血红素加氧酶-1诱导对鼠肝缺血再灌注损伤的保护作用

目的研究血红素加氧酶-1(heme oxygenase-1,HO-1)在鼠肝缺血再灌注损伤肝组织中的表达及其作用。方法建立小鼠部分肝脏热缺血再灌注损伤模型,36只清洁级Balb/C小鼠随机分为3组: 假手术组(S组)、缺血/再灌注损伤组(I/R组)、HO-1诱导剂氯化高铁血红素(hemin)预处理组(HM组)。免疫组化半定量分析肝组织HO-1蛋白的表达,检测血清AST和ALT,肝组织丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,并观察肝组织的病理变化。结果与S组比较,I/R组HO-1蛋白表达显著增强,hemin预处理后,HO-1蛋白表达较I/R组增高(P<0．01)。I/R组AST,ALT活性和MDA的含量显著高于S组,而HM组均显著低于I/R组(P<0．01);I/R组SOD活性下降,而HM组显著高于I/R组(P<0．01)。HM组病理损伤程度明显轻于I/R组。结论 HO-1在鼠肝缺血再灌注损伤肝组织中表达上调,对肝脏具有保护效应。     

细胞穿透肽PEP-1介导血红素加氧酶-1对大鼠肠缺血再灌注损伤的影响

目的 评价细胞穿透肽PEP-1介导血红素加氧酶-1(HO-1)对大鼠肠缺血再灌注损伤的影响.方法 雄性SD大鼠18只,周龄7～9周,体重210～260 g,采用随机数字表法,将大鼠随机分为3组(n=6):假手术组(S组)、肠缺血再灌注组(IR组)和融合蛋白PEP-1/HO-1+肠缺血再灌注组(HO组).采用夹闭肠系膜上动脉45 min,恢复灌注120 min的方法制备大鼠肠缺血再灌注损伤模型.HO组夹闭肠系膜上动脉前30 min,左侧髂静脉注射融合蛋白PEP-1/HO-1 0.5 mg,S组不夹闭肠系膜上动脉,余操作同IR组.于再灌注120 min时处死大鼠取小肠组织,称重后计算肠湿/干重比,测定丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和HO-1活性,免疫组化法检测肠组织HO-1蛋白的表达,光镜下观察肠组织结构并进行损伤评分.结果 与S组比较,IR组和HO组肠湿/干重比和MDA含量升高,SOD活性降低,HO-1活性和蛋白表达水平升高,损伤评分升高(P＜0.05);与IR组比较,HO组肠湿/干重比、MDA含量降低,SOD活性升高,HO-1活性和蛋白表达水平升高,损伤评分降低(P＜0.05).HO组大鼠肠组织病理学损伤较IR组减轻.结论 细胞穿透肽PEP-1可将HO-1成功导人大鼠肠组织中的细胞并减轻肠缺血再灌注损伤.

Abstract：

Objective To investigate the effects of heme oxygenase-1 (HO-1) mediated by cell penetrating peptide PEP-1 on intestinal ischemia/reperfusion (I/R) injuiy in tats. Methods Eighteen male SD rats aged 7-9 weeks weighing 210-260 g were randomly divided into 3 groups (re = 6 each): sham operation group (group S) , I/R group and PEP-1/HO-1 + I/R group (group HO) . To establish a model of intestinal I/R injury, intestines were exteriorized and the superior mesenteric artery was exposed and occluded for 45 min ischemia, and then the clamp was removed for 120 min reperfusion. The PEP-1/HO-1 fusion protein 0.5 mg was injected via the left iliac vein 30 min prior to ischemia in group HO. The superior mesenteric artery was exposed but not occluded in group S. At the end of reperfusion, the rats were sacrificed and intestinal tissues obtained to determine the intestinal wet/ dry ratio, malondialdehyde (MDA) level, activities of superoxide dismutase (SOD) and HO-1, and HO-1 protein expression. The histological changes in the intestinal mucosa were examined and the injuiy was scored. Results Compared with group S, the intestinal wet/dry ratio, MDA level, HO-1 activity, HO-1 protein expression and injury score were significantly increased, while the SOD activity was significantly decreased in groups I/R and HO ( P ＜ 0.05) . Compared with group I/R, the intestinal wet/dry ratio, MDA level and injury score were significantly decreased, while the SOD activity, HO-1 activity and HO-1 protein expression increased in group HO ( P ＜ 0.05) . The pathologic changes were significantly attenuated in group HO compared with group I/R.Conclusion HO-1 protein can be successfully delivered into intestinal tissues by PEP-1 and has protective effects against intestinal I/R injury.     

Protective effect of ischemic postconditioning on lung ischemia-reperfusion injury in rats and the role of heme oxygenase-1

To investigate the effect of ischemic postconditioning (IPO) on acute lung ischemia-reperfusion (I/R) injury and the protein expression of haeme oxygenase-1 (H0-1), a cytoprotective defense against oxidative injury. Methods: After being anesthetized with chloralhy-drate, forty-eight healthy SD rats were randomly divided into 6 groups (8 in each): sham operation group (S group); I/R group: left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group: left lung hilum was clamped for40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Hemin (HM)+ I/R group: hemin, an inducer of HO- 1 was injected intraperitoneally at 40 μmol.kg-1·day-1 for two con-secutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX+IPO group: zinc protoporphyrin Ⅸ, an inhibitor of HO-1 was injected intraperitoneally at 20 mg·kg-1 24 hours prior to 40 minutes clamping of left lung hilum; and HM+S group: HM was administered as in the HM+I/R group without inducing lung I/R. Arterial partial pressure of oxygen (PaO2) and malondialdehyde (MDA) content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-his-tochemical technique and for light microscopic examination. Results: The PaO2 was significantly lower in all the experimental groups compared with sham group (90 mm Hg ±11 mm Hg). However, the values ofPaO2 in IPO (81 mm Hg ±7 mm Hg) and HM+I/R (80 mm Hg±9 mm Hg) were higher than that in I/R (63 mm Hg±9 mm Hg) and ZnPPIX+IPO (65 mm Hg±8 mm Hg) groups (P<0.01). The protein expression of HO-1 in lung tissue was significantly increased in I/R group compared with S group (P<0.01). While the HO-1 protein expression was higher in IPO and HM+I/R groups as compared with I/R group (P<0.05, P<0.01). The lung wet/ dry (W/D) weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM+S groups (P<0.01), accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment (P<0.01, IPO or HM+I/R vs. I/R). The protective effect of IPO was abolished by ZnPPIX. Condusion: Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-1 that leads to reduced post-ischemic oxidative damage.     

血红素加氧酶-1对乳鼠心肌细胞缺氧复氧损伤的影响

目的 探讨血红素加氧酶-1(HO-1)对乳鼠心肌细胞缺氧复氧损伤的影响.方法 新生SD大鼠8只,日龄1～3 d,原代培养心肌细胞,随机分为4组:正常对照组(C组)常规培养8 h;缺氧复氧组(HR组)采用缺氧2 h,复氧6 h的方法制备心肌细胞缺氧复氧模型;血晶素组(Hemin组)缺氧前24 h及缺氧即刻,培养基中加入Hemin,终浓度为20 μmol/L;血晶素+锌原卟啉组(Hemin+ZnPP组)缺氧前24 h及缺氧即刻培养基中同时加入Hemin及ZnPP,终浓度均为20 μmol/L.各组细胞均接种于35 mm培养皿(2 ml/皿)或50 ml培养瓶(3 ml/瓶),每组45皿和3瓶.于复氧结束后采用蛋白印迹法测定心肌细胞HO-1表达,台盼蓝染色法测定心肌细胞存活率,应用全自动生化分析仪测定细胞培养液乳酸脱氧酶(LDH)活性,超声破碎细胞离心后取上清,采用硫代巴比妥酸法测定细胞MDA水平,黄嘌呤氧化酶法测定细胞SOD活性.结果 与C组比较,其余3组培养液LDH活性、心肌细胞MDA水平及HO-1表达升高,心肌细胞存活率及SOD活性降低(P＜0.05).与HR组比较,Hemin组培养液LDH活性、心肌细胞MDA水平降低,HO-1表达、心肌细胞存活率及SOD活性升高(P＜0.05),Hemin+ZnPP组上述指标差异无统计学意义(P＞0.05).HR组和Hemin+ZnPP组细胞缺氧复氧损伤明显,Hemin组细胞缺氧复氧损伤减轻.结论 HO-1可减轻乳鼠心肌细胞缺氧复氧损伤.     

缺血预处理对大鼠缺血再灌注心肌HIF-1α和HO-1的影响

目的 探讨缺血预处理对大鼠缺血再灌注心肌低氧诱导因子1α(HIF-1α)和血红素加氧酶1(HO-1)的影响.方法 健康雄性SD大鼠48只,体重220～280 g,随机分为4组(n=12):假手术组(S组)、缺血再灌注组(IR组)、缺血预处理+缺血再灌注组(IP组)和缺血预处理+缺血再灌注+HO-1抑制剂组(HI组).采用结扎左冠状动脉前降支30 min再灌注120 min的方法建立心肌缺血再灌注模型.S组仅在冠状动脉下穿线;IP组于缺血前采用结扎/放松左冠状动脉前降支各5 min,重复3次的方法行缺血预处理;HI组于缺血预处理前1 d腹腔注射锌原卟啉Ⅸ 10 ms/ks,其余同IP组.于再灌注结束时测定心肌HIF-1α、HO-1的mRNA和蛋白表达、HO-1活性、SOD活性及MDA含量,计算心肌梗死面积,取动脉血样测定血清TNF-α和IL-6的浓度.结果 与S组比较,IR组、IP组和HI组心肌SOD活性降低,MDA含量升高,血清TNF-α和IL-6的浓度升高(P＜0.01);与IR组比较,IP组心肌SOD活性升高,MDA含量降低,血清TNF-α和IL-6浓度降低,心肌HIF-1α和HO-1的mRNA和蛋白表达上调,HO-1活性升高,心肌梗死面积减小(P＜0.01);与IP组比较,HI组心肌SOD活性降低,MDA含量升高,血清TNF-α和IL6浓度升高,心肌HO-1的mRNA和蛋白表达下调,HO-1活性降低,心肌梗死面积增加(P＜0.05或0.01),心肌HIF-1α的mBNA和蛋白表达差异无统计学意义(P＞0.05).结论 缺血预处理减轻大鼠心肌缺血再灌注损伤的机制与HIF-1α诱导HO-1活性增强有关.     

Hyperglycemia in streptozotocin-induced diabetic rat increases infarct size associated with low levels of myocardial HO-1 during ischemia/reperfusion

This study investigated the role of heme oxygenase (HO)-1 in the cardiac tissue injury of acute ischemia/reperfusion (I/R) in diabetic streptozotocin (STZ)-induced hyperglycemic rats. The effects of 1) hemin, an inducer of HO expression and activity, and 2) zinc protoporphyrin IX (ZnPP-IX), an inhibitor of HO activity, have also been investigated on the tissue injury by I/R and some mediators released in these circumstances. STZ hyperglycemic rats had impaired levels of HO-1 within the cardiac tissue and increased myocardial infarct size (IS) following I/R, as compared with the nondiabetic rats. In these rats, administration of hemin 4 mg/kg 18 h before I/R increases the levels of HO-1 within the tissue. However, the values of HO-1 assayed in these circumstances were significantly lower (P < 0.01) than those assayed in nondiabetic animals subjected to the same procedures; IS was much more extended (P < 0.01) than in the parent nondiabetic group. STZ hyperglycemic rats also predisposed the heart to produce high levels of the cytokines interleukin (IL)-1beta and CXCL8. Subsequent I/R further increased (P < 0.01) the cytokine production, an effect partly prevented by hemin treatment. This recovered the huge number of infiltrated polymorphonuclear (PMN) leukocytes within the cardiac tissue associated with the STZ hyperglycemic state and I/R damage.     

氯胺酮对兔肺缺血/再灌注损伤后细胞凋亡和Caspase-3mRNA表达的影响

目的 观察氯胺酮对兔肺缺血/再灌注损伤后细胞凋亡和Caspase-3 mRNA表达的影响.方法 90只兔建立单肺缺血再灌注模型后,被随机分成3组（每组30只）：对照组（C组）、缺血/再灌注组（I/R组）和氯胺酮组（KET组）.每组30只兔子又平均分成再灌注后1小时、3小时、5小时组.检测各组超氧物歧化物（SOD）活性、丙二醛（MDA）浓度、肿瘤坏死因子α（TNF-α）含量和凋亡指数（AI）变化.图像分析TUNEL染色和原位杂交对肺细胞凋亡及Caspase-3mRNA表达.结果各相同时间点I/R组比C组SOD活性显著降低（P〈0.01）,而MDA、TNF-α含量和AI明显升高（P〈0.01）;与I/R组比较,相同时间点KET组SOD活性升高,而MDA、TNF-α含量和AI则有不同程度降低（P〈0.01或P〈0.05）.肺再灌注后TUNEL法检测阳性细胞主要分布在肺泡上皮细胞和血管内皮细胞,Caspase-3 mRNA表达主要分布在血管内皮细胞;每个时间点I/R组Caspase-3 mRNA表达相比C组显著增加,同时肺细胞凋亡也显著增加.然而,使用氯胺酮后,两者都有明显减少.结论氯胺酮可通过减少缺血/再灌注后MDA、TNF-α含量,提高SOD活性,降低caspase-3 mRNA表达而抑制肺细胞凋亡,减轻再灌注后兔肺损伤.     

Protective effect of hemoglobin—induced heme oxygenase—1 on injured lungs caused by limb ischemia—reperfusion in rats

OBJECTIVE: To determine the role of hemoglobin (HB) induced heme oxygenase-1 (HO-1) in injured lungs caused by limb ischemia-reperfusion (I/R) in rats. METHODS: A rat model of ischemia in the hind limbs was made by clamping the infrarenal aorta with a microvascular clip, and lung injury occurred after reperfusion. To induce the expression of HO-1 in the lungs, Hb was administrated intraperitoneally at 16 hours before reperfusion. Northern blotting and Western blotting were used to detect the expression of HO-1 in the lungs, and the carboxyhemoglobin (COHb) level in arterial blood was assayed. The effect of hemoglobin (Hb) on the injured lungs after limb I/R was determined by measuring the changes of lung histology, polymorphonuclear (PMN) count, malondialdehyde (MDA) content and wet-to-dry weight ratio (W/D). Zinc protoporphyrin (ZnPP), an inhibitor of HO, was used to determine whether HO-1 was induced by Hb after lung injury. RESULTS: Hb led to a significant increase in HO-1 mRNA and protein expression in the lungs, accompanied by the increase of COHb level in arterial blood. Compared with the sham controls, the lung PMN count, MDA content and W/D significantly increased at 4 hours after limb I/R, which reversed by the pretreatment with Hb at 16 hours before reperfusion. ZnPP blocked this protective role of Hb in the injured lungs. CONCLUSIONS: Hb can induce the lung HO-1 expression, which plays an important role in the defense against I/R induced lung injury in rats.     

亚甲蓝预处理对大鼠肝缺血再灌注肺损伤的保护作用

目的研究肝缺血再灌注后肺损伤的机制以及亚甲蓝的保护作用。方法 36只SD大鼠随机分为假手术组（S组,n=12）、缺血再灌注组（I/R组,n=12）和亚甲蓝处理组（MB组,n=12）。阻断肝门30分钟后开放血流,建立大鼠全肝缺血再灌注模型。I/R组与MB组分别于肝门阻断前10分钟腹腔注射亚甲蓝10mg/kg或相应剂量生理盐水,于再灌注1小时取血、处死动物。假手术组不阻断肝门,于上述相应时间点注射生理盐水与取血、处死动物。肝肺病理切片光镜观察、肺干湿重比、肺组织丙二醛（MDA）含量、髓过氧化物酶（MPO）活力、血清TNF-α和IL-8含量。结果病理结果显示,亚甲蓝组缺血再灌注后肺损害程度较缺血再灌注组减轻。缺血再灌注组较假手术组肺组织干湿重比、MDA含量、MPO活性和血清TNF-α和IL-8含量升高（P〈0.01）,而亚甲蓝组较缺血再灌注组肺组织干湿重比和血清TNF-α和IL-8含量（P〈0.01）,MDA含量和MPO活性（P〈0.05）均有下降。结论肝缺血再灌注会导致肺损伤,缺血前给予亚甲蓝对大鼠肝I/R后肺损伤具有有保护作用。     

Effect of radix paeoniae rubra on expression of p38 MAPK/iNOS/HO-1 in rats with lipopolysaccharide-induced acute lung injury

Objective: To investigate the effect of radix paeoniae rubra (RPR) on expression of p38 mitogen activated protein kinase ( MAPK )/iNOS/HO-1 in rats with lipopolysaccharide-induced acute lung injury and explore the molecular mechanism.Methods: Forty healthy male Wistar rats, weighing 200-250 g, aged 6-8 weeks (mean =7 weeks), provided by the Experimental Center, Medical College, Wuhan University, Wuhan, China, were employed in this study.Under anesthesia with 7% chloraldurat (5 ml/kg body weight) through intraperitoneal injection, the trachea of the rat was exposed and an arterial puncture needle pricked into the trachea via cricothyroid membrane. Then they were randomly divided into five groups: 8 rats receiving 1 ml normal saline through the puncture needle (Group A),8 receiving 1 ml lipopolysaccharide (LPS, 2.5 mg/kg,Group B), 8 receiving LPS and RPR (30 mg/kg, pumped through the femoral vein for 2 hours, Group C ), 8 receiving RPR 2 hours before dripping LPS ( Group D),and 8 receiving hemin (75 μmol/L through intraperitoneal injection) 18 hours before dripping LPS (Group E). After 6 hours of LPS dripping, blood samples were obtained through the carotid artery to perform blood gas analysis,then all the rats were exsanguinated to death and specimens of lung tissues were obtained. The pathomorphological changes of the lung tissues were observed. The expression of p38 MAPK/iNOS/HO-1, the neutrophil ratio, protein content in alveolar irrigating solution and malonaldehyde (MDA) content in the lung tissues were also detected.Results: Compared with Group A, the expression of p38 MAPK, iNOS and HO-1 markedly increased in Groups B, C, D, and E (P ＜0.01). But in Groups C, D, and E,the expression of p38 MAPK and iNOS were significantly lower than that of Group B, while expression of HO-1 was obviously higher than that of Group B ( P ＜ 0.05 ). The protein content, the ratio of neutrophils in bronchoalveolar lavage fluid ( BALF), the content of MDA and the activities of serum NO in Group B were significantly higher than those of Group A ( P ＜ 0.01 ). There was a significant decrease in the level of arterial bicarbonate and partial pressure of oxygen in Group B (P ＜ 0.01). Compared with Group B, these indexes of lung injury were significantly lower while the levels of arterial bicarbonate and partial pressure of oxygen increased significantly in Groups C, D,and E (P ＜ 0.05 or P ＜ 0.01 ). Under light microscope, the pathological changes induced by LPS were significantly attenuated by RPR and hemin.Conclusions: The high expression of MAPK plays an important role in lipopolysaccharide-induced acute lung injury. Protective effect of RPR on lipopolysaccharideinduced acute lung injury may be related to the inhibition of the abnormal high expression of p38 MAPK/iNOS/HO-1.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.     

肢体缺血预处理对兔肺缺血再灌注损伤的影响

目的 探讨肢体缺血预处理对兔肺缺血再灌注损伤的影响.方法 健康日本大耳白兔18只,体重2.0～2.5 kg,雌雄不拘,随机分为3组(n=6):假手术组(S组)开胸后左侧肺门穿线但不结扎,旷置观察340 min;缺血再灌注组(IR组)开胸旷置100 min,阻断左侧肺门,左肺不张后60 min再灌注180 min;肢体缺血预处理组(L组)捆绑双后肢10 min,松开10 min,反复3次后恢复灌注,60 min后阻断左侧肺门60 min,再灌注180 min.于缺血前、再灌注15、30、60、120、180 min时采集左颈内动脉血样行血气分析,计算呼吸指数(R1);于再灌注180 min时处死动物,取左肺上叶组织,测定超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性及丙二醛(MDA)含量,计算肺湿干重比(W/D);取左肺下叶行支气管肺泡灌洗,计算肺通透性指数;取左肺中叶组织,观察肺组织病理学,进行弥漫性肺泡损伤(DAD)评分.结果 与s组比较,IR组RI、MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分升高,SOD活性降低(P<0.05或0.01);与IR组比较,L组RI,MDA含量、MPO活性、肺W/D、肺通透性指数和DAD评分降低,SOD活性升高(P<0.05或0.01);L组和S组间上述指标比较差异无统计学意义(P>0.05).L组和S组肺组织病理损伤程度较IR组减轻.结论 肢体缺血预处理可减轻兔肺缺血再灌注损伤.