CO2气腹对糖尿病兔胰腺功能影响的实验研究

目的探讨二氧化碳（CO2）气腹对糖尿病兔胰腺功能的影响。方法利用四氧嘧啶制作糖尿病兔模型,建立不同压力气腹,观察气腹前和气腹后0、2、6及12h各时间点血糖、淀粉酶、胰岛素、C肽、胰腺组织SOD活性及MDA含量的变化。结果气腹结束后,血糖、淀粉酶、胰岛素、C肽浓度和MDA含量较气腹前上升（P〈0.05）,SOD活性较气腹前下降（P〈0.05）。气腹结束后12h,10mmHg（1mmHg=0.133kPa）气腹组血糖、淀粉酶、胰岛素、C肽浓度和MDA含量与气腹前比较差异无统计学意义（P〉0.05）,15mmHg气腹组血糖、淀粉酶、胰岛素、C肽浓度和MDA含量仍较气腹前升高（P〈0.05）;SOD活性在2组均未恢复至气腹前水平（P〈0.05）。10mmHg和15mmHg气腹组相应时相之间,血糖和胰岛素变化差异无统计学意义（P〉0.05）,淀粉酶、C肽浓度、MDA含量和SOD活性变化差异有统计学意义（P〈0.05）。结论CO2气腹对糖尿病兔胰腺功能有损伤作用,损伤程度与气腹压力相关,较低的气腹压引起的胰腺损害更易逆转。     

CO2气腹对慢性肺功能不全兔肺功能影响的实验研究

目的探讨腹腔镜手术中建立的CO2气腹对慢性肺功能不全兔肺功能的影响和损伤机制. 方法依据随机原则,将50只健康雄性日本大耳白兔分为4组,即正常对照组(N0:n=5,免气腹),实验对照组(T0:n=5,免气腹),10 mmHg气腹实验组(T10:n=20, 10 mmHg气腹),15 mmHg气腹实验组(T15:n=20, 15 mmHg气腹).兔肺气肿模型稳定后,建CO2气腹,压力为10 mmHg(1.33 kPa)和15 mmHg(2.00 kPa)2种,作用时间2 h.分别在气腹前后各时点通过脉冲振荡法测4组肺功能(呼吸总阻力、中心阻力、总气道阻力). 结果兔肺气肿模型稳定后呼吸总阻力、中心阻力、总气道阻力升高.与气腹前相比,气腹结束时呼吸总阻力、中心阻力、总气道阻力显著下降(q=17.824, P<0.05;q=69.643, P<0.0.5;q=9.315,P<0.05),气腹后2 h表现为各值升至最高(q=48.631,P<0.05;q=107.842,P<0.05;q=57.213, P<0.05),此后开始降低,气腹后18 h升至比气腹结束时略高状态(q=26.313, P<0.05;q=73.499,P<0.05;q=23.547,P<0.05).15 mmHg(2.00 kPa)压力下变化更为显著. 结论在CO2 气腹条件下,慢性肺功能不全机体易发生血流动力学紊乱和肺通气障碍、顺应性降低,导致肺功能损伤,且气腹压力越高损伤越显著.     

肝肺撞击伤伴失血后CO2气腹对兔动脉血气影响的实验研究

目的探讨肝肺撞击伤伴失血后二氧化碳（CO：）气腹对兔动脉血气的影响及其机制。方法制作创伤性失血兔模型，按不同失血量（6ml／kg、12ml／kg、22ml／kg）及C02腹压（5mmHg、10mmHg、15mmHg）将75只新西兰大白兔按随机数字表分为9组（每组6只）。观察建立气腹前、气腹0．5h、2h及撤去气腹后0．5h呼吸频率（RR）、动脉血气（ABG）的变化和死亡率。结果大白兔在建立气腹前：随失血量的增加，RR、PaCO2上升显著；pH值先升高后降；PaO2则持续下降。大白兔在建立CO2气腹后：随时间延长，5mmHg、10mmHg压力组的RR先增后降；pH值、PaO2持续下降，PaCO2持续升高，而且在相同失血量的情况下各组间的pH值、PaO2随压力升高而降低，15mmHg气腹组RR及PaCO2显著高于其他组。在相同压力条件下，5mmHg、10／11／11Hg气腹压力组随失血增多RR加快、PaCO2增高，pH值、PaO2下降。撤去气腹后0．5h，各组内RR、PaO2、pH、PaCO2值向正常恢复。结论一定气腹压力（〈10mmHg）对创伤伴失血（〈12ml／kg）自主呼吸兔ABG的影响是可逆的；而高气腹压力（15mmHg）或大白兔失血量在12ml／kg以上时建立气腹将引起致死性后果。     

亚低温对肝缺血再灌注损伤的保护作用

目的　探讨亚低温对肝缺血再灌注损伤的保护作用机制。方法　将 18只犬随机分为 3组 :非缺血对照组 (n =6 )、缺血再灌注组 (n =6 )和亚低温处理组 (肝周充填碎冰块造成肝脏亚低温 ,n =6 )。对各组肝上下腔静脉血进行谷丙转氨酶 (ALT)、谷草转氨酶(AST)、乳酸脱氢酶 (LHD )以及丙二醛 (MDA)和超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT)、谷胱甘肽过氧化酶 (GSH PX)活性及总抗氧化 (TAX )能力测定。结果　全肝缺血再灌注后ALT ,AST ,LDH和MDA含量明显上升 (P <0 .0 1) ,SOD ,CAT ,GSH PX活性及TAX能力明显下降 (P <0 .0 1) ;而亚低温处理组与缺血再灌注组比较 ,ALT ,AST ,LDH和MDA含量明显下降 (P <0 .0 1) ,SOD ,CAT ,GSH PX活性及TAX能力明显上升 (P <0 .0 1,P <0 .0 5 )。结论　亚低温能增强肝组织自身抗氧化能力 ,减轻肝缺血再灌注后氧自由基对肝脏的损伤。     

脑死亡供体鼠吸入一氧化碳对受体鼠移植肺损伤的影响

目的 评价脑死亡供体鼠吸入一氧化碳(CO)对受体鼠移植肺损伤的影响.方法 雄性Wistar大鼠24只,体重250～300 g,随机分为3组(n=8),接受非脑死亡供体肺组(NBD组)供体鼠颅内置入Fogarty导管,但不诱导脑死亡,观察2.5 h;接受吸入氧气的脑死亡供体肺组(BDO2组)供体鼠确认脑死亡后吸入40%氧气2 h;接受吸入CO的脑死亡供体肺组(BDCO组)供体鼠确认脑死亡后吸入40%氧气和0.025%CO混合气2 h.处理结束后取供体左肺,进行原位异体肺移植,受体鼠每30 min进行一次动脉血气分析.肺移植成功后2 h处死受体鼠,采集右股动脉血样,采用嘌呤氧化酶法测定血浆超氧化物歧化酶(SOD)活性;采用硫代巴比妥酸法测定丙二醛(MDA)浓度;采用ELISA法测定血浆白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α和IL-10浓度.计算移植肺组织湿/干重比(W/D);测定移植肺组织髓过氧化物酶(MPO)活性,并进行移植肺组织损伤评分.结果 与C组比较,BDO2组和BDCO组PaO2/FiO2、BE、pH值和血浆SOD活性、IL-10浓度降低,移植肺组织W/D、MPO活性、损伤评分和血浆MDA、IL-6、TNF-α浓度升高(P<0.05);与BD02组比较,BDCO组PaO2/FiO2、BE、pH值和血浆SOD活性、IL-10浓度升高,移植肺组织W/D、MPO活性、损伤评分和血浆MDA、IL-6、TNF-α浓度降低(P<0.05).结论 脑死亡供体鼠吸入CO 2 h可减轻受体鼠移植肺损伤,其机制可能是吸入CO提高了移植肺的抗氧化能力,减轻了移植后局部和全身炎性反应.     

褪黑素对梗阻性黄疸大鼠肝损伤保护作用的实验研究

目的探讨氧化性损伤在大鼠梗阻性黄疸肝功能损害发生中的作用以及褪黑素对其的保护作用。方法成年雄性SD大鼠64只,采用完全随机化法随机分为正常对照组（CN组,n=16）、假手术组（SO组,n=16）、胆总管结扎组（BDL组,n=16）和胆总管结扎＋褪黑素治疗组（BDL＋MT组,n=16）。应用胆总管结扎法建立梗阻性黄疸模型,褪黑素治疗组大鼠手术前1 d至手术后7 d连续腹腔注射褪黑素0.5 mg（/kg.d）,每日10∶00给药。分别于手术后第4 d和第8 d两个时间点采集标本,检测血浆中总胆红素（TBIL）、丙氨酸转氨酶（ALT）、门冬氨酸转氨酶（AST）、碱性磷酸酶（AKP）及γ-谷氨酰转肽酶（GGT）水平变化,比色法测定肝组织匀浆中丙二醛（MDA）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-Px）含量或活力变化,采用TUNEL法检测肝组织细胞凋亡,并计算肝细胞凋亡指数（AI）。结果与CN组和SO组比较,BDL组大鼠血浆TBIL、ALT、AST、AKP、GGT水平和肝组织MDA含量明显升高（P〈0.05,P〈0.01）,SOD、CAT、GSH-Px活力或GSH含量显著降低（P〈0.01）,AI增加（P〈0.01）;褪黑素治疗可使血浆TBIL、ALT、AST、AKP、GGT和肝组织MDA含量显著降低,SOD、CAT、GSH-Px活力或GSH含量明显升高（P〈0.01）,AI减少（P〈0.01）。BDL组肝组织MDA含量与血浆TBIL、ALT、AKP、AST、GGT水平均呈显著正相关（P〈0.01）,GSH、SOD、CAT、GSH-Px与血浆TBIL、ALT、AKP、ALT、AST水平分别均呈显著负相关（P〈0.01）;BDL组肝组织MDA含量的变化与AI呈正相关（P〈0.01）,而GSH含量及SOD、CAT、GSH-Px活力分别与AI呈负相关（P〈0.01）。结论大鼠梗阻性黄疸时,肝组织自由基大量产生介导的氧化性损伤及其细胞凋亡,参与了肝功能损害的发生、发展。褪黑素对大鼠梗阻性黄疸肝功能损害有一定程度的保护作用,其机制可能与其拮抗肝组织过氧化和细胞凋亡有关。     

外源性一氧化碳改善供体肺功能的实验研究

目的观察一氧化碳(CO)对长时间低温保存的供体肺的保护作用。方法建立大鼠肺移植离体肺灌注实验模型:SD大鼠24只随机分为空白对照组、实验组(CO组),每组6对作为肺移植的供体鼠和受体鼠。对照组大鼠供肺移植全程吸入100%氧气直至再灌注后1h;CO组移植全程吸入500×10-6CO和O2的混合气,并且供体肺在冷保存的12h内肺内仍充盈着CO和O2的混合气,余同对照组。于供体肺循环灌注l,20,40,60min测定供肺氧合后动脉血氧分压(PaO2)、平均肺动脉压、气道峰压;灌注结束后测定肺组织湿干比、丙二醛(MDA)含量、髓过氧化物酶(MPO)活性、白细胞介素8(IL-8)的含量。结果作为受体的12只(每组6只)进入结果分析:①CO组供体肺的PaO2在再灌注20、40、60min明显高于对照组,平均动脉压、气道峰压分别在再灌注20、40、60min和40、60min明显低于对照组(P<0.05);②与空白对照组比较,CO组供体肺再灌注后湿干比、MDA、MPO、IL-8含量均明显降低(P<0.05)。结论在肺移植的全程吸入低剂量CO可以减轻供肺的缺血再灌注损伤,改善供肺功能。     

缺血预处理对家兔肢体缺血再灌注后肺抗氧化系统的影响

目的：观察肢体缺血预处理对家兔肢体缺血再灌注后肺损伤时肺抗氧化系统的影响并探讨其机制。方法：健康家兔30只，随机分为假手术对照组（SC）、缺血再灌注组（IR）和缺血预处理组（IPC），每组10只。实验结束时，取肺组织测定超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—PX）、黄嘌呤氧化酶（XOD）活性和丙二醛（MDA）、一氧化氮（N0）含量，同时计算肺系数及进行肺病理学检查。结果：肢体缺血再灌注后肺组织SOD、GSH-PX活性和NO含量显著下降，XOD活性和MDA含量明显增高，肺系数升高，肺组织病变明显，肢体缺血预处理可明显缓解上述变化。结论：家兔肢体缺血再灌注后，肺抗氧化功能下降参与肺脏的损伤过程，肢体缺血预处理对这种肺损伤有明显的保护作用。     

丹参和β-七叶皂甙钠对烧伤后急性肺损伤治疗作用的实验研究

目的：探讨丹参和β-七叶皂甙钠对烧伤后急性肺损伤的治疗作用及其可能机制。方法：采用大鼠30%TBSAⅢ度烫伤模型，将45只大鼠随机分为假烫组、盐水组、丹参组、β-七叶皂甙钠组及联合组，烫伤后24h取静脉血侧外周血白细胞粘附聚集（LAA），取肺组织检测髓过氧化物酶（MPO）、丙二醛（MDA）、超氧化物歧化酶（SOD）含量。结果：丹参组、β-七叶皂甙钠组及联合组外周血LAA、肺组织MPO及MDA均低于盐水组，联合组最低。丹参组、β-七叶皂甙钠组及联合组SOD较盐水组明显增高，联合组最高。外周血LAA与肺组织MPO含量呈正相关。结论：丹参及β-七叶皂甙钠均可减轻中性粒细胞（PMN）在肺内的聚集、粘附，减轻氧自由基（OFR）及其代谢产物对肺组织的损伤，增强SOD对机体的保护作用，联合应用效果更佳。     

星状神经节阻滞对兔机械通气所致肺损伤的保护作用

目的 探讨星状神经节阻滞(stellate ganglion block,SGB)对兔呼吸机相关性肺损伤(ventilator associated lunginjury,VALI)的影响. 方法 40只成年日本大耳兔按随机数字表法分为两组(每组20只):空白对照组(Ⅰ组)和SGB组(Ⅱ组).Ⅰ组全身麻醉气管插管后椎旁注入生理盐水(0.5 ml),Ⅱ组全身麻醉气管插管后给予SGB.分别于机械通气后1 h(T1)、2 h(T2)、4 h(T3)、6 h(T4)4个时间点经耳缘静脉抽取静脉血3ml后处死白兔,检测血清丙二醛(malondialdehyde,MDA)、TNF-α浓度及超氧化物歧化酶(superoxide dismutase,SOD)活性;取左肺组织测量湿/干重比(wet/dry,W/D);取一部分右肺组织H-E染色后光镜和电镜观察其病理变化,另一部分匀浆后检测MDA含量、髓过氧化物酶(myeloperoxidase,MPO)及SOD活性. 结果 与Ⅰ组比较,Ⅱ组肺组织的W/D[(6.07±0.12)比(8.58±0.48)]和SOD活性[(64±10) U/mg比(77±11) U/mg]明显降低(P＜0.01);Ⅱ组肺组织的MDA含量[(0.89±0.12) μmol/g比(0.63±0.11) μmoFg]和MPO活性[(0.46±0.09) U/g比(0.28±0.07)U/g]明显升高(P＜0.01).H-E染色后光镜和电镜观察Ⅱ组肺组织病变轻于Ⅰ组.与Ⅰ组比较,Ⅱ组血清MDA、TNF-α在T2～T4时间点降低(P＜0.05),Ⅱ组血清SOD在T2-T4时间点升高(P＜0.05). 结论 SGB可以减轻机械通气兔肺组织的损伤,产生肺保护作用.     

Effects of carbon dioxide pneumoperitoneum on free radical formation in lung and liver tissues

BACKGROUND: The purpose of this study was to investigate the possible effects of carbon dioxide (CO2) pneumoperitoneum on free radical formation and lipid peroxidation in the lung and liver tissues of rats. METHODS: For this study, 50 male Sprague-Dawley rats were divided into five equal groups: control (group 1); sham operation (group 2); 5, 10, or 15 mmHg (group 3, 4, or 5) pneumoperitoneum with CO2 groups. At the end of the procedures, the rats were killed, and perfusion was performed via vena jugularis with cold Ringer's lactate. After the perfusion procedure, the lung and liver were harvested, and the supernatant fractions of the lungs and livers were assayed for superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA). RESULTS: Both the lung and liver CAT activities were elevated consistently and significantly in the order of the study groups, as compared with the previous groups (p < 0.01 for all comparisons). The lung and liver SOD levels were elevated in groups 4 and 5, as compared with the other groups (p < 0.05). The lung MDA was significantly higher in groups 3 and 4, but not in group 5. Significant elevation in liver MDA was noted only in the 5-mmHg pnemoperitoneum group (p < 0.05). CONCLUSIONS: These results indicate that CO2 pneumoperitoneum applied with 5, 10, or 15 mmHg pressure increases the formation of free oxygen radicals, which is counterbalanced by increased SOD and CAT activities of the lung and liver tissues. This effect of CO2 pneumoperitoneum on free radicals and lipid peroxidation appears to be pressure dependent in rats. The mechanism underlying this pressure dependency is still under investigation.     

The effects of methylene blue on lung injury in septic rats

PURPOSE: We aimed to investigate the effects of methylene blue (MB) on NO production, myeloperoxidase (MPO) activity, antioxidant status and lipid peroxidation in lung injury during different stages of sepsis in rats. MATERIAL AND METHODS: Rats were randomly divided into 4 groups (n = 20): group C, sham operated; group CMB, sham operated and receiving MB (25 mg/kg, i.p.); group S, sepsis; group SMB, sepsis and receiving MB (25 mg/kg, i.p.). Sepsis was induced by cecal ligation and puncture (CLP). The MB dose was administered after CLP. Each group was subdivided into two subgroups (n = 10) which were sacrificed at 9 or 18 h after the surgical procedure. The levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) and MPO activity, total nitrite/nitrate and malondialdehyde (MDA) in the lung tissue were measured. Lung injury was graded from 1 (injury to 25% of the field) to 4 (diffuse injury) by the pathologist. RESULTS: In group SMB, while SOD and CAT increased in both early and late sepsis periods, GSH-PX increased significantly only in the early sepsis period when compared with group S. Increase in lung MPO activity after CLP-induced sepsis was prevented by MB administration. MB significantly decreased to nitrite/nitrate and MDA levels both in early and late sepsis periods when compared with group S (p < 0.05). Group S showed a marked increase in neutrophil infiltration into the interstitial space and thickening of the alveolar septa, whereas the alveolar damage score was lower in the SMB group (p < 0.05). CONCLUSION: MB reduced the MPO activity and lipid peroxidation by both decreasing oxidative stress and NO overproduction in the lungs, which resulted in the attenuation of lung injury after CLP-induced sepsis in rats.     

Lycopene inhibits caspase-3 activity and reduces oxidative organ damage in a rat model of thermal injury

Oxidative stress has been implicated in various pathological processes including burn induced multiple organ damage. This study investigated the effects of lycopene treatment against oxidative injury in rats with thermal trauma. Under ether anesthesia, shaved dorsum of the rats was exposed to 90°C bath for 10s to induce burn and treated either vehicle (olive oil) or lycopene (50mg/kg orally). Rats were decapitated 48 h after injury and the tissue samples from lung and kidney were taken for histological analysis and the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT) and caspase-3 activities. Proinflammatory cytokines, TNF-α and IL-1β, were assayed in blood samples. Severe skin scald injury caused a significant decrease in GSH levels, SOD and CAT activities, and significant increases in MDA levels, MPO and caspase-3 activities of tissues. Similarly, plasma TNF-α and IL-1β were elevated in the burn group as compared to the control group. Lycopene treatment reversed all these biochemical indices. According to the findings of the present study, lycopene possesses antiinflammatory, antiapoptotic and antioxidant effects that prevents burn-induced oxidative damage in remote organs.     

Re-Protective Effects of Pre- and Post-Laparoscopy Conditioning,Zinc, Pentoxifylline,and N-acetylcysteine in an Animal Model of Laparoscopy-Induced Ischemia/Reperfusion Injury of the Kidney

Background. Pneumoperitoneum (P) created to facilitate laparoscopy (L) is associated with splanchnic hypoperfusion, ischemia/reperfusion (I/R) injury, and oxidative stress. Aim. This study investigated the effects of pre- and post-laparoscopic conditioning, zinc, pentoxifylline (PTX), and N-acetylcysteine (NAC) on markers of I/R injury in an animal model. Methods. Sprague-Dawley male rats (n?=?56, weight range 300–350 g) were randomly placed in one of seven treatment groups. Except for group C (control group who underwent a sham operation without pneumoperitoneum), pneumoperitoneum was created in all using CO₂ insufflation under a pressure of 15 mmHg. Group L (laparoscopy) was subjected to 60 min of pneumoperitoneum. Group Lpre (laparoscopic preconditioning plus laparoscopy) was subjected to 5 min of insufflation and 5 min of desufflation followed by 60 min of pneumoperitoneum. Group Lpost (laparoscopy plus laparoscopic post-conditioning) was subjected to 60 min of pneumoperitoneum and 60 min of desufflation followed by 5 min of insufflation and 5 min of desufflation. The laparoscopy plus zinc (LZ), PTX (LP), and NAC (LNAC) groups received a single intraperitoneal injection of zinc (50 mg/kg), pentoxifylline (50 mg/kg), or N-acetylcysteine (150 mg/kg) 5 min before the desufflation period. Animals were sacrificed at the end of the experiments, and kidney samples were tested for malondialdehyde (MDA), catalase (CAT), glutathione peroxidase (GPX), and superoxide dismutase (SOD). Results. MDA levels, as an indicator of oxidative stress in kidney tissue samples, were significantly higher in all pneumoperitoneum groups compared to Group C, except for Group Lpre. The pattern of change in tissue levels of SOD, GPX, and catalase was variable in the different treatment groups. Conclusions. In this animal model of renal ischemia/reperfusion injury, laparoscopy caused renal ischemia as evidenced by elevated markers of tissue ischemia-reperfusion injury. This effect was significantly attenuated by post-laparoscopy conditioning, zinc, pentoxifylline, and N-acetylcysteine, but not by pre-laparoscopy conditioning.     

Starvation-related alterations in free radical tissue defense mechanisms in rats

Alterations in endogenous free radical-scavenging defense mechanisms of rat tissues after body weight loss (induced by starvation for 72 h) associated with hypoinsulinemia were investigated. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and glutathione (GSSG) reductase as well as levels of reduced glutathione (GSH) were examined in several tissues and in erythrocytes. A complex pattern of changes was observed. CAT activities were increased in the heart and pancreas and decreased in the liver. SOD levels were decreased in the heart and increased in the kidney and pancreas. GSH-PX activities were increased only in the kidney, and levels of GSH were decreased only in the liver of starved animals. Erythrocytes from starved animals showed no alterations in the levels of major free radical-scavenging enzymes. However, GSSG reductase levels were lower in erythrocytes from starved animals, and this was associated with an increased susceptibility to H2O2-induced GSH depletion. Paradoxically, H2O2-induced malondialdehyde (MDA) production in erythrocytes from starved animals was lower than that in control erythrocytes. Our results suggest that, in studies of experimental diabetes, attention must be given to the influence of body weight loss per se on the biochemical alterations associated with this disease.     

The effect of carbon dioxide pneumoperitoneum on free radicals

Background: Carbon dioxide is usually preferred as the insufflating agent for laparoscopic surgery because it is readily available, noncombustible, and chemically stable. It is still questionable, however, if CO₂ pneumoperitoneum has any effect on free radicals and lipid peroxidation. The purpose of this study was to investigate the possible effects of CO₂ pneumoperitoneum on free radicals and lipid peroxidation in the erythrocytes of rats. Methods: Fifty male Sprague-Dawley rats were divided into five equal groups: controls, a sham-operation group, and three groups of 5, 10, or 15 mmHg pneumoperitoneum with CO₂. At the end of the procedure, blood was collected and the erythrocytes were separated from the plasma. The resultant supernatant fractions of erythrocytes were assayed for superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA). Results: SOD activities of the 5 and 10 mmHg pneumoperitoneum groups were significantly lower than those of the sham operation group. SOD activity was greater in the 15 mmHg pneumoperitoneum group than in any of the other groups, and this activity was significantly different from that seen in the 5 and 10 mmHg pneumoperitoneum groups (p < 0.05). No significant changes were observed in the CAT activities of the study groups (p > 0.05). MDA level was increased in the 5 mmHg pneumoperitoneum group; this result was statistically different from the control and 15 mmHg pneumoperitoneum groups (p < 0.05). No significant differences were found in the CAT activities for the study groups. On the other hand, the SOD activities of the 5 and 10 mmHg pneumoperitoneum groups were significantly lower than those of the sham and the 15 mmHg pneumoperitoneum group (p < 0.05 for all comparisons). Conclusions: These results indicate that CO₂ pneumoperitoneum applied with 5–10 mmHg pressure increases the formation of free oxygen radicals by inhibiting SOD activity and that the accumulation of free radicals elevates the level of MDA, a metabolite of lipid peroxidation. The effect of CO₂ pneumoperitoneum on free radicals and lipid peroxidation is pressure-dependent in rats. The mechanism underlying this pressure dependency is still under investigation. Received: 16 December 1999/Accepted: 14 February 2000/Online publication: 10 May 2000     

Pretreatment with edaravone reduces lung mitochondrial damage in an infant rabbit ischemia-reperfusion model

Purpose

Free radical scavenger edaravone has been approved as a new drug for treatment of stroke patients. The purpose of this study was to examine whether pretreatment with edaravone could attenuate ischemia-reperfusion (IR)-induced lung damage in infant rabbits.

Methods

New Zealand White rabbits (Experimental Animal Center, Nanjing Medical University, Nanjing, China) at age from 15 to 21 days were subjected to sham operation, IR, or edaravone plus IR. Ischemia/reperfusion was induced by clamping the right pulmonary hilum for 1 hour and then removal of the clamp for 4 hours. Edaravone (1 mg/kg, intravenous) was given 5 minutes before ischemia. Concentrations of reactive oxygen species-hydroxyl radical (ROS-HR) and malondialdehyde (MDA), and activities of glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) in the lung tissue were measured. Mitochondrial membrane potential, swelling rate, and ultrastructure of the lung were analyzed, and histologic condition of the lung was evaluated.

Results

Edaravone pretreatment reduced markedly the productions of ROS-HR and MDA and increased the activities of GSH-PX and SOD. It attenuated both IR-induced decrease in mitochondrial membrane potential from 60% to 14% and IR-induced increase in mitochondrial swelling. As results, the mitochondrial and lung tissue damages were less, leading to an improved survival rate in IR rabbits pretreated with edaravone compared with IR rabbits without the treatment.

Conclusion

Edaravone pretreatment reduces the IR-induced lung mitochondrial damage in infant rabbits.     

The effect of hypericum perforatum on kidney ischemia/reperfusion damage

It has been revealed in recent studies that Hypericum Perforatum (HP) is influential on cancer, inflammatory diseases, bacterial and viral diseases, and has neuroprotective and antioxidant properties. In this study, we investigated the effect of HP, which is known to have antioxidant and anti-inflammatory effects, on kidney I/R damage. Male Sprague–Dawley rats were divided into three groups, and each of the groups had eight rats: The Control Group; the Ischemia/Reperfusion (I/R) Group; and the IR?+?HP Group which was treated with 50?mg/kg of HP. The right kidneys of the rats were removed, and the left kidney developed ischemia during the 45th min, and reperfusion occurred in the following 3rd h. The histopathological findings and also the level of Malondialdehyde (MDA), Glutathione (GSH) and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX) enzyme activations in the renal tissues were measured. Blood Urea Nitrogen (BUN), Creatinin (Cre) from serum samples were determined. The levels of BUN, Cre, and kidney tissue MDA increased at a significant level, and the SOD, CAT, and GSH-PX enzyme activity decreased at a significant level in the I/R group, compared with the Control Group (p?p?相似文献   

Effect of a pneumoperitoneum on systemic cytokine levels, bacterial translocation, and organ complications in a rat model of severe acute pancreatitis with infected necrosis

Background Infection of pancreatic necrosis (IPN) is strongly associated with sepsis and multiple organ dysfunction and is an absolute indication for surgery. Patients with IPN are critically ill at the time of surgery and may benefit from a minimally invasive approach with reduced surgical trauma. Recently, several minimally invasive necrosectomy techniques have been reported. However, the effects and potential dangers of a pneumoperitoneum in IPN cases are unknown. This study aimed to determine the effects of a pneumoperitoneum on systemic cytokine levels, bacterial translocation, and systemic organ complications in a rat model of IPN. Methods For this study, IPN was induced in Wistar rats using retrograde intraductal infusion of 3% taurocholate. After 8 h, the animals were subjected to either laparoscopy (pneumoperitoneum at 8 mmHg) or laparotomy for 1 h and killed after 1 or 3 h. Severe acute pancreatitis with IPN was proved by serum amylase and lipase, histology, tissue activity of myeloperoxidase (MPO), and bacteriology. Systemic levels for interleukin-10 (IL-10), IL-6, tumor necrosis factor-alpha (TNF-α), and lipopolysaccarides were determined by enzyme-linked immunoassay (ELISA). Systemic organ damage and dysfunction were evaluated using MPO activity (lung), serum creatinine (kidney), and serum aminotransferases (liver). Results Necrotizing pancreatitis developed in all the animals. Most of the animals (85%) had proven infected necrosis. Elevated cytokine levels and deteriorated organ parameters demonstrated systemic inflammation and organ failure. Although there was a tendency toward a higher level of proinflammatory cytokines after laparotomy, there were no significant differences between laparotomy and laparoscopy. Furthermore, these alterations were not accompanied by any differences in bacterial translocation (lipopolysaccharides), systemic organ damage, or mortality between laparoscopy and laparotomy. Conclusions In the current model of infected pancreatic necrosis, a pneumoperitoneum did not result in increased cytokine release or bacterial translocation. However, the putative advantage of less surgical trauma with the laparoscopic approach did not play a significant role in the setting of severe acute pancreatitis with IPN.