其抑制RAGE合成与激活有关。

乌司他丁对体外循环心脏手术后心肌损伤及缺血再灌注相关病理环节的影响

目的:研究乌司他丁对体外循环心脏手术后心肌损伤及缺血再灌注相关病理环节的影响。方法:选择在四川省绵阳市中心医院进行体外循环下瓣膜置换术的患者作为研究对象,随机分为接受乌司他丁+磷酸肌酸钠干预的实验组、接受磷酸肌酸钠干预的对照组。手术前及手术后24小时,测定血清中心肌损伤标志物、凋亡分子、炎症分子、氧化应激分子的含量及外周血中炎症分子、氧化应激分子的表达强度。结果:两组手术后血清中cTnI、CK-MB、H-FABP、sFasL、sTWEAK、Caspase-3、Caspase-8、IL-1β、TNF-α、ICAM1、MDA、NO的含量及外周血中TLR4、NLRP3、NOX2、iNOS的表达强度均较手术前显著升高且实验组患者手术后血清中cTnI、CK-MB、H-FABP、sFasL、sTWEAK、Caspase-3、Caspase-8、IL-1β、TNF-α、ICAM1、MDA、NO的含量及外周血中TLR4、NLRP3、NOX2、iNOS的表达强度均显著低于对照组。结论:乌司他丁对体外循环心脏手术后心肌损伤及缺血再灌注相关的细胞凋亡、炎症反应、氧化应激反应均具有改善作用。

乌司他丁对心脏直视术中缺血-再灌注损伤的保护作用

目的 研究乌司他丁对心肺转流 (CPB)心脏直视手术中缺血 再灌注损伤的保护作用。方法 2 0例择期CPB心脏瓣膜手术患者随机均分为对照组 (C组 )和乌司他丁组 (U组 )。C组不给药 ,U组给予乌司他丁 10 0万U(其中 30万U为麻醉诱导前给予 ,40万U预充体外循环机内 ,30万U为开放升主动脉后给予 )。分别于麻醉诱导后 (T1)、阻断升主动脉 30分钟 (T2 )、再灌注 1小时(T3 )、再灌注 2小时 (T4 )及再灌注 3小时 (T5)各时间点取静脉血用ELISA法测定样本中下列各指标的水平 :肿瘤坏死因子 α(TNF α)、白细胞介素 6 (IL 6 )、白细胞介素 8(IL 8)。结果 两组血清中TNF α、IL 6、IL 8的浓度 ,都是在再灌注后与手术前值及阻断主动脉 30分钟的值相比有明显的增加(P <0 0 5 ) ;在T3 、T4 、T5三个时点U组的TNF α、IL 6、IL 8的释放明显低于对照组 (P <0 0 5 )。结论 在CPB过程中乌司他丁可以通过抑制炎性介质TNF α、IL 6和IL 8的释放而减轻缺血

小鼠肺缺血再灌注损伤模型的建立与评估

目的探索一种用显微外科技术制备小鼠肺缺血再灌注损伤模型的方法,并对其效果进行评估。方法将30只C57BL/6J小鼠随机分成2组(缺血再灌注组和假手术组),每组15只。缺血再灌注组采用无创血管夹夹闭左肺门60min,再灌注120min,建立肺缺血再灌注模型。获取标本,检测肺湿干重比值,用光镜和电镜观察肺组织结构变化。结果肺缺血再灌注组湿干重比值明显高于假手术组(P<0.01),光镜、电镜下均可观察到严重的肺损伤改变。结论成功建立了小鼠肺缺血再灌注损伤模型,且方法简单,易于操作,成功率高,为肺缺血再灌注损伤机制研究提供了一种可行的模型。

沐舒坦对瓣膜置换患者血浆细胞因子和丙二醛、超氧化物歧化酶的影响

目的 探讨不同剂量沐舒坦对瓣膜置换患者血浆细胞因子和自由基水平的影响。方法 将 30例瓣膜置换术患者随机分为三组 :对照组 (C组 )、沐舒坦 1组 (M1组 ,6 0mg)和沐舒坦 2组(M 2组 ,12 0mg) ,每组各 10例。沐舒坦组分别于麻醉后切皮前加入半量沐舒坦 ,另半量则加入预充液中。分别于麻醉后切皮前 (T1)、心肺转流 (CPB) 30min(T2 )、开主动脉 30min(T3 )、停CPB 1h(T4)、术后 4h(T5)、2 4h(T6)测定血浆TNF α、IL 1β、IL 10和丙二醛 (MDA)浓度及超氧化物歧化酶(SOD)活性。结果 三组TNF α、IL 1β、IL 10、MDA和SOD在CPB后均升高 (P <0 0 5～ 0 0 1) ;M1组和M 2组TNF α于T2 ～T6时较C组低 (P <0 0 5～ 0 0 1) ;M1组IL 1β于T5时较C组低 ,M 2组则于T2 ～T5低于C组 ,于T3 ～T4低于M 1组 (P <0 0 5～ 0 0 1) ;M 1组IL 10仅于T2 时较C组升高 ,M2组则于T2 ～T5时较C组升高 (P <0 0 5 ) ;M2组MDA于T2 、T3 、T5时较C组和M 1组低 (P<0 0 5 ) ;C组SOD活性于T2 ～T5下降 ,M1组和M2组则无明显变化 ,M 2组于T2 ～T5时较C组高(P <0 0 5 )。结论 CPB心脏手术可促发炎性和抗炎细胞因子及自由基的释放 ;沐舒坦可抑制CPB心脏手术所致的全身性炎性反应 ,减少自由基的产生 ,从而减轻缺血 再灌注损伤 ,且有?

不同途径注入乌司他丁对心内直视术心肌保护的比较

目的观察乌司他丁经不同途径注入对心内直视手术围心肺转流（CPB）期心肌缺血-再灌注损伤的影响。方法选择45例心功能Ⅱ或Ⅲ级需在CPB下行单纯人工二尖瓣置换术的风湿性瓣膜病患者，随机分为三组，每组15例，A组：乌司他丁以12000U／kg半量加在停跳液500m1中，另半量加入预充液中；B组：麻醉诱导后锯胸骨前经颈内静脉缓慢推注乌司他丁12000U／kg的半量，另半量加入预充液中；C组：用等量的生理盐水。于切皮前（]r0）、CPB30min（T1）、主动脉开放后1h（T2）、6h（T3）、24h（T4）抽取静脉血测定血浆中肌酸磷酸激酶同工酶（CK—MB）、中性粒细胞弹性蛋白酶（NE）、血浆白细胞介素6（IL-6）、白细胞介素10（IL-10）、血浆肿瘤坏死因子α（TNF-α）。结果与T0时比较，T1～T1时三组cK—MB、NE、IL-6、IL-10及TNF-α均明显升高（P〈0．05）；与C组比较，T2～T4时A、B组CK—MB、NE、IL-6、TNF-α均明显降低及IL-10明显升高（P〈0．05）；与B组比较，T3、T4时A组CK—MB、NE、IL6、TNF-α均明显降低及IL-10明显升高（P〈0．05）。结论乌司他丁对CPB下行心内直视手术对心肌缺血一再灌注损伤具有保护作用，抑制炎症因子的释放，乌司他丁加入停跳液的保护作用优于传统的静脉给药效果。

阿卡地新对体外循环心肌缺血再灌注损伤模型犬心肌能量代谢的影响

目的:探讨阿卡地新对体外循环(CPB)心肌缺血再灌注损伤(MIRI)模型犬心肌能量代谢的影响。方法:将犬随机分为对照组、模型组和阿卡地新低、高剂量组(0.8、3.2 mg/kg),每组6只。所有犬行CPB术,除对照组外,其余各组犬建立MIRI模型,并于主动脉阻断60 min后灌注含相应药物的St.Thomas心脏停搏液。分别于转流前和再灌注15、60、90 min时检测并计算心肌葡萄糖和游离脂肪酸(FFA)摄取率、静脉窦血浆中肌酸激酶同工酶(CK-MB)含量、线粒体中三磷酸腺苷(ATP)含量;分析左心室收缩压(LVSP)和左心室舒张末期压(LVEDP);检测心肌组织中腺苷酸活化蛋白激酶(AMPK)mRNA表达和磷酸化AMPK(p-AMPK)蛋白表达。结果:各组犬转流前的所有指标差异均无统计学意义(P>0.05);转流后,与对照组比较,模型组和各给药组犬3个时间点的心肌葡萄糖摄取率、FAA摄取率、ATP含量、AMPK mRNA表达、p-AMPK蛋白表达和LVSP均明显降低(P<0.05),LVEDP和血浆中CK-MB含量均明显升高(P<0.05)。与模型组比较,各给药组犬3个时间点的心肌葡萄糖摄取率、FAA摄取率、ATP含量、AMPK mRNA表达、p-AMPK蛋白表达和LVSP均明显升高(P<0.05),LVEDP和血浆中CK-MB含量均明显降低(P<0.05),其中高剂量组较低剂量组变化更明显(P<0.05)。结论:阿卡地新可促进AMPK磷酸化,有助于心肌葡萄糖和FFA的摄取,促使心肌线粒体中ATP增加,有助于减轻CPB术后MIRI。

大鼠心肺复苏后肺组织的损伤及其影响因素

目的 :研究心肺复苏后大鼠肺组织细胞的损伤及其可能的影响因素。 方法 :选择健康 SD雄性大鼠 16只 ,随机均分为对照组和复苏组 ,采用琥珀酰胆碱 (0 .15 mg/ 10 0 g)窒息合并冰氯化钾 (0 .5 mol/ L,0 .12 ml/ 10 0 g,4℃ )致大鼠心跳骤停 ,停跳 5 min后开始心肺复苏 ,制备大鼠呼吸心跳骤停 -心肺复苏模型。复苏后 3h取动脉血行血气分析 ,取静脉血离心采用放射免疫法测定血清中 TNF- α含量 ,取肺组织测定湿干质量比值 (W/ D)、髓过氧化酶 (MPO)活性和丙二醛 (MDA)含量 ,通过光镜和电镜观察肺组织细胞结构的变化。 结果 :心肺复苏后 3h较对照组大鼠肺 W/ D值明显升高 (P<0 .0 5 ) ,Pa O2 降低 ,血清中 TNF- α含量、肺组织 MDA含量和 MPO活性明显升高 (P<0 .0 5 ) ,光镜、电镜观察结果显示肺组织细胞结构均有较明显受损的征象。结论 :心肺复苏后早期大鼠存在肺组织细胞损伤 ,肺功能受损 ,血清 TNF-α升高 ,氧自由基生成增多 ,中性粒细胞(PMN)在肺组织聚集可能参与了复苏后肺组织细胞损伤的过程。