钙敏感受体在大鼠心肌缺血/再灌注损伤中的作用

目的观察钙敏感受体在大鼠心肌缺血/再灌注损伤中的作用及其机制。方法30只Wistar大鼠随机分为3组(每组10只):假手术组(sham组)、缺血/再灌注组(I/R组)和钙敏感受体激动剂组(Gdcl3组),采用冠状动脉结扎和松结的方法,制备大鼠在体心肌缺血/再灌注损伤模型。分别测定血清一氧化氮(NO)、丙二醛(MDA)、超氧化物歧化酶(SOD)和乳酸脱氢酶(LDH)水平,光镜及透射电镜下观察心肌结构病理变化。结果I/R组血清LDH、MDA水平明显高于sham组(P<0.01),NO、SOD低于sham组(P<0..01);Gdcl3组血清LDH、MDA水平明显高于I/R组(P<0.01),而NO、SOD低于I/R组(P<0.01)。光镜及透射电镜下可观察到Gdcl3组心肌结构破坏,心肌细胞呈灶状或片状坏死;线粒体损伤,核皱缩,核染色质边集,其病理学改变程度较I/R组严重。结论钙敏感受体激活可使氧自由基产生增加,减少NO含量,降低SOD活性,加重心肌缺血/再灌注损伤。     

白藜芦醇对大鼠肠缺血再灌注损伤的保护作用

目的 探讨白藜芦醇(resveratro1,RES)对实验性大鼠肠缺血再灌注肠黏膜损伤的保护作用.方法 24只成年雄性SD大鼠随机分为假手术组(SO)、缺血再灌注损伤组(I/R)、RES治疗组.SO组仅分离肠系膜上动脉(SMA)根部而不夹闭.肠缺血再灌注损伤组(I/R)和RES治疗组均用无损伤血管夹夹闭SMA根部后分别立即经阴茎背静脉注射生理盐水、RES(20 mg/kg),45 min之后放松血管夹形成再灌注.各组大鼠均于制模后6 h采集标本.检测血清和回肠组织中的超氧化物歧化酶(SOD)和丙二醛(MDA)的含量,TUNEL法检测肠黏膜上皮细胞凋亡率,并观察肠黏膜病理变化.结果 小肠缺血再灌注后,血清及小肠组织中反映氧化损伤程度的MDA明显升高,SOD则明显减少,小肠黏膜上皮细胞凋亡,应用RES后能显著改善上述改变.结论 白藜芦醇对肠缺血再灌注损伤具有保护作用,其机制可能与通过抗氧化作用及抑制肠黏膜上皮细胞凋亡有关.

Abstract：

Objective To study the protective effects of resveratrol (RES) on intestinal ischemia-reperfusion injury in rats.Methods Twenty-four SD rats were randomly divided into the sham operation group,intestinal ischemia-reperfusion injury (I/R) group and resveratrol treated (RES) group.The intestinal ischemia injury was induced by superior mesenteric artery occlusion for 45 minutes,and then the blood supply to the intestine was restored to cause reperfusion injury.After 6 hours' reperfusion,the rats were sacrificed and intestine was collected.Of the RES group,the rats were subjected to I/R injury,and treated with 20 mg/kg resveratrol by intravenous injection immediately after the mesenteric artery was clamped.Superoxide Dismutase (SOD) and Malonaldehyde (MDA) levels in serum and intestine were measured.Apoptotic intestinal epithelial cells were detected by TUNEL methods.The histological injury of the intestine was also examined.Results Compared with the sham operated rats,MDA levels in the serum and intestine as well as the apoptotic epithelial cells were significantly increased in the rats subjected to I/R (MDA in serum and intestine 4.63±0.53 vs 1.32±0.40;8.60± 0.98 vs 4.13±0.86,P＜0.01;apoptotic index 66.63 ± 1.71 vs 46.72 ± 1.50,P＜0.01 ).However,the SOD levels in the serum and intestine were decreased (49.21±4.38 vs 86.65±6.14;351.03 ± 21.46 vs 468.93 ± 16.21,P＜0.01).In the rats subjected to I/R injury but received resveratrol treatment,the epithelial cells apoptosis and MDA levels in serum and intestine were decreased,and SOD levels in serum and intestine increased (P＜0.05).Conclusions Resveratrol protects intestine from ischemia-reperfusion injury in rats.     

氨力农对大鼠在体肺缺血再灌注损伤的保护作用

目的：探讨氨力农对在体肺缺血再灌注（I/R）损伤的保护作用。方法：夹闭大鼠左肺门1.5 h,再灌注2 h,建立在体缺血再灌注模型。将24只SD大鼠随机分成假手术组,缺血再灌注组（I/R组）和氨力农组（AMR组）,AMR组缺血前30 min给予颈静脉注射氨力农10 mg/kg,再灌注前5 min颈静脉注射氨力农10 mg/kg。再灌注2 h后采颈动脉血检测血气、白细胞介素-1β（IL-1β）、白细胞介素-8(IL-8)、肿瘤坏死因子-α（TNF-α）;摘取左肺测湿干比、超氧化物歧化酶（SOD）活力、丙二醛（MDA）含量并行病理学检查。结果：再灌注2 h后,动脉血氧分压和二氧化碳分压3组间差异无显著性;I/R组肺湿干比和MDA（nmol/mg prot）含量分别为5.3±0.5和0.66±0.16,显著高于假手术组,AMR组上述指标降低至4.8±0.2和0.51±0.09;SOD（U/mg prot）在I/R组为39.3±3.0 ,AMR组为54.7±6.8,较I/R组升高;I/R组血清IL-1β（pg/mL）、IL-8 （pg/mL）、TNF-α(pg/mL)含量分别为22.08±3.85,21.92±5.56,30.50±3.77较假手术组显著升高, AMR组上述指标为16.66±3.02,14.73±2.75和 22.48±3.82,较I/R组低。病理学结果显示：三组动物肺组织结构基本正常,假手术组和AMR组无充血,I/R组充血明显且较其他两组炎症细胞明显增多。结论： 氨力农对肺缺血再灌注损伤具有保护作用,可能与其抗氧化和抑制炎症因子分泌有关。［中国当代儿科杂志,2007,9（3）：233-236］     

宫内窒息胎鼠肝组织一氧化氮及氧自由基作用的研究

研究表明肝脏缺血缺氧及再灌注(I/R)损伤中一氧化氮(NO)和氧自由基有重要作用.本文研究宫内窒息胎鼠在I/R过程中其肝组织超氧化物歧化酶(SOD)、丙二醛(MDA)、NO变化,以及肝脏病理变化.     

山楂叶总黄酮对大鼠肾缺血/再灌注损伤的保护作用

目的探讨山楂叶总黄酮(TFHL)对大鼠肾缺血/再灌注(I/R)的作用。方法采用在体夹闭双侧肾动脉60min后恢复灌注的方法复制大鼠肾I/R损伤的模型,夹闭动脉前30min静脉注射TFHL30或60mg/kg。检测再灌注1、24h后血清BUN、血Scr及TNF-α和IL-1水平及再灌注24h后肾组织丙二醛(MDA)和超氧化物歧化酶(SOD)水平。结果TFHL能显著降低I/R导致的血清BUN和Scr升高,增加尿量,减少TNF-α和IL-1产生,提高肾组织SOD活性,减少MDA生成。结论TFHL能明显减轻肾I/R损伤,有效改善肾功能,其机制与TFHL减少脂质过氧化反应,减少细胞因子TNF-α和IL-1水平有关。     

丹参注射液对肠缺血再灌注所致肝损伤保护作用的实验研究

目的观察再灌注前给予丹参注射液对大鼠肠缺血再灌注(I/R)致肝损伤的影响,为丹参注射液的外科应用提供理论依据。方法将24只wister大白鼠,随机分为A、B、C三组。B、C两组分别于再灌注前静注生理盐水、丹参注射液,以A组为对照。测定所有动物血清中ALT,AST和LDH含量,血清和肝组织中超氧化物歧化酶(SOD),丙二醛(MDA)活性以及肝组织中细胞色素C氧化酶活力,对肝组织进行HE染色。结果C组肝组织及血清中各项指标均接近A组(P>0.05),与B组比较差异显著(P<0.05～0.01);肝组织病理切片光镜观察C组肝组织细胞仅轻度受损,而B组肝细胞中重度损伤。结论再灌注前给予适量的丹参注射液对大鼠肠I/R所致的肝损伤具有明显的保护作用。     

生脉注射液对青春前期大鼠睾丸扭转/复位缺血再灌注的保护作用

目的观察青春前期大鼠睾丸单侧扭转复位后对双侧睾丸氧自由基的远期影响,探讨生脉注射液对其的保护作用。方法 5周龄健康SD雄性大鼠24只,随机分为实验组(生脉注射液组)、对照组(9 g.L-1盐水组)和假手术组,每组8只。实验组和对照组建立左侧睾丸扭转复位模型,假手术组游离睾丸,不予扭转。于术后7周取各组大鼠双侧睾丸,分别测定大鼠睾丸组织内超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)活性和丙二醛(MDA)水平。结果与对照组比较,实验组和假手术组大鼠双侧睾丸中SOD活性升高,NOS活性和MDA水平下降(Pa<0.05)。与假手术组比较,实验组大鼠双侧睾丸组织中SOD活性下降,NOS活性和MDA水平升高(Pa<0.05)。结论生脉注射液可提高大鼠睾丸组织中的SOD活性,提高机体抗氧化能力,清除氧自由基,抑制脂质过氧化反应,减轻MDA对细胞膜的损伤,对睾丸缺血再灌注损伤具有一定的保护作用。     

二氧化硫预处理对心肌缺血再灌注损伤大鼠二氧化硫/天门冬氨酸氨基转移酶体系的影响

目的 探讨二氧化硫(SO2)预处理对心肌缺血再灌注损伤大鼠的保护作用及对心肌组织中SO2/天门冬氨酸氨基转移酶(AAT)体系的影响.方法　24只健康清洁级雄性Wistar大鼠随机分为假手术组、缺血再灌注组(I/R组)、SO2预处理组(I/R+S组).结扎大鼠左侧冠状动脉30 min,再灌注120 min,制备心肌缺血再灌注模型;I/R+S组大鼠在缺血前10 min用1 μmoL·kg-1SO2颈外静脉注射预处理.采用全自动生化检测仪检测大鼠血浆CK和LDH水平,用高效液相色谱法测定其心肌组织中SO2水平,采用蛋白免疫印迹法检测其心肌组织AAT1和AAT2蛋白表达水平.结果 缺血再灌注后,I/R组及IR+S组血浆CK、LDH水平均较假手术组明显增高(P＜0.01,0.05),I/R+S组血浆CK、LDH水平较I/R组均明显降低(Pa＜0.05).与假手术组比较,I/R组大鼠心肌组织匀浆中SO2水平显著降低(P＜0.05),I/R+S组无明显变化;I/R+S组SO2水平较I/R组显著增高(P＜0.01).I/R组大鼠心肌组织AAT1蛋白表达较假手术组显著降低(P＜0.01),I/R+S组与假手术组比较差异无统计学意义(P＞0.05),而I/R+S组AAT1蛋白表达则较I/R组显著增高(P＜0.01);AAT2蛋白表达在3组间的差异无统计学意义(P＞0.05).结论　SO2预处理可明显降低心肌缺血再灌注大鼠血浆中心肌酶活性,具有心肌保护作用,并对心肌组织中SO2/AAT体系具有上调作用.     

左旋精氨酸对模拟缺血再灌注乳兔培养窦房结细胞损伤的保护作用

目的 观察模拟缺血再灌注(IR)培养乳兔窦房结细胞(SANC)损伤及左旋精氨酸(L-Arg)的保护作用.方法 对SANC模拟低糖缺氧培养,添加L-Arg和L-Arg 加 L-NAME(L-Arg抑制剂)与培养细胞共同孵育,吖啶橙(AO)标记细胞凋亡,检测细胞内过氧化物歧化酶(SOD)活性、丙二醛(MDA)、总一氧化氮合酶(NOS)、氧化亚氮(NO)水平.细胞分为正常对照组、I120R120 组、I120R120加L-Arg组、I120R120加L-Arg加L-NAME组4组.结果 凋亡细胞体积明显缩小,核呈黄绿色,断裂为多个碎块状,由膜包裹着凸起于细胞表面呈黄绿色凋亡小体.与I120R120组凋亡率[(5.21±1.59)%]比较,I120R120加L-Arg组凋亡率[(8.70±3.10)%]显著降低(P<0.01);I120R120加L-Arg组细胞SOD活性[(46 820±14 450) U/g]较I120R120组 [(25 030±8 440) U/g]显著上升,而I120R120加L-Arg组MDA[(5.55±3.71)mmol/g]、NO[(3.65±1.02) U/g]和NOS[(3.73±0.24) μmol/L]较I120R120组MDA[(8.42±4.21)mmol/g]、NO[ (4.62±1.20) U/g]和NOS[(4.96±0.52) μmol/L]显著下降(Pa<0.05);而I120R120加L-Arg加L-NAME组各指标较I120R120组无显著性差异(Pa>0.05).结论 补充NO合成底物L-Arg能清除自由基,增加SOD活性,增强细胞抗氧化损伤能力,可能是阻断氧自由基所介导的细胞凋亡机制之一.     

心肌缺血预适应家兔血浆内皮素及血清一氧化氮水平变化的意义

目的探讨心肌缺血预适应家兔血浆内皮素(ET)及血清一氧化氮(NO)水平的变化,探讨其在心肌缺血预适应过程中的作用。方法16只新西兰大耳白兔随机分为2组。缺血再灌注组(I/R组):结扎其冠状动脉左室支40min后再灌注120min;缺血预适应组(IP组):先予缺血预适应的过程,结扎冠状动脉左室支5min,放松冠脉血管后再灌注5min,反复操作3次,再按照I/R组进行操作。实验开始前取血测定血清CK、LDH、NO及血浆ET水平,2组动物均在结扎左室支40min、再灌注120min复测NO及ET水平,观察NO和ET变化。结果IP组阻断40min及再灌注120min血浆ET水平及LDH升高低于I/R组,二组比较差异有统计学意义(Pa<0.01),血清NO水平升高多于I/R组,二组比较差异有统计学意义(P<0.01)。IP组再灌注120min,CK水平升高于I/R组,心肌损伤程度小于I/R组。结论心肌缺血预适应家兔NO及ET水平发生明显变化,缺血预适应过程中NO水平升高增强了心肌对缺血的耐受性,ET水平降低减少了心肌缺血过程中其对心肌的损伤。     

The nitric oxide donor molsidomine prevents ischemia/reperfusion injury of the adult rat small intestine

It is suggested that gastrointestinal mucosal blood flow depends on a balanced release of vasoactive substances from the endothelium. The present study investigated the effects of molsidomine on the small intestine after ischemia-reperfusion (I/R) injury in four groups of 10 rats each composed: (1) SO, sham operation; (2) untreated I/R; (3) ML, I/R plus molsidomine pretreatment; (4) L-NAME, I/R plus N-omega-nitro-L-arginine methyl ester pretreatment. Intestinal ischemia for 45 min and reperfusion for 60 min were applied. Ileum specimens were obtained to determine the tissue level of malondialdehyde (MDA) and histologic changes. Mean MDA levels in the SO, untreated I/R, ML, and L-NAME groups were 95.60 +/- 2.59, 136.90 +/- 4.35, 121.10 +/- 3.38, and 137.40 +/- 4.42 nmol/g wet tissue, respectively. Although the MDA level in the ML group was higher than in the SO group ( P < 0.0001), it was significantly lower compared to the untreated I/R and L-NAME groups ( P < 0.0001, P < 0.0001). Mucosal injury scores (MIS) in groups 1-4 were 0.2 +/- 0.42, 3.9 +/- 0.73, 1.5 +/- 0.70, and 4.1 +/- 0.56, respectively. In group 3 the MIS was significantly lower than in groups 2 and 4 ( P < 0.0001, P < 0.0001). Molsidomine plays a role in attenuating reperfusion injury of the small intestine by depression of tissue MDA levels and MIS and regulates post-ischemic intestinal perfusion while restoring the intestinal microcirculatory blood flow and histologic injury.     

Orchiectomy or testosterone receptor blockade reduces intestinal mucosal damage caused by ischemia-reperfusion insult

The aim of the present study was to investigate whether orchiectomy or administration of flutamide an antagonist of the testosterone receptor can reduce oxidative stress and histologic damage in the rat small bowel subjected to mesenteric ischemia/reperfusion (I/R) injury. A total of 32 Sprague-Dawley rats were divided into four groups. Group 1 was control (sham), group 2 was I/R, group 3 was I/R plus orchiectomy (orchiectomy was performed 14 days before I/R), group 4 was I/R plus flutamide (flutamide was given throughout 14 days before mesenteric IR). Rats were subjected to 45 min of mesenteric ischemia followed by 3 h of reperfusion. The levels of ileal malondialdehyde (MDA) and nitric oxide (NO) were found to be significantly lower in orchiectomy and flutamide treatment groups compared with I/R group (P < 0.05). The histopathological injury scores were consistent with the MDA and NO levels. These results suggest that castration or testosterone receptor blockade decreases the level of intestinal I/R injury in male rats and it is an another example for disease variations based on gender differences.     

Serum cytosolic beta-glucosidase activity in a rat model of necrotizing enterocolitis

The diagnosis of necrotizing enterocolitis (NEC) is made from a combination of clinical and radiographic findings. There are no useful screening biochemical markers of intestinal injury. The serum concentration of cytosolic beta-glucosidase (CBG), an enzyme found primarily in enterocytes, is markedly elevated in animal models of ischemia and bowel obstruction. We hypothesized that in a rat model of NEC, serum CBG activity would significantly increase before microscopic evidence of severe intestinal injury. Cohorts of 2-wk-old Sprague-Dawley rats (n = 10/cohort) were anesthetized and underwent laparotomy with occlusion of the superior mesenteric artery (SMA). Platelet-activating factor (200 microg/animal) was injected in the proximal duodenum. Serum and intestinal samples were obtained at time 0 (control) and 30, 60, and 90 min of ischemia (I) and after 90 min of I followed by 60 min of reperfusion (I/R). Histopathologic injury was categorized as either no or minimal injury or mural necrosis by two masked investigators and CBG activity was measured by ELISA. Data were analyzed with Fisher's exact test and ANOVA. Only the I/R group had significantly greater mural necrosis compared with the control group (90% versus 0%, respectively, p < 0.001). In contrast, CBG activity was significantly elevated after only 90 min of I and after I/R (15.1 +/- 5.6 and 16.4 +/- 4.3 units/mL, respectively, p < 0.05). We conclude that serum CBG is elevated before transmural intestinal injury in this model and may have utility as an early marker of ischemia in patients at risk for NEC.     

雌激素对青春期雌性大鼠肠缺血再灌注损伤的保护作用

目的：探讨雌激素对肠缺血再灌注损伤的影响。方法：取雌性青春期大鼠，分为卵巢切除组（20只）、对照组（10只）、雌二醇组（10只），大剂量雌二醇组（20只）。观察肠缺血30min再灌注60min后肠粘膜损伤程度(Chiu氏评分法），测定血清雌二醇，NO2^－／NO3^-和丙二醛水平。结果：雌二醇组和大剂量雌二醇组的Chiu氏评分法和丙二醛低于卵巢切除组，而NO2^-／NO3^－高于卵巢切除组。雌二醇Chiu氏评分法呈负相关，与NO2^-／NO3^3－呈正相关，结论：雌激素对青春期雌性大鼠肠缺血再灌注损伤有一定的保护作用。     

The protective effects of trimetazidine on testicular ischemia and reperfusion injury in rats

This study was designed to investigate the protective effect of trimetazidine [TMZ; 1-(2, 3, 4-trimethhoxibenzyl)-piperazine dihydrochloride], as an antioxidant agent, on torsion–detorsion-induced biochemical and histopathological changes in experimental testicular ischemia/reperfusion injury in rats. Twenty-seven male Wistar rats weighing 180–220 g were divided into five groups: control (C, n = 4), sham-operated (S, n = 4), ischemia (I, n = 6), ischemia–reperfusion (I/R, n = 6) and ischemia–reperfusion + trimetazidine (I/R + TMZ; n = 7). Control rats were used for basal normal values. In group I, 2 h torsion of the left testis was performed. In I/R and I/R + TMZ groups, following 2 h of torsion, 4 h detorsion of the testis was performed. In ischemia and I/R groups, physiologic saline was administered orally for 7 days, and the rats in I/R + TMZ group were pretreated orally with 5 mg/kg day TMZ for 7 days before inducing ischemia. At the end of each experiment, ipsilateral orchiectomies were performed for the tissue levels of malondialdehyde (MDA), glutathione peroxidase (GPx) enzyme activities and histopathological examinations in all groups. MDA levels were significantly reduced and GPx enzyme activities were significantly increased in testes in I/R+TMZ pretreated group compared to group I and I/R. The mean seminiferous tubular diameter (MSTD) and Johnsen’s score were significantly better in I/R+TMZ group than groups I and I/R. Pretreatment with TMZ decreased germ cell apoptosis and caspase-3 expression in the ischemic testis. The present results show that TMZ has a protective activity in the testicular injury caused by I/R, and provide the first evidence of the role of TMZ for the prevention of I/R-induced testicular injury.     

Effects of whole-body hypoxic preconditioning on hypoxia/reoxygenation-induced intestinal injury in newborn rats.

PURPOSE: The precise cause of necrotizing enterocolitis (NEC) is elusive. Ischemia and reperfusion injury of the intestine has been considered to be a major contributing factor for NEC. Ischemic preconditioning is defined as one or more brief periods of ischemia with intermittent reperfusion that protects tissues against a sustained period of subsequent ischemia. Contribution of preconditioning to hypoxia/reoxygenation-induced intestinal injury in newborn rats has not been evaluated previously. METHODS: The study was carried out on 1-day-old Wistar albino rat pups. Whole-body hypoxia and reoxygenation (H/R) was achieved by 10 min hypoxia using 95 % N (2) + 5 % CO (2) followed by 10 min reoxygenation with 100 % oxygen. Whole body hypoxic preconditioning (HP) cycles were performed with 3 min hypoxia and 5 min reoxygenation. Thirty-three pups were randomly allocated into 4 groups. Group 1 served as untreated controls. The pups in group 2 were subjected to H/R only. In groups 3 and 4, 1 cycle and 3 cycles of HP were performed prior to H/R, respectively. Animals were killed at the end of the protocols. Intestine specimens were obtained to determine the histological changes, as well as to measure the tissue malondialdehyde (MDA) and nitric oxide (NO) levels, and xanthine oxidase (XO) and myeloperoxidase (MPO) activities. RESULTS: The microscopic lesions in H/R rat pups were virtually the same as those seen in neonatal NEC, with severe destruction of villi and crypts, in some cases extending to the muscularis. In both HP groups, the lesions were found to be milder. H/R resulted in a marked elevation in MDA and NO levels, and XO and MPO activities compared to the untreated controls. Both 1 cycle and 3 cycles of HP prior to H/R resulted in an obvious decrease in all biochemical parameters. Differences of the biochemical results between both HP groups were not statistically significant. CONCLUSION: This study revealed that whole-body hypoxic preconditioning is beneficial for hypoxia/reoxygenation-induced intestinal injury in newborn rats.     

双歧杆菌对内毒素损伤幼年大鼠肠道血管内皮细胞粘附分子－1的影响

目的：双歧杆菌是肠黏膜屏障中生物屏障的主要成分,参与了宿主的消化、营养、代谢、吸收、免疫及抗感染过程,然而其具体的作用机制目前还不清楚。该研究欲探讨双歧杆菌对内毒素损伤幼年大鼠血清和回肠组织的丙二醛（MDA）含量和小肠绒毛间质血管内皮细胞粘附分子-1（ICAM-1）表达的影响。方法：腹腔注射内毒素制造内毒素损伤动物模型（模型组,E组）,治疗组（T组）提前7 d给予双歧杆菌灌胃,同时设对照组（C组,腹腔注射生理盐水）,于不同时间点处死后检测血清和肠组织中MDA的含量,并用免疫组织化学和逆转录-聚合酶链反应（RT-PCR）方法检测小肠组织ICAM-1蛋白质和核酸水平的变化。结果：E组血清和小肠MDA含量较对照组增加,以6 h增加明显（肠组织：99.88±12.62 nmol/mg prot vs 84.25±12.96 nmol/mg prot,P<0.05;血清：1.67±0.30 nmol/mL vs 1.13±0.20 nmol/mL,P<0.05）;T组MDA含量（6 h：肠组织92.75±9.28 nmol/mg prot;血清1.17±0.23 nmol/mL）较E组下降;E组小肠组织ICAM-1蛋白质和核酸表达增加,分别以6 h和2 h为著,T组改变低于E组（P<0.05）。 结论：内毒素损伤幼鼠血清和小肠MDA含量增加,同时ICAM-1蛋白质和mRNA表达增加,外源性给予双歧杆菌能降低内毒素组MDA和ICAM-1的增加,表明双歧杆菌能通过抑制大鼠体内的MDA含量和ICAM-1的表达而起到一定的肠道保护作用。［中国当代儿科杂志,2007,9（4）：375-378］     

Effects of rapid rewarming on cerebral nitric oxide production and cerebral hemodynamics after hypothermia therapy for kainic acid-induced seizures in immature rabbits

BACKGROUND: The aim of the present study was to investigate whether rapid rewarming after hypothermia therapy during seizures alters the endogenous nitric oxide (NO) production in and around hippocampus, cortical cerebral blood flow (cCBF), and mean arterial blood pressure (MABP) in immature rabbits. METHODS: The hypothermic rabbits (rectal temperatures, 33 degrees C) were given kainic acid (KA; 12 mg/kg, i.v; at 0 min), followed by cooling (33 degrees C) for 60 min (at 60 min), then either rewarming (RW; 33-37 degrees C) was started (KA[+]RW[+] group, n = 7) or cooling was continued (KA[+]RW[-] group, n = 7) for another 60 min (at the end 120 min). In the KA(-)RW(+) group (n = 5), 0.5 mL normal saline was given (at time 0 min), followed by cooling (33 degrees C) for 60 min (at 60 min), then rewarming to 37 degrees C was started with observation for another 60 min (at the end 120 min). NO production in and around hippocampus was continuously measured by an NO-selective electrode, cCBF by laser Doppler flowmetry, cortical electroencephalogram (EEG), rectal and cerebral temperatures, and MABP during the experiment. Comparisons were made of these parameters between the values at 60 min and 120 min after the KA administrations. RESULTS: KA administration induced abnormal discharges in both KA(+)RW(+) and KA(+)RW(-) groups at the same degree. The KA(+)RW(+) group had a significant increase in %NO, and significant decreases in %cCBF and MABP after rapid rewarming, compared with before rewarming. In the KA(+)RW(-) group, there were no significant changes in %NO, %cCBF, and MABP between values at 60 and 120 min. These changes after rapid rewarming in the KA(+)RW(+) group were different from those with only elevation in brain temperature from 33 to 37 degrees C without seizures (KA[-]RW[+] group). CONCLUSIONS: These results suggest that rapid rewarming after hypothermia therapy induces an increase in the NO production in and around hippocampus and the decreases in cCBF and MABP during seizures in immature rabbits.