缺血预处理联合后处理对大鼠肾缺血再灌注损伤的影响

目的 评价缺血预处理联合后处理对大鼠肾缺血再灌注损伤的影响.方法 健康雄性SD大鼠30只,体重250～280 g,随机分为5组(n=6):假手术组(S组)、缺血再灌注组(I/R组)、缺血预处理组(IP组)、缺血后处理组(IPo组)和缺血预处理联合后处理组(IP+IPo组).S组仅开腹,游离双侧肾脏,分离双侧肾蒂但不夹闭.采用夹闭双侧肾蒂45 min、再灌注6 h的方法 制备肾缺血再灌注模型.IP组夹闭双侧肾蒂5 min,再灌注5 min,反复3次,余操作同I/R组;IPo组夹闭双侧肾蒂45 min后,再灌注10 8,缺血10 s,反复3次,再灌注6 h.于再灌注6 h时,经心脏抽血后迅速处死大鼠取肾,测定血清肌酐(Cr)和尿素氮(BUN)的浓度;采用硫代巴比妥酸法测定肾组织丙二醛(MDA)含量,采用黄嘌呤氧化酶法测定肾组织超氧化物歧化酶(SOD)活性;光镜下观察肾组织病理学结果 ;TUNEL法检测肾组织凋亡细胞,计算凋亡指数(AJ).结果 与S组比较,其余各组血清Cr和BUN的浓度升高,肾组织SOD活性降低,MDA含量和AI升高(P<0.05);与I/R组比较,IP组、IPo组和IP+IPo组血清Cr和BUN的浓度降低,肾组织SOD活性升高,MDA含量和AJ降低(P<0.05),肾损伤减轻;与IP组和IPo组比较,IP+IPo组肾组织SOD活性升高,AI降低(P<0.05),肾损伤减轻.结论 缺血预处理联合后处理可减轻大鼠肾缺血再灌注损伤,较单独应用时效果好.     

乳化异氟醚预处理对大鼠肾缺血再灌注损伤的影响

目的 评价乳化异氟醚预处理对大鼠肾缺血再灌注损伤的影响.方法 选择雄性SD大鼠32只,体重220～300 g,10～ 13周龄,采用随机数字表法,将其分为4组(n=8):假手术组(S组)、肾缺血再灌注组(I/R组)、乳化异氟醚预处理组(E组)和脂肪乳剂预处理组(I组).I/R组、E组和I组采用夹闭左侧肾蒂45 min后恢复再灌注的方法建立肾缺血再灌注模型.E组和I组分别静脉输注8%乳化异氟醚、30%脂肪乳剂4ml·kg-·h-30 min,洗脱15 min后制备模型.于再灌注3h时采集腹主动脉血样5ml,测定血清肌酐(Cr)、胱抑素C(Cys C)、TNF-α、IL-6、IL-10浓度;取左肾组织,行HE染色,光镜下观察病理学结果,并行肾脏近曲小管坏死程度分级.结果 与S组比较,其余3组血清Cr、Cys C、TNF-α、IL-6、IL-10浓度及肾脏近曲小管坏死程度均升高(P＜0.05);与I/R组和I组比较,E组血清Cr、Cys C、TNF-α、IL-6浓度及肾脏近曲小管坏死程度均降低(P＜0.05),血清IL-10浓度升高(P＜0.05).I/R组和I组上述各指标比较差异无统计学意义(P＞0.05).I/R组和I组肾组织病理学损伤严重,E组肾组织病理学损伤明显减轻.结论 8％乳化异氟醚预处理可减轻大鼠肾缺血再灌注损伤,其机制可能与抑制全身炎性反应有关.     

缺血预处理与肝脏缺血再灌注损伤的研究

目的 :观察缺血预处理对肝脏再灌注损伤的影响。方法 :通过构建正常大鼠和肝硬化大鼠肝脏 70 %的原位热缺血再灌注损伤模型 ,比较缺血预处理和无预处理组及间歇阻断肝门法对再灌注损伤的影响 ;以肝功酶、能量代谢和过氧化损伤等生物化学指标、组织学病理和细胞超微结构的形态学指标 ,观察不同预处理条件对结果的影响。结果 :各项指标显示 ,正常大鼠中 ,缺血预处理与无预处理组相比 ,可显著减轻再灌注损伤 (P <0 .0 5 ) ,与间歇性阻断肝门组相比也有显著性意义 (P <0 .0 5 ) ;在各个缺血预处理组内 ,缺血预处理 5min(IPC5min)组较IPC10min组和IPC5min× 2 组效果好 (P <0 .0 5 ) ,证实缺血预处理对肝硬化大鼠肝脏再灌注损伤有保护作用。结论 :缺血预处理可减轻肝脏再灌注损伤 ,并优于间歇性阻断肝门法 ,是一种应用方便、效果较好、前景广阔的阻断肝脏血供的新方法     

七氟醚预处理对大鼠肺缺血再灌注时肺组织血管紧张素转化酶mRNA表达的影响

目的 探讨七氟醚预处理对大鼠肺缺血再灌注时肺组织血管紧张素转化酶(ACE) mRNA表达的影响.方法 成年雄性SD大鼠54只,体重250 ～ 320 g,采用随机数字表法,将其分为3组(n=18):假手术组(S组)仅游离左肺门,但不阻断;肺缺血再灌注组(I/R组)采用阻断左肺门45 min后再灌注120 min的方法制备大鼠肺缺血再灌注模型;七氟醚预处理组(SP组)吸入2.1％七氟醚30min,停止吸入后10 min时后制备肺缺血再灌注模型.于再灌注30、60和120 min时随机取6只大鼠,处死取肺组织,测定湿/干重比(W/D比),采用比色法测定髓过氧化物酶(MPO)活性,采用RT-PCR法测定ACE mRNA的表达,光镜下观察肺组织病理学结果.结果 与S组比较,I/R组和SP组再灌注各时点肺组织W/D比、MPO活性和ACE mRNA表达水平均升高(P＜0.05);与I/R组比较,SP组再灌注各时点肺组织W/D比、MPO活性和ACE mRNA表达水平降低(P＜0.05).SP组肺组织病理学损伤较I/R组减轻.结论 七氟醚预处理可能通过下调ACE mRNA的表达从而减轻大鼠肺缺血再灌注损伤.     

丙泊酚对大鼠急性肾缺血再灌注损伤的影响

目的 探讨丙泊酚预处理对急性肾缺血再灌注损伤(acute renal ischemia reperfusion injury ,ARIRI)的保护作用及其机制.方法 采用完全随机研究设计(randomized controlled trial,RCT),健康近交系清洁级的雄性SD大鼠63只,随机分为3组:假手术组(A组)、缺血再灌注组(B组)、丙泊酚预处理组(C组),每组21只SD大鼠.采用切除右侧肾,用无损伤微动脉夹夹闭左侧肾蒂60分钟后解除阻断,建立大鼠急性肾缺血再灌注损伤模型.用24号套管针股静脉穿刺置管,实验过程中各组使用微量注射泵注入不同注射液.分别于手术前15分钟、再灌注后2小时、24小时留取血和肾组织标本同时处死大鼠,检测血清尿素氮(BUN)、肌酐(Cr)、超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及观察这三个时点肾组织的病理学改变.结果 丙泊酚预处理组各个时点的肾组织病理学变化均轻于缺血再灌注组.缺血再灌注组中血清BUN、Cr、MDA和TNF-α水平增加均高于丙泊酚预处理组(p＜0.05),丙泊酚预处理组血清SOD、IL-6水平均高于缺血再灌注组(p＜0.05).结论 丙泊酚预处理组血清BUN、Cr、MDA、TNF-α、SOD、IL-6水平与缺血再灌注组均有统计学差异.结果 表明丙泊酚能减少氧自由基释放,抑制和减少炎症反应,在急性肾缺血再灌注损伤能起到保护肾脏的作用.     

硫化氢预处理延迟相对大鼠心肌缺血-再灌注损伤的保护作用

目的探讨硫化氢预处理延迟相对大鼠心肌缺血-再灌注损伤的保护作用。方法将30只健康成年SD雄性大鼠随机分为三组:假手术组(S组)、缺血-再灌注组(IR组)和硫化氢组(H组)。S组仅开胸并分离冠状动脉左前降支,但不阻断血流150min;IR组行冠状动脉左前降支阻断30min,再灌注120min;H组予以静脉注射NaHS0.05mg/kg,给药后24h同IR组处理。再灌注结束后检测血清超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量和心肌梗死面积,电镜观察各组心肌细胞超微结构变化。结果与IR组比较,H组MDA含量降低,SOD活性增高(P<0.05),心肌梗死面积减少(P<0.05),电镜下H组心肌细胞损伤程度减轻。结论硫化氢预处理延迟相对大鼠缺血-再灌注心肌具有保护作用,与抗氧化反应有关。     

缺血预处理对大鼠急性缺血-再灌注肾细胞凋亡的影响

目的:探讨缺血预处理对急性肾缺血-再灌注细胞凋亡的影响。方法:采用8 min缺血加5 min再灌注预处理在体肾缺血-再灌注模型(I45 min I-R 6h),将实验动物随机分为正常(A组)、假手术(S组)、单纯缺血(B组)、缺血再灌注(C组)、预处理(D组)五组,采用透射电镜、流式细胞仪检测肾细胞凋亡和细胞增殖周期,利用光学显微镜进行组织学观察,同时测定血清中尿素氮(BUN)、肌酐(Cr)及MDA含量。结果:与A、S组相比,C组细胞凋亡率显著增高(P<0.01);与C组相比,D组细胞凋亡率和细胞增殖指数均降低(P<0.01),G0/G1时段增加(P<0.01),肾组织损伤病理评分显著降低(P<0.05),同时肾超微结构破坏较轻。结论:缺血预处理对急性肾缺血-再灌注有保护作用,可以减轻急性肾缺血-再灌注引起的细胞凋亡,其作用机制可能与调节细胞增殖周期有关。     

苦参碱预处理对预防大鼠肝脏缺血再灌注损伤的作用观察

目的:探讨苦参碱(MT)预处理对大鼠肝脏缺血再灌注损伤的影响.方法:50只雄性SD大鼠随机分为5组:假手术组(SO组)、缺血再灌注组(NS组)和不同剂量MT(3.75、7.5、15 mg/kg)预处理组(MT1、2,3组).动物麻醉后分别经门静脉注入生理盐水或MT,然后阻断左、中叶肝蒂45 min,造成70%肝脏缺血,SO组仅行分离不阻断,再恢复供血40 min.术后采集下腔静脉血测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)水平,取肝组织测定超氧化物歧化酶(SOD)与丙二醛(MDA)水平,并行肝组织病理学观察.结果:MT预处理组血清ALT、AST、LDH水平及肝组织MDA含塞低于NS组,肝组织SOD含量则高于NS组;M丁预处理组肝细胞形态学异常改变较NS组明显减轻.结论:MT预处理可减轻大鼠肝脏缺血再灌注损伤,其机制可能与提高肝组织SOD含量,抑制脂质过氧化,保护线粒体有关.     

mito-KATP通道在缺血后处理减轻大鼠肾缺血再灌注损伤中的作用

目的 评价线粒体ATP敏感性钾通道(mito-KATP通道)在缺血后处理减轻大鼠肾缺血再灌注损伤中的作用.方法 健康成年雄性SD大鼠35只,体重250～280 g,随机分为5组(n=7):假手术组(S组)仅分离双侧肾蒂,暴露45 min不夹闭;肾缺血再灌注组(I/R组)夹闭双侧肾蒂缺血45 min,再灌注6 h制备大鼠肾缺血再灌注模型;缺血后处理组(Ipo组)夹闭双侧肾蒂缺血45 min,再灌注10 s,缺血10 s,反复3次,再灌注6 h;mito-KATP通道阻断剂5-羟葵酸+I/R组(5-HD+I/R组)缺血前30 min腹腔注射5-HD 10 mg/kg,余处理同I/R组;缺血后处理+5-HD组(5-HD+Ipo组)缺血前30 min腹腔注射5-HD 10 mg/kg,余处理同Ipo组.于再灌注6 h时采集心脏血样,取肾并分离肾小管上皮细胞,测定血清Cr和BUN的浓度、肾小管上皮细胞线粒体膜电位、细胞内活性氧(ROS)含量和游离Ca2+浓度.结果 与S组比较,I/R组、Ipo组、5-HD+I/R组和5-HD+Ipo组血清Cr和BUN的浓度、肾小管上皮细胞内游离Ca2+浓度和ROS含量升高,线粒体膜电位降低(P＜0.05);与I/R组比较,Ipo组血清Cr和BUN的浓度、肾小管上皮细胞内游离Ca2+浓度和ROS含量降低,线粒体膜电位升高(P＜0.05),5-HD+I/R组和5-HD+Ipo组上述指标差异无统计学意义(P＞0.05);与Ipo组比较,5-HD+I/R组和5-HD+Ipo组血清Cr和BUN浓度、肾小管上皮细胞内游离Ca2+浓度和ROS含量升高,线粒体膜电位降低(P＜0.05).结论 mito-KATP通道的开放参与了缺血后处理减轻大鼠肾缺血再灌注损伤的过程.     

麦角新碱预处理对减轻大鼠移植肝缺血再灌注损伤的作用

目的 探讨使用外源性药物麦角新碱预处理对减轻大鼠移植肝缺血再灌注损伤的作用.方法 在大鼠的门静脉-左肾静脉搭桥、肝后下腔静脉内置管分流法自体原位肝移植模型中,于肝门阻断前10 min经大鼠尾静脉注射麦角新碱;观察移植肝缺血前和再灌注后5 min、30 min、2 h时血清一氧化氮(NO)和血浆内皮素1(ET1)水平以及NO/ET1的比值变化;测定血清丙氨酸转氨酶(ALT)酶学差异和肝组织内三磷酸腺苷(ATP)和丙二醛(MDA)含量变化;再灌注2 h取肝组织检测肝细胞、肝小叶超微结构.结果 应用麦角新碱预处理的大鼠移植肝缺血前门脉血浆中ET1升高(P＜0.01),但再灌注后5 min、30 min时,血浆中ET1水平降低(P＜0.05);而缺血前NO/ET1比值降低(P＜0.01),再灌注后5 min时,NO/ET1比值升高(P＜0.01);再灌注后ALT的升高有逐渐降低趋势;再灌注后2 h肝细胞内超微结构的损害程度减轻.结论 使用麦角新碱预处理能减轻大鼠移植肝缺血再灌注损伤.移植肝缺血再灌注损伤的靶细胞是肝血窦内皮细胞,NO/ET1比值平衡可能是影响移植肝微循环血流量变化的调节因素.     

CO_2气腹对大鼠胃肠动力和十二指肠组织一氧化氮、丙二醛含量的影响

目的:建立大鼠CO2气腹模型,观察不同气腹压力对大鼠胃肠动力指标及十二指肠组织一氧化氮、丙二醛含量的影响。方法:随机将36只大鼠按不同气腹压力(0 mmHg,10 mmHg,15 mmHg)分为三组,每组均接受2 h气腹时程的处理,观察不同气腹压力下胃排空率及小肠推进比的变化趋势,以及十二指肠组织一氧化氮、丙二醛水平的变化。结果:气腹2 h时,低压组(10 mmHg)较气腹前胃残留率显著升高,小肠推进比显著下降(P<0.05),一氧化氮下降非常明显(P<0.05),丙二醛有升高趋势,但差异无统计学意义(P>0.05);高压组(15 mmHg)各指标变化更为显著(P<0.01)。结论:CO2气腹使胃残留率增加,小肠推进比下降,十二指肠一氧化氮含量减低,丙二醛升高,随着气腹压力的增高,此作用显著增强。     

The effects of carbon dioxide pneumoperitoneum on tyrosine hydroxylase activity

PURPOSE: The aim of this study is to investigate the effects of carbon dioxide (CO2) pneumoperitoneum on tyrosine hydroxylase (TH) activity and total protein (TP) levels. METHODS: Forty male Sprague-Dawley rats were randomized into 10 groups, each consisting of 10 rats. Groups 1 and 2 consisted of anesthesia and sham-operated control rats, respectively. In the study groups, 10 mm Hg (group 3) and 15 mm Hg (group 4) pneumoperitoneum with CO2 were accomplished. At the end of the procedures, the brains and adrenals were removed quickly, and the hypothalamus and adrenal medulla separated, weighed, and homogenized. TH activity and TP levels were determined. RESULTS: The adrenal medulla TP and TH activity levels were decreased consistently and this decrease was significant in the sham and pneumoperitoneum groups compared with the control group (P<0.05). The adrenal medulla TP and TH activity levels were reduced significantly in group 4, as compared with the other groups (P<0.05). Elevation of hypothalamic TH activity in group 4 was significantly higher than in the other groups (P<0.05). CONCLUSIONS: These results indicate that CO2 pneumoperitoneum applied with 10 and 15 mm Hg pressure gradually decreases the adrenal medulla TH activity; TH is an indispensable enzyme for the biosynthesis of catecholamines. CO2 pneumoperitoneum with 15 mm Hg pressure significantly elevated hypothalamus TH activity.     

CO2气腹对大鼠重症急性胰腺炎胰腺病理及IL-6、E-选择素、P-选择素的影响

目的 研究腹腔镜手术时CO2气腹对SD大鼠重症急性胰腺炎病变局部、血淀粉酶、白细胞介素-6(IL-6)、E-选择素和P-选择素的影响. 方法 雄性SD大鼠50只,随机分为3组:CO2气腹组(n=20),5%牛磺胆酸钠胆胰管逆行注射方法制备SAP动物模型后,以气腹机向大鼠腹腔内注入CO2(压力12 mm Hg,维持30 min);SAP组(n=20):建立SAP模型后关腹,不充入CO2;单纯手术组(n=10):仅开腹翻动胰腺后关腹.各组均于术后2.5 h处死动物,取静脉血测定血淀粉酶、白细胞介素-6、E-选择素和P-选择素的水平,并进行胰腺组织病理学检查. 结果 与单纯手术组相比,CO2气腹组和SAP组病理学评分、血清淀粉酶、白细胞介素-6、E-选择素和P-选择索均明显升高,差异有统计学意义(P=0.000).与SAP组相比,CO2气腹组血白细胞介素-6明显降低,差异有统计学意义P=0.000;病理学评分(P=0.294)、血清淀粉酶(P=0.073)、E-选择素(P=0.126)和P-选择素(P=0.213)的差异无统计学意义. 结论 对于SAP大鼠,CO2气腹对白细胞介素-6有一定的抑制作用;对胰腺病理变化及E-选择素和P-选择素无明显影响.     

CO2气腹下缺氧诱导因子-1α与血管内皮生长因子在大鼠肝癌中的表达及其意义

目的 观察不同CO2气腹压力条件下,大鼠移植性肝癌中缺氧诱导因子(HIF)-1α与血管内皮生长因子(VEGF)表达的变化.方法 制作大鼠Walker-256移植性肝癌模型,将48只肝痛模型随机分为4组,给予不同气腹压力0、5、10、15 mm Hg(1 mm Hg=0.133 kPa),恒定一定时间及流量.术后处死全部大鼠,切取肝肿瘤,4%甲醛固定后行苏木素-伊红(HE)染色,免疫组织化学染色检测HIF-1α及VEGF表达.结果 随着CO2气腹压力的增加,HIF-1α、VEGF在肿瘤模型上的表达逐渐增强(P＜0.05),各组肝癌组织中HIF-1α VEGF呈正相关关系(其r分别为0.835、0.714、0.761、0.781).结论 随着CO2气腹压力的增加,HIF-1α与VEGF的表达逐渐增加,且HIF-1α与VEGF呈正相关.CO2气腹促进肿瘤生长和转移可能与HIF-1α VEGF有一定关系.     

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.     

Impact of carbon dioxide and helium insufflation on cardiorespiratory function during prolonged pneumoperitoneum in an experimental rat model

BACKGROUND: Experimental studies on laparoscopic surgery are often performed in rats. However, the hemodynamic and respiratory responses related to the pneumoperitoneum have not been studied extensively in rats. Therefore, the aim of this study was to investigate in spontaneously breathing rats the effects of CO2 and helium, insufflation pressure, and duration of pneumoperitoneum on blood pressure, arterial pH, pCO2, pO2, HCO3-, base excess, and respiratory rate. METHODS: Five groups of 9 Brown Norway rats were anesthetized and underwent CO2 insufflation (6 or 12 mmHg), helium insufflation (6 or 12 mmHg), or abdominal wall lifting (gasless control) for 120 min. Blood pressure was monitored by an indwelling carotid artery catheter. Baseline measurements of mean arterial pressure (MAP), respiratory rate, arterial blood pH, pCO2, pO2, HCO3-, and base excess were recorded. Blood gases were analyzed at 5, 30, 60, 90, and 120 min during pneumoperitoneum, and MAP and respiratory rate were recorded at 5 and 15 min and at 15-min intervals thereafter for 2 h. RESULTS: CO2 insufflation (at both 6 and 12 mmHg) caused a significant decrease in blood pH and increase in arterial pCO2. Respiratory compensation was evident since pCO2 returned to preinsufflation levels during CO2 insufflation at 12 mmHg. There was no significant change in blood pH and pCO2 in rats undergoing either helium insufflation or gasless procedures. Neither insufflation pressure nor the type of insufflation gas had a significant effect on MAP over time. CONCLUSION: The cardiorespiratory changes during prolonged pneumoperitoneum in spontaneously breathing rats are similar to those seen in clinical practice. Therefore, studies conducted in this animal model can provide valuable physiological data relevant to the study of laparoscopic surgery.     

Effect of small bowel perforation during laparoscopy on end-tidal carbon dioxide: observation in a small animal model

INTRODUCTION: There are currently no reports in the literature regarding changes in end-tidal carbon dioxide (ETCO(2)) when the small bowel is deliberately or inadvertently perforated during laparoscopic surgery. The aim of this study was to assess the influence of small bowel perforation during laparoscopy on ETCO(2) in a rat model. MATERIALS AND METHODS: Two groups of Wistar rats (n = 8/group) were anesthetized, tracheostomized, and mechanically ventilated at a fixed tidal volume and respiratory rate. After a stabilization phase of 30 min, CO(2) pneumoperitoneum was established to 5 mmHg in one group and 12 mmHg in the other group, and maintained for 30 min. A small bowel perforation was then created and pneumoperitoneum was reestablished for another 30 min. Blood pressure, heart rate, peak ventilatory pressure, and ETCO(2) were recorded throughout the experiment. RESULTS: No significant changes in blood pressure throughout the experiment were noted in either group. The ventilatory pressure increased in both groups after the induction of pneumoperitoneum. In the 5 mmHg group, there was a modest increase in ETCO(2) following the induction of pneumoperitoneum (from 39.4 +/- 1.9 to 41.1 +/- 1.4, P = 0.014), and a further increase following the small bowel perforation (from 41.1 +/- 1.4 to 42 +/- 0.8, P = 0.007). In the 12 mmHg group, there was no change in ETCO(2) after the induction of pneumoperitoneum; however, there was a substantial increase in ETCO(2) following bowel perforation (35.0 +/- 2.0 to 49.8 +/- 7.1, P = 0.002). CONCLUSIONS: ETCO(2) increases when the small bowel is perforated during CO(2) pneumoperitoneum. This increase seems more substantial under higher pneumoperitoneal pressures. Small bowel injury may enable the diffusion of CO(2) through the bowel mucosa, causing ETCO(2) elevation. Therefore, an abrupt increase in ETCO(2) observed during laparoscopy may indicate small bowel injury.     

CO2气腹对肝硬变大鼠门脉血流影响的实验研究

目的　探讨CO2 气腹对肝硬变大鼠门脉血流量的影响。　方法　制作肝硬变大鼠模型 ,施加不同压力的气腹 ,分别测平均动脉压、门静脉压力、下腔静脉压、门静脉血流 ,计算门静脉阻力。　结果　平均动脉压、下腔静脉压在不同气腹压力下无明显变化 ,两组大鼠门静脉压力在 10mmHg时出现显著差异 ,随着压力的升高而升高。正常大鼠的门静脉血流量在 2 0mmHg下与 0mmHg下比较有显著差异 ,而肝硬变大鼠的门静脉血流量在 10mmHg下与 0mmHg下比较已有显著差异。正常大鼠门静脉阻力随着压力的升高在 10mmHg时出现显著差异 ,以后继续升高 ,肝硬化大鼠门静脉阻力随着压力的升高持续升高。　结论　CO2 气腹致肝硬化大鼠门静脉血流减少 ,且减少程度重于正常大鼠     

Carbon dioxide pneumoperitoneum alters acute-phase response induced by lipopolysaccharide

BACKGROUND: As laparoscopic surgery continues to expand in scope, septic patients will be exposed to carbon dioxide (CO2) pneumoperitoneum in increasing numbers. The biologic advantages or disadvantages of laparoscopic surgery in the setting of sepsis/inflammation are not known. In a rat model, we investigated whether CO2 pneumoperitoneum alters the inflammatory response induced by bacterial lipopolysaccharide (LPS). METHODS: Male rats were injected via the penile vein with LPS (1 mg/kg). Five hours later, the animals (n = 5) were subjected to CO2 pneumoperitoneum (group I) for 1h; the animals of group II (n = 5) served as controls (no pneumoperitoneum). At 6 h, all animals were killed and the liver harvested for analysis of hepatic acute-phase gene expression. Total RNA was isolated and analyzed by Northern blot hybridization with probes for alpha-2 macroglobulin (A2M) and detected by autoradiography. The film in the linear range of exposure was quantitated using an imaging system. The signal intensity corresponding to A2M mRNA was normalized by the signal corresponding to 28S rRNA detected by staining with methylene blue. RESULTS: The mRNA levels in group II was 6.5 +/- 0.9 vs 2.8 +/- 0.4 in group I. As compared with rats that received LPS only, those that received a combination of LPS and CO2 showed a reduction in A2M mRNA levels (57.4%, p = 0.006). CONCLUSIONS: These data demonstrate that the presence of CO2 pneumoperitoneum reduces the inflammatory response established by LPS. This finding challenges the generally accepted notion that smaller incisions alone account for the observed benefits of laparoscopic surgery. It further suggests that CO2 pneumoperitoneum - aided laparoscopic surgery impedes the inflammatory response and may therefore offer specific benefits over conventional surgery.     

Videoendoscopic endotracheal intubation in the rat: a comprehensive rodent model of laparoscopic surgery

BACKGROUND: Peritoneal absorption of CO(2) during abdominal insufflation in laparoscopy may disrupt the acid-base equilibrium and alter the physiological response to stress. Current nonventilated rodent models of laparoscopy do not manage the CO(2) load of pneumoperitoneum, but ventilated surgical rodent models are invasive (tracheotomy) and may independently induce the inflammatory response. MATERIALS AND METHODS: A comprehensive rodent model of laparoscopy was developed. Rats were randomized to receive anesthesia alone, anesthesia plus CO(2) pneumoperitoneum, or anesthesia plus CO(2) pneumoperitoneum with videoendoscopic intubation and mechanical ventilation. Arterial blood-gas analysis was performed at baseline and after 30 min of intervention. RESULTS: Baseline pH, pCO(2), and HCO(3)(-) arterial blood gas parameters were normal for all rats. After 30 min, pCO(2) and pH changed slightly but remained normal among rats receiving anesthesia alone (pCO(2) = 46.5 +/- 1.9; pH = 7.365 +/- 0.009) whereas animals receiving anesthesia plus CO(2) pneumoperitoneum that were dependent on spontaneous respiration for ventilation developed significant hypercarbic acidosis (pCO(2) = 53.2 +/- 1.9, P < 0.05; pH = 7.299 +/- 0.011, P < 0.001). This acidosis was completely corrected with increased minute ventilation in intubated rats receiving mechanical ventilation (pCO(2) = 36.8 +/- 1.5, P < 0.001; pH = 7.398 +/- 0.011, P < 0.001). CONCLUSIONS: CO(2) pneumoperitoneum induces significant hypercarbic acidosis in nonventilated rats. Noninvasive endotracheal intubation is feasible in the rat with videoendoscopic assistance. Our noninvasive rodent model of laparoscopic surgery controls for anesthesia- and capnoperitoneum-related acid-base changes and provides an environment in which the biological response to pneumoperitoneum can be studied precisely.