心脏直视手术再灌注时血浆和心肌组织氧自由基及超微结构改变的观察

为进一步探讨心脏直视手术患者血浆、心肌组织氧自由基变化及临床意义，对１５例心脏直视手术患者血浆、心肌组织丙二醛（ＭＤＡ）含量及超氧化物歧化酶（ＳＯＤ）活性进行测定，并对心肌组织进行超微结构观察。结果表明，血浆ＭＤＡ含量在体外循环过程中逐渐升高，心脏复跳后较缺血期更明显，而血液ＳＯＤ活性呈下降趋势；心肌组织缺血再灌注后ＭＤＡ含量较心脏停跳前、停跳后明显增加，而ＳＯＤ活性降低。心脏复跳后，心肌组织超微结构损害较停跳后更明显．这一结果提示，心肌组织氧自由基的产生主要是在再灌注期，是心肌缺血再灌注损伤的重要原因。     

应用搏动性体外循环患者血浆丙二醛和超氧化物歧化酶的动态变化

对２０例心脏直视手术病人分别应用搏动性与非搏动性体外循环，动态观察体内丙二醛（ＭＤＡ）和超氧化物歧化酶（ＳＯＤ）变化。结果显示搏动组患者体外循环期间主动脉阻断及开放后血中ＳＯＤ升高，而ＭＤＡ无明显变化。提示搏动性灌注可能通过提高机体的抗氧自由基能力而改善组织的氧代谢。     

实验性缺血再灌注心肌顿抑与一氧化氮的关系及东莨菪碱对其影响

目的探讨体外循环缺血再灌注心肌顿抑与心肌一氧化氮（ＮＯ）产生之间的关系及东莨菪碱对其影响。方法１２只绵羊，随机均分为：对照组和实验组：即东莨菪碱治疗组。常规建立体外循环，对照组主动脉阻断同时灌注冷停搏液（本院配方）；实验组，停搏液中加入东莨菪碱１７．５μｇ／ｋｇ。于主动脉阻断前、再灌注５分钟、再灌注３０分钟取冠状窦血检测ＮＯ、肌酸激酶（ＣＫ）、环磷酸鸟苷（ｃＧＭＰ）浓度，取心肌测定丙二醛（ＭＤＡ）含量，相应时点监测心功能。结果再灌注５分钟和３０分钟时，对照组心肌血的ＮＯ、ＣＫ、ｃＧＭＰ、ＭＤＡ均明显升高，与主动脉阻断前相比差异有显著性（Ｐ＜０．０５或＜０．００１），和实验组相同时间点相比差异有显著性（Ｐ＜０．０５或＜０．０１）。两组再灌注５分钟和３０分钟时心肌功能均降低，对照组较实验组更为显著。再灌注后ＮＯ的变化与心肌ＭＤＡ和ＣＫ之间呈正相关（Ｐ＜０．０５和０．０１）。结论缺血再灌注心肌顿抑与ＮＯ产生增加有关，大量释放的ＮＯ提高心肌组织ｃＧＭＰ，参与心肌细胞脂质过氧化损害心肌功能。东莨菪碱减少ＮＯ产生、保护顿抑心肌的作用可能与其抗脂质过氧化有关。     

川芎嗪对老龄鼠再灌注肾损伤中一氧化氮的作用研究

目的 观察川芎嗪对老龄鼠肾缺血再主中一氧化氮合酶（ＮＯＳ）和一氧化氮（ＮＯ）的影响及对肾脏的保护作用。方法 制做老龄鼠肾缺血再灌注模型,分为用川芎嗪组和未用川芎嗪组,检测缺血６０ｍｉｎ,再灌注１５ｍｉｎ和２４ｈ的肾组织ＮＯＳ、ＮＯ及丙二醛（ＭＤＡ）浓度。结果 缺血再灌注后肾组织中ＮＯＳ明显升高（Ｐ〈０．０１）,ＮＯ明显升高（Ｐ〈０．０１）,ＭＤＡ明显升高（Ｐ〈０．０１）,与此结果相比,用川芎嗪组Ｎ     

丹参注射液及血栓通注射液对缺血再灌注大鼠肾脏的影响

本文研究了丹参注射腋（ＳＭ）及以三七皂甙为主要成分的血栓通注射液（ＡＲ）对缺血再灌注大鼠肾脏的影响。将Ｗｉｓｔａｒ大鼠肾蒂夹闭造成缺血１ｈ再灌注前１０ｍｉｎ分别给大鼠尾静脉注射ＳＭ及ＡＲ，于再灌注１５ｍｉｎ测定肾皮质ＳＯＤ，ＧＳＨｐｘ活力及ＧＳＨ，ＧＳＳＧ含量。于再灌注２４ｈ后检查大鼠血肌酐含量，并进行病理学检查。结果发现，ＳＭ和ＡＲ起到了相当于活性氧清除剂的作用，显著地改善了大鼠肾脏的再灌注性损伤，无论是肾脏的功能或形态均较未用药组有显著的改善；肾皮质ＳＯＤ及ＧＳＨｐｘ的活力亦受到有效的保护；肾皮质ＧＳＨ含量显著低于未用药组。     

家兔心肌缺血再灌注时中性粒细胞胞浆游离钙、MDA、SOD变化规律比较

目的通过对比观察青、老年家兔心肌缺血再灌注时外周血中性粒细胞（ＰＭＮｓ）胞浆游离钙（［Ｃａ~（２＋）］ｉ）、丙二醛（ＭＤＡ）及超氧化物歧化酶（ＳＯＤ）的变化规律，探索上述变化对老年兔心肌缺血再灌注损伤的影响特征，并寻找一种可替代心肌组织标本作为判断再灌注损伤的检测指标。方法５年龄及６月龄家兔实验性心肌缺血３０分钟、再灌注３０、９０、３６０分钟，分别取外周血ＰＭＮｓ及心肌组织测定ＭＤＡ、ＳＯＤ、ＰＭＮ［Ｃａ~（２＋）］ｉ和心肌组织钙。结果青、老年组ＰＭＮ［Ｃａ~（２＋）］ｉ、ＭＤＡ于缺血期均明显升高，至再灌注时更显著，而ＳＯＤ活性则明显降低（Ｐ值均＜０．０１）；上述改变在老年组更明显（Ｐ值＜０．０５及０．０１）。ＰＭＮ［Ｃａ~（２＋）］ｉ、ＭＤＡ、ＳＯＤ的变化分别与心肌钙、ＭＤＡ、ＳＯＤ的变化呈正相关（ｒ值分别为０．９２９２、０．９４３６和０．９８６７）。结论钙超载、氧自由基不但共同参与心肌缺血再灌注损伤，且老年期对致损因子更敏感。ＰＭＮｓ指标测定可作为判断心肌缺血再灌注损伤程度的可靠方法。     

风湿性心脏病二尖瓣球囊扩张术前后氧自由基变化的观察

心脏缺血和再灌注过程中，氧自由基的生成、代谢和消除是影响心肌损伤严重程度的重要因素。本文对２０例风心病二尖瓣窄狭患者经皮穿刺球囊成形术后较术前的氧自由基的代谢产物丙二醛（ＭＤＡ）明显增高（Ｐ＜０．０５）以及内源性氧自由基清除剂超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶（ＧＳＨ─Ｐｘ）下降，但无显著差异（Ｐ＞０．０５），仍基本符合缺血／再灌注损伤规律。     

川芎嗪对肝缺血再灌注损伤防护作用的实验研究

采用大鼠肝缺血再灌注损伤模型，观察了川芎嗪对肝缺血再灌注损伤的防护作用。结果提示：川芎嗪可显著减少血清转氨酶、ＬＤＨ的溢出；减轻肝缺血再灌注后肝细胞病理性损伤；明显降低肝组织ＬＰＯ、ＴＸＢ２的升高；维持缺血及再灌注期ＳＯＤ活性。川芎嗪通过抑制肝缺血再灌注时氧自由基产生，提高组织抗氧化能力，维持Ｗ／Ｋ平衡，对肝缺血再灌注损伤起到保护作用     

氧自由基在肝硬化大鼠休克再灌注肝损伤中的作用

采用电子自旋共振（ＥＳＲ）直接测定肝硬化大鼠在休克再灌注时肝组织中氧自由基（ｏｘｙｇｅｎ ｆｒｅｅ ｒａｄｉｃａｌｓ，ＯＦＲ）的变化，同时检测丙二醛（ＭＤＡ），超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅ ｄｉｓｍｕｔａｓｅ，ＳＯＤ），并进行肝组织病理检查。结果显示，休克后３０分钟ＯＦＲ即有明显增高，再灌注后１５分钟进一步增高，肝硬化大鼠增高更为明显。ＭＤＡ再灌注后显著增高，ＳＯＤ肝硬化大鼠再灌注后才有显     

川芎嗪对肝缺血再灌注损伤保护作用的实验研究

采用大鼠肝缺血再灌注损伤模型，观察了川芎嗪对肝缺血再灌注损伤的防护作用，结果提示川芎嗪可显著减少血清转氨酶，ＬＤＨ的溢出，减轻肝缺血再灌注后肝细胞病理性损伤，明量降低肝组织ＬＰＯ，ＴＸＢ２的升高，维持缺血及再灌注期ＳＯＤ活性，川芎嗪通过抑制肝缺血再灌注时氧自由基产生，提高组织抗氧化能力，维持Ｔ／Ｋ平衡，对肝缺血再灌注损伤起到保护作用。     

The protective effect of adrenomedullin on renal injury, in a model of abdominal aorta cross-clamping

Renal injury induced by aortic ischemia-reperfusion (IR) is an important factor in the development of postoperative acute renal failure following abdominal aortic surgery. The aim of this study was to examine the effect of adrenomedullin (AM) on kidney injury induced by infrarenal abdominal aortic IR in rats. Thirty-two Wistar Albino rats were randomized into four groups (eight per group) as follows: Control group, IR group (120-minute ischemia and 120-minute reperfusion), IR?+?AM group (a bolus intravenously of 0.05 μg/kg/min AM), and control?+?AM group. At the end of the experiment, blood and kidney tissue specimens were obtained for biochemical analysis. Immunohistological evaluation of the rat kidney tissues was also done. IR significantly increased (p?相似文献   

缺血预处理对兔缺血再灌注脊髓血流量的影响

目的　研究缺血预处理 (IP)对缺血再灌注早期兔脊髓血流量的影响。方法　往置入腹主动脉的Swan Ganz导管气囊内注气建立兔脊髓缺血模型。将实验兔分为缺血组、预处理组和假手术组。应用激光多普勒血流量图像仪测量缺血期及再灌注 4h内的腰髓血流量。结果　在缺血 30min时 ,缺血组兔腰髓血流量 (2 3.0 % )和预处理组兔腰髓血流量 (36 .4 % )与各自基础值 (10 0 % )相比均有明显下降 (P <0 .0 1)。再灌注刚开始时 ,缺血组和预处理组兔腰髓血流量迅速回升 ,并超过基础值。再灌注 5 0min后 ,缺血组与预处理组兔相比 ,腰髓血流量 (85 .9% ,114 .3% )开始明显下降 (P <0 .0 5 )。再灌注 90min以后下降更为显著 (P <0 .0 1)。预处理组兔腰髓血流量在再灌注 4h内均高于基础值 ;假手术组兔腰髓血流量一直在基础值波动。结论　缺血预处理可通过提高缺血再灌注早期的脊髓血流量而对脊髓缺血再灌注损伤产生保护作用     

胰腺血运阻断安全性的实验研究

目的探讨大鼠胰腺不同血运阻断时间的损伤程度，确定合适的没有明显缺血再灌注损伤的大鼠胰腺热缺血时间。方法将成年雄性SD大鼠60只随机分为5组：A组，正常对照组；B组，10min缺血组；C组，20min缺血组；D组，30min缺血组；E组，60min缺血组，每组各12只。通过钳闭大鼠腹腔干和肠系膜上动脉，建立大鼠胰腺的缺血再灌注损伤模型，对不同血运阻断时间的胰腺组织进行光、电镜检查和相关血清丙二酰二醛（MDA）、超氧化歧化酶（SOD）、一氧化氮（NO）、淀粉酶（AMS）等生化指标检测。结果不同热缺血时间的大鼠胰腺组织的病理变化及其MDA、SOD、NO、AMS等生化指标间均存在差异，B组无明显缺血再灌注损伤，C组出现缺血再灌注损伤，D组有显著的缺血再灌注损伤，E组有严重的缺血再灌注损伤。结论胰腺血运阻断时间不能超过20min，最好不超过10min。     

Clinical-functional and morphological changes in the large intestine in patients with chronic abdominal ischemia]

The article presents a study of clinical variants of ischemic lesions of the large intestine (ILLI) in patients with the chronic abdominal ischemia (CAI) syndrome. There was an examination of 42 patients with putative ILLI, who had a cardiovascular pathology at the background, which led to significant hemodynamic disorders of the blood flow in unpaired visceral branches of the abdominal aorta. The authors performed a complex diagnostics of ILLI including anamnestic and clinical data, laboratory and morphological assessment of the large intestine and vessels providing its blood supply. Based on the data collected, other functional and organic diseases of the large intestine (LI) were excluded. It was revealed that the final result of ILLI differed depending on the ischemia degree--from reversible functional disorders to high-grade organic lesions of the LI. Each clinical variant of ILLI has its own clinical manifestations as well as functional, organic and morphological peculiarities of changes in the LI revealed by a laboratory and histological examination of the LI.     

The protective effect of melatonin on renal ischemia-reperfusion injury in the rat

Oxygen free radicals are considered to be important components involved in the pathophysiological tissue alterations observed during ischemia-reperfusion (I/R). In this study, we investigated the putative protective effects of melatonin treatment on renal I/R injury. Wistar albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 1, 3, 6, 24, 48 hr or 1 wk of reperfusion. Melatonin (10 mg/kg, s.c.) or vehicle was administered twice, 15 min prior to ischemia and immediately before the reperfusion period. At the end of the reperfusion periods, rats were decapitated. Kidney samples were taken for histological examination or the determination of renal malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and protein oxidation (PO). Serum creatinine and blood urea nitrogen (BUN) concentrations were measured for the evaluation of renal function. The results revealed that I/R induced nephrotoxicity, as evidenced by increases in BUN and creatinine levels at each time point, was reversed by melatonin treatment. The decrease in GSH and increases in MDA, MPO and PO induced by I/R indicated that renal injury involves free radical formation. As melatonin administration reversed these oxidant responses, improved renal function and microscopic damage, it seems likely that melatonin protects kidney tissue against oxidative damage.     

脑缺血再灌注肾脏组织损伤老年大鼠ATP酶和自由基代谢的变化及其意义

目的 从ATP酶活性变化和自由基损伤方面研究老年大鼠脑缺血再灌注肾脏损伤机制。方法 青年（5-6月龄）和老年（20-22月龄）大鼠均分为模型组和正常对照组。观察大鼠全脑缺血30min再灌注60min后肾脏组织形态和肌酐（Cr)。尿素氮（BUN），丙二醛（MDA）含量及超氧化物岐化酶（SOD），ATP酶的活性，结果 青年和老年模型组大鼠肾脏组织形态和功能均出现明显的病理改变，老年模型组较青年模型组严重，青年模型组和老年模型组肾脏组织MDA含量和MDA/SOD比值分别高于青年对照组和老年对照组，老年模型组肾脏组织Na^ -K^ -ATP酶和Ca^2 -ATP酶活性低于青年模型组；老年对照组肾脏Ca^2 -ATP酶活性低于青年对照组，老年模型组肾脏Ca^2 -ATP酶活性低于老年对照组。结论 脑缺血再灌注肾脏损伤老年大鼠较青年大鼠严重。ATP酶活性降低和自由基损伤可能是其主要机制之一，由于老年大鼠ATP酶活性和自由基代谢的增龄变化使这些病理改变较青年明显并具有一定特点。     

Melatonin protects from ischemia/reperfusion-induced renal injury in rats: this effect is not mediated by proinflammatory cytokines

The pathophysiologic mechanisms leading to acute ischemic renal failure are not completely understood. Melatonin, a compound with well-known antioxidant properties, reduces IR-induced renal injury. The purpose of the present study was to investigate the changes in levels of tumor necrosis factor (TNF)-alpha, IL-beta, and IL-6 in postischemic reperfused renal tissue, and to determine whether the protective effect of melatonin is related the modulation of the production of these inflammatory molecules. Male Wistar albino rats were unilaterally nephrectomized and subjected to 1 hr of renal pedicle occlusion followed by 2 hr or 24 hr of reperfusion. Melatonin (10 mg/kg, i.p.) or vehicle was administrated at 10 min prior to ischemia. After 24 hr of the reperfusion, following decapitation, kidney samples were taken both for histologic examination and for the determination of malondialdehyde (MDA), myeloperoxidase (MPO) activity, total antioxidant capacity (TAC), total oxidative stress (TOS), creatinine, and blood urea nitrogen (BUN). These were measured in serum samples. TNF-alpha, IL-beta, and IL-6 were measured in kidney samples after 2 hr of reperfusion. IR caused a significant increase in renal MDA, MPO, TOS, creatinine, and BUN while decrease TAC without any change in TNF-alpha, IL-beta, and IL-6 levels. Melatonin treatment reduced the biochemical indices without any change in the cytokine levels and ameliorated histopathologic alterations induced by IR. The protective effect of melatonin on IR-induced renal injury is related to its antioxidant properties but not to proinflammatory cytokines.     

山楂提取物对心肌缺血/再灌注损伤的保护作用

目的探讨山楂提取物对大鼠心肌缺血/再灌注损伤（IR I）的保护作用。方法建立大鼠心肌缺血/再灌注模型,在缺血前给予山楂提取物处理,观察动脉压和心律失常的改变,测定血液中乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）和丙二醛（MDA）的变化。结果预先给予山楂提取物可降低血液中LDH和MDA含量,提高SOD活性,降低血压,有抗心律失常作用。结论山楂提取物对大鼠心肌IR I具有一定的保护作用。     

云芝多糖防止缺血再灌注心肌早期损伤

为了探讨云芝多糖对心肌缺血再灌注损伤的预防作用，制备犬心肌缺血再灌注损伤模型，输血再灌注组不用药物干预，云芝多糖组手术前2天每天口服云芝多糖150mg/kg。在缺血再灌注过程不同时间点测定左心室舒张压，超声心功能和冠状静脉窦血浆丙二醛浓度，心肌标本行透射电镜检查。结果发现，缺血再灌注组再灌注前和再灌注早期左心室舒张压显著升高，云芝多糖组仅再灌注前左心室舒张压升高，再灌注前两组缺血心肌节段收缩期增厚百分率显著下降，并表现为矛盾运动，再灌注期两组缺血心肌节段收缩期增厚百分率呈进行性改善，至再灌注120min两组均未恢复至结扎前水平，且云芝多糖组显著高于相应时间咪缺血再灌注组；左心室射血分数的变化趋势与缺血心肌节段收缩期增厚百分率相似，但恢复较快，云芝多糖组于再灌注90min即恢复至结扎前水平。缺血再灌注组再灌注期丙二醛浓度明显升高，至再灌注120min尚未恢复至结扎前水平。而云芝多糖组再灌注早期丙二醛浓度升高，但回降较快，于再灌注30min即恢复至结扎前水平，缺血再灌注组心肌组织水肿，心肌细胞少部分肌丝断裂，收缩带模糊，线粒体轻度肿胀，脱颗粒，胞质水肿；云芝多糖组心肌组织除轻微水肿外，未见其它明显结构改变，结果提示，云芝多糖对缺血再灌注早期心肌有显著保护作用。     

Topiramate ameliorates abdominal aorta cross-clamping induced liver injury in rats

Background and Aim:

Ischemia/reperfusion (I/R) injury in the liver occurs after a prolonged period of ischemia followed by restoration of hepatic blood perfusion. During the surgery of abdominal aorta, I/R injury causes damage to lower extremities and many organs, especially liver. The antioxidant and tumor necrosis factor-alpha (TNF-α) suppression effects of topiramate (TPM) have been reported in several studies. We evaluated the potential protective effect of TPM on cellular damage in liver tissue during I/R injury.

Materials and Methods:

Thirty male Wistar albino rats were divided into three groups: Control, I/R, and I/R plus TPM (I/R + TPM) groups. Laparotomy without I/R injury was performed in the control group. After laparotomy, cross-ligation of infrarenal abdominal aorta was applied for 2 h in I/R groups that was followed by 2 h of reperfusion. TPM (100 mg/kg/day) was orally administrated to the animals in the I/R + TPM group for seven consecutive days before I/R procedure.

Results:

The I/R group''s TNF-α and interleukin-6 (IL-6) levels were significantly higher than those of the control (P = 0.010; P = 0.002) and I/R + TPM groups (P = 0.010; P = 0.002, respectively). Asymmetric dimethyl arginine (ADMA) levels of I/R group were higher than the control (P = 0.015) and I/R + TPM groups. I/R caused serious histopathological damage to liver tissue; however, TPM led to very low histopathological changes.

Conclusion:

Our data demonstrated that TPM treatment prominently decreases the severity of liver I/R injury. TPM pretreatment may have preventive effects on liver injury via I/R during intra-abdominal surgery.