卡巴胆碱对肠缺血/再灌注大鼠中性粒细胞CD11b/CD18表达和血清可溶性细胞间黏附分子-1浓度的影响

目的:观察胆碱能激动剂卡巴胆碱对肠缺血/再灌注大鼠中性粒细胞(PMN)上CD11b/CD18表达和血清可溶性细胞间黏附分子-1(sICAM-1)浓度的调节作用。方法:54只雄性Wistar大鼠随机分为假手术组(N组)、肠缺血/再灌注组(GI/R组)及卡巴胆碱干预组(Car组)。采用夹闭肠系膜上动脉45min后恢复灌流的方法制成GI/R模型;卡巴胆碱组在肠缺血15min后经幽门注入卡巴胆碱(100μg/kg)。于肠缺血45min(I45)及再灌注1h(R1)、2h(R2)、6h(R6)取肠系膜上静脉血,双抗体夹心酶联免疫吸附(ELISA)法测定血清sICAM-1浓度,流式细胞仪检测PMN上CD11b/CD18表达率。结果:肠系膜上静脉血中PMN表面黏附分子CD11b/CD18的表达在肠缺血和再灌注后各时相点均增加(P<0.01),R2和R6时增加幅度较大;卡巴胆碱干预组R6时CD11b/CD18阳性PMN比例减少(P<0.05)。血清sICAM-1浓度在R1～R6时均升高(P<0.05),而给予卡巴胆碱的动物R6时降低(P<0.05),其值接近N组。结论:卡巴胆碱能降低肠缺血/再灌注大鼠PMN上CD11b/ C...     

缺血后适应在兔急性肠系膜缺血再灌注损伤模型中的作用

目的 观察缺血后适应干预措施能否减轻兔急性肠系膜缺血再灌注损伤.方法 将雄性新西兰兔120只随机分为空白对照(Con)组(仅开腹显露SMA)、缺血再灌注(I/R)组[肠系上动脉(superior mesenteric artery,SMA)缺血30 min后持续灌注120 min]、缺血后适应1(IpostC1)组(SMA缺血30 min后行3个循环的灌注30 s/阻断30 s,再持续灌注117 min)、缺血后适应2(IpostC2)组(SMA缺血30 min后行3个循环的灌注60s/阻断60 s,再持续灌注114 min),每组30只.干预后采集各组兔处理后下腔静脉血及部分肠道组织标本,试剂盒测定血清及肠道组织内丙二醛(MDA)、髓过氧化酶(MPO)水平,HE染色,Chiu 6级评分法观察肠黏膜损伤情况. 结果 与对照组比较,I/R组及IpostC1组、IpostC2组血清及肠道组织中MDA、MPO水平明显增加(P＜0.01),肠黏膜损伤评分明显升高(P＜0.01).与I/R组相比,IpostC1组血清和肠道组织中MDA、MPO水平及肠黏膜损伤评分明显降低(P＜0.01),而IpostC2组血清和肠道组织中MDA、MPO水平及肠黏膜损伤评分无明显降低(P＞0.05).结论 缺血后适应可明显降低兔急性肠系膜缺血再灌注损伤后下腔静脉血和肠道组织中MDA、MPO水平及肠黏膜损伤.     

外源性碱性成纤维细胞生长因子对肠道缺血再灌注损伤的保护作用及机制

目的　探讨碱性成纤维细胞生长因子 (bFGF)对大鼠缺血性损伤的保护作用及其分子机制。方法　利用肠系膜上动脉夹闭 (SMA) 4 5min后松夹造成缺血再灌注 (I/R)损伤作为动物模型。将 78只Wistar大鼠随机分为假手术组 (A组 )、生理盐水对照治疗组 (B组 )、bFGF抗体预处理组 (C组 )和bFGF治疗组 (D组 )。A组分离SMA但不夹闭 ,45min后活杀动物 ,其余各组分别于松夹后 2、6、2 4和 48h活杀动物 ,取血浆检测二氨氧化酶 (DAO)含量 ,取小肠组织利用免疫组织化学技术检测磷酸化 p38钙调蛋白依赖性蛋白激酶 (MAPK)及SAPK/JNK的活性 ,并行苏木素 伊红(HE)染色于光镜下观察病理形态学改变。结果　HE染色结果显示 ,I/R损伤后 6h肠屏障功能损伤最严重 ,D组在再灌注 48h损伤较B组及C组减轻。损伤后 6h ,D组DAO含量 (2 .55± 1 .2 2 )低于C组 (2 .86± 0 .94) (P <0 .0 5)。p38MAPK及SAPK/JNK在正常小肠组织表达极少 ,I/R损伤后表达量增高。p38MAPK染色主要位于小肠隐窝 ,少量存在于绒毛尖处。B组及C组磷酸化 p38MAPK在 6h表达量达高峰 ,而D组在 2h达高峰。SAPK/JNK在各组表达均呈弱阳性 ,于再灌注后 2 4h表达量达峰值 ,组间无明显区别。结论　外源性bFGF对肠I/R损伤有保护作用 ,其保护机制可能与损伤早期激活p38MAPK信号     

肠道部分缺血再灌注损伤诱发外周血淋巴细胞凋亡

目的：观察肠道部分缺血再灌注(I/R)损伤过程中外周血淋巴细胞凋亡及其在植物血凝素(PHA)刺激下增殖能力的变化。方法：大耳白兔55只,分为肠部分I/R组、假手术对照组、正常对照组,用自行设计的血流阻断器阻断SMA血流50%,维持4h,制作肠道部分缺血再灌注损伤动物模型。采用流式细胞术(AnnexinV/PI双染法)测定外周血淋巴细胞凋亡变化,采用免疫组织化学方法观察外周血淋巴细胞caspase-3蛋白的表达,采用MTT比色法测定外周血淋巴细胞增殖能力。结果：肠道缺血期外周血淋巴细胞凋亡率明显升高,肠道再灌注期后外周血淋巴细胞凋亡比例骤然减少;外周血淋巴细胞caspase-3表达与凋亡改变呈相同趋势;肠部分I/R损伤后外周血淋巴细胞增殖能力明显降低。结论：肠道部分I/R损伤后,外周血T-淋巴细胞增殖功能明显受抑,外周血淋巴细胞凋亡变化与细胞内caspase-3的表达有关。     

瘦素对肠缺血/再灌注损伤大鼠肝脏功能的影响及其机制

目的:探讨瘦素(leptin)对大鼠肠缺血/再灌注(I/R)损伤时肝脏的保护作用及其机制。方法:99只Wistar大鼠随机分成11组:假手术组,肠缺血45min再灌注15min、30min、1h、3h、6h的肠I/R损伤组和相应时间点的leptin治疗组,每组9只大鼠。肠I/R损伤组和leptin治疗组建立大鼠肠I/R损伤模型;leptin治疗组于再灌注的同时腹腔注射leptin0.2mg/kg。假手术组术后1h处死,其余各组大鼠于相应时间点处死,检测血清丙氨酸转氨酶(ALT),肝组织中白细胞介素-6(IL-6)、IL-10和超氧化物歧化酶(SOD)水平的动态变化。结果:肠I/R组血清ALT随着时间变化逐渐升高,肝组织中的IL-6水平于再灌注3h显著升高,而IL-10水平基本处于平稳的波动状态,SOD活性于再灌注早期呈略微下降趋势,1h后逐步回升至假手术组水平;leptin治疗后血清ALT水平基本稳定在较低水平,再灌注3h后,肝组织IL-6水平较损伤组明显降低,同时SOD活性显著提高,IL-10水平于再灌注15min时突然增高,随即恢复到假手术组水平。结论:leptin对大鼠肠I/R造成的肝脏功能损伤具有改善作用,可能与其调节肝组织中的细胞因子释放、提高肝脏的抗氧化损伤能力有关。     

肠缺血再灌注对小肠功能的影响

目的从不同角度探讨大鼠肠缺血再灌注对小肠屏障、吸收、通透和传输等功能的影响,为更深入地研究肠道损伤及其保护提供防治依据.方法以Wistar大鼠肠缺血再灌注(I/R)作模型,将动物随机分为健康对照(C)、肠系膜上动脉夹闭1h(I)、夹闭后再灌1h(R 1h)、2h(R 2h)和4h(R 4h)共5个组.分别测血或小肠组织的二胺氧化酶(DAO)、D-乳酸、D-木糖、肠传输、脂质过氧化物(MDA)和髓过氧化物酶(MPO),并作小肠普通光镜检查.结果R 1h和R 4h组的血浆DAO显著升高(P<0.05),小肠DAO各组有不同程度的降低,R 2h组降低显著,血浆和小肠DAO的变化呈负相关(r=-0.648,P<0.05).缺血和再灌注后各时相点血D-乳酸浓度升高,其中R 1h和R 2h升高显著(P<0.05).缺血再灌后肠道D-木糖的吸收增加,小肠的传输显著加快.结论肠缺血和再灌注后小肠的屏障、吸收、通透和传输功能均显示不同程度的改变.     

不同分子量和取代级的羟乙基淀粉溶液对兔凝血功能的影响

目的观察家兔输注羟乙基淀粉(贺斯,HES)HES 450/0.7、HES 200/0.62、HES 200/0.5和HES130/0.4后的凝血功能变化。方法 家兔40只,随机分为5组(n=8):组I:HES 450/0.7;组Ⅱ:HES200/0.62;组Ⅲ:HES 200/0.5;组Ⅳ:HES 130/0.4;组Ⅴ:0.9％NaCl。按10 ml·kg-1·h-1输注胶体,共3 h,于输注前、输注1 h、2 h、3 h测定凝血酶原时间(PT)、部分凝血活酶时间(APTT)、纤维蛋白原(FIb)及血栓弹性描记图TEG(R、K、α角及MA)。结果 (1)输注30 ml·kg-1后,组I:R(16.1±1.9)min、K(6.0±2.1)min,α(35±9)deg,MA(45±5)mm(P<0.01);组Ⅱ:R(15.4±1.0)min,K(7.0±2.1)min,α(34±5)deg,MA(38±9)mm(P<0.01)。(2)输注20 m1·kg-1后五组PT均延长(P<0.05)。(3)组I、组Ⅱ输注30ml·kg-1后APTT显著延长(P<0.05)。(4)组I输注30ml·kg-1后FIb显著降低(P<0.05)。结论HES 450/0.7与HES 200/0.62大剂量输注对凝血功能有显著影响,HES 200/0.5与HES 130/0.4则无明显损害。     

卡巴胆碱改善重度烫伤大鼠胃血流量和胃排空功能的初步研究

目的:探讨不同剂量卡巴胆碱对烫伤大鼠胃血流量和胃排空功能的影响.方法:40只Wistar雄性大鼠,随机分为假烫组(n=5)、单烫组(n=5)和口服卡巴胆碱组(n=30),后者又根据卡巴胆碱剂量不同分为20、40、60、80、100、120 μg/kg组(每组5只).假烫组大鼠均给予0.1%酚红溶液1.5 ml灌胃.单烫组和口服卡巴胆碱组大鼠均经30%TBSAⅢ度烫伤后立即给予0.1%酚红溶液1.5 ml灌胃,口服卡巴胆碱组于伤后0.5 h给予相应剂量卡巴胆碱 1 ml生理盐水灌胃.大鼠均于伤后2 h处死,观察不同剂量卡巴胆碱对大鼠胃血流量及胃排空率的影响.结果:烫伤后大鼠胃排空率为(29.50±13.42)%,明显低于假烫组(92.19±5.24)%,P＜0.01.伤后2 h胃血流量从伤前的(476.00±71.24)U降低到(103.60±51.28)U,P＜0.01.烫伤后给予不同剂量卡巴胆碱均能增加胃排空率和胃血流量,但以60 μg/kg最为显著(P＜0.01).结论:卡巴胆碱对烧伤休克大鼠胃血流量和胃排空有显著促进作用,最佳剂量为60μg/kg.     

缺血预处理对肺缺血再灌注损伤中细胞因子生成的影响

目的　探讨缺血预处理 (IPC)对肺缺血再灌注 (I/R)损伤的保护作用及其对细胞因子生成的影响。　方法　 36只大白兔分为 3组 :对照组、I/R组和IPC组。通过阻断左肺门造成兔在体I/R损伤 ,观察IPC对肺I/R损伤的保护作用 ,指标为肺组织湿干重比、肺通透性指数及支气管肺泡灌洗液(BALF)中白细胞分类计数 ;以双抗体夹心酶联免疫吸附试验法检测血清中肿瘤坏死因子α(TNFα)、白细胞介素 6(IL 6)、白细胞介素 8(IL 8)的含量。　结果　肺I/R损伤后 ,I/R组肺组织湿干重比、肺通透性指数及BALF中性粒细胞百分比分别为 9 73± 1 1 4、(41 62± 5 77)× 1 0 - 4和 (58 1± 1 0 0 ) % ;IPC组分别为 6 2 3± 0 69、(2 0 31± 4 0 3)× 1 0 - 4和 (2 3 8± 5 2 ) % ,两组差异有极显著意义 (P <0 0 1 )。I/R组血清TNFα、IL 6和IL 8含量分别为 (0 90 78± 0 1 0 6 2 )、(0 2 1 3 7± 0 0 598)和 (0 72 1 1± 0 0 979)ng/ml,IPC组分别为 (0 7478± 0 0 843)、(0 1 2 71± 0 0 0 89)和 (0 590 3± 0 0 746)ng/ml,较I/R组显著降低 (P <0 0 1 )。　结论　IPC对I/R损伤有显著的保护作用 ,机理可能与其抑制炎性细胞因子TNFα、IL 6和IL 8的合成和释放 ,从而减轻中性粒细胞的浸润与激活有关。     

肠道部分缺血再灌注损伤过程中外周血中性粒细胞凋亡变化及其机制

目的:研究兔肠道部分缺血再灌注(I/R)损伤过程中外周血中性粒细胞(PMN)凋亡的变化及机制。方法:大耳白兔55只,分为肠部分 I/R 组、假手术对照组、正常对照组,用自行设计的血流阻断器阻断肠系膜上动脉(SMA)血流50%,维持4h,制作肠道部分缺血再灌注操作动物模型:采用流式细胞术(AnnexinV/PI 双染法)测定外周血 PMN 凋亡变化,采用放免法测定血浆内 IL-6和 TNF-α水平,采用免疫组织化学方法观察外周血 PMNcaspase-3蛋白的表达,同时观察脏器功能和病理形态学改变。结果:肠部分 I/R 组,在肠道缺血期血浆 IL-6T 和TNF-α水平及外周血 PMN 凋亡比例均明显升高;在肠道再灌注期至术后1d 外周血 PMN 凋亡比例骤然减少,而血浆 IL-6和 TNF-α在肠道再注期处于较高水平:外周血 PMN caspase-3蛋白在肠道缺血期呈现高表达,而在再灌注期后表达明显降低。结论:肠道 I/R 全过程中 PMN 的凋亡与多种信号启动 caspase-3蛋白的表达正相关。在肠道缺血期,IL-6及 TNF-α可能是外周血 PMN 的凋亡过程的诱导分子或促进分子:而在肠道再灌注期,外周血 PMN 凋亡锐减可能是导致 TNF-α、IL-6等细胞因子进一步增加的原因。     

Oral administered nonabsorbable antibiotics prevent endotoxemia in primates following intestinal ischemia

Plasma lipopolysaccharide (LPS) concentrations have been found to increase during a temporary occlusion of the superior mesenteric artery (SMA). We have attempted to show, by a prophylactic oral administration of a nonabsorbable antibiotic to monkeys subjected to an SMA occlusion shock, that the increased LPS is intestinal in origin. A total of eight monkeys were subjected to a temporary occlusion of the SMA. Four monkeys received prophylactic oral administration of a nonabsorbable antibiotic, while the rest acted as controls. The plasma LPS concentrations before occlusion in the control and the kanamycin group were 0.069 +/- 0.006 and 0.092 +/- 0.005 ng/ml, respectively. At the end of the 1-hr occlusion period the plasma LPS concentration in the controls increased to 0.09 +/- 0.009 ng/ml (P less than 0.1) and peaked to 0.378 +/- 0.103 ng/ml (P less than .001) within 20 min of reperfusion. Thereafter, the plasma LPS concentration returned slowly to baseline. In the kanamycin group the plasma LPS concentration remained at baseline throughout both the occlusion and reperfusion periods. These data suggest that the origin of the increased plasma LPS concentration seen following temporary occlusion of the SMA is from the gut, and is information of possible importance in patients about to undergo intestinal surgery.     

GLP-2alpha accelerates recovery of mucosal absorptive function after intestinal ischemia/reperfusion

BACKGROUND/PURPOSE: The authors' previous laboratory results have shown that rats treated for 3 days with intravenous GLP-2alpha, a synthetic protease-resistant form of glucagonlike peptide-2, showed increased mucosal mass and absorptive function when compared with saline-treated controls after intestinal ischemia/reperfusion (I/R). This study was designed to explore the temporal relationship between injury that occurs secondary to intestinal I/R and recovery of mucosal absorptive function with and without GLP-2alpha treatment. METHODS: Each of 18 male Sprague-Dawley rats (300 to 333 g) was subjected to superior mesenteric artery occlusion for 30 minutes, during which time a jugular venous catheter was placed and connected to a subcutaneous infusion pump. Rats were divided into 4 groups based on the type and duration of infusion as follows: group 1, systemic saline at 1 microL/h for 24 hours (n = 5); group 2, systemic GLP-2alpha at 100 microg/kg/d for 24 hours (n = 5); group 3, systemic saline at 1 microL/h for 72 hours (n = 4); and group 4, systemic GLP-2alpha at 100 microg/kg/d for 72 hours (n = 4). Immediately after the infusions, (14)C-galactose and (14)C-glycine absorption was measured using an in vivo, closed-recirculation technique and expressed as micromoles per square centimeter intestine +/- SEM. Statistical analysis was performed using analysis of variance. RESULTS: Twenty-four hours after intestinal I/R injury, there was a decrease in substrate absorption but no significant difference between the saline and GLP-2alpha-treated groups (galactose absorption, 1.13 +/- 0.09 in group 1 v 1.35 +/- 0.11 in group 2, P =.15; glycine absorption, 1.18 +/- 0.13 in group 1 v 1.34 +/- 0.15 in group 2, P =.36). However, after the 72-hour infusion, absorption of galactose and glycine was significantly increased in the rats receiving GLP-2alpha as compared with the saline-infused control group (galactose absorption, 1.24 +/- 0.13 in group 3 v 1.88 +/- 0.10 in group 4, P <.01; glycine absorption, 1.64 +/- 0.07 in group 3 v 2.05 +/- 0.08 in group 4, P <.05). Compared with previously determined levels of absorption in normal, uninjured rat intestine (1.50 +/- 0.12 micromol/cm(2) for galactose and 1.85 +/- 0.17 micromol/cm(2) for glycine), after I/R a 72-hour infusion of GLP-2alpha increased galactose absorption 26% (P <.05) and glycine absorption 11% (P =.29) beyond baseline. CONCLUSIONS: When initiated at the time of intestinal I/R, a continuous infusion of GLP-2alpha accelerated recovery of mucosal absorptive function in rats. Remarkably, carbohydrate absorption at 72 hours was increased to a level significantly greater than that in normal, uninjured rat intestine. J Pediatr Surg 36:570-572.     

血管扩张刺激磷蛋白在失血性休克肠屏障功能障碍中的作用

目的 观察大鼠小肠上皮血管扩张刺激磷蛋白(vasodilator stimulated phosphoprotein,VASP)在失血性休克肠屏障功能障碍中的作用.方法 实验分为正常组、休克1、2、4 h组及休克2 h+环磷腺苷组,每组8只.测定各组血清二胺氧化酶(diamine oxidase,DAO)活性、血浆D-乳酸含量,并观察其与VASP表达的关系.结果 VASP磷酸化激动剂环磷腺苷可明显增强失血性休克2 h时VASP表达,降低血清DAO活性和血浆D-乳酸含量,与未加环磷腺苷组比较差异有统计学意义(t=18.62,9.28,2.83,P<0.05).失血性休克后大鼠血清DAO活性显著增高,而VASP表达明显降低,两者旱负相关(r=-0.95,P<0.05).结论 VASP降低是导致失血性休克大鼠肠屏障功能障碍的因素.环磷腺苷能改善肠屏障功能障碍.     

Lactate in the diagnosis of acute intestinal vascular occlusions

The diagnostic value of lactate in acute occlusion of intestinal vessels was investigated in two groups of patients: Group 1 included 86 patients with reconstructions of aorta and intestinal arteries: The lactate-concentrations measured during uncomplicated postoperative course over 24 hours remained within the normal range of 4.31 +/- 1.06 mmol/l. Only in 3 patients with acute postoperative occlusion of intestinal arteries, lactate rose to high pathologic levels up to 59.94 mmol/l. In 10 patients after reconstruction of acute mesenteric artery occlusion the postoperative lactate levels enforced the decision in 9 cases against and in one patient to second look operation. Group 2 included 36 patients with acute abdomen: In 18 patients with intestinal vascular occlusions the mean value of lactate was 7.45 +/- 2.86 mmol/l, in 18 patients without intestinal ischemia lactate was only 1.94 +/- 1.02 mmol/l. The statistical difference is significant. In summary, the results of this study document the reliable value of lactate for the diagnosis of acute occlusions of intestinal vessels during pre- and postoperative course.     

Ischemic preconditioning protects intestine from prolonged ischemia

Ischemic preconditioning (IP), obtained by exposure to brief periods of vascular occlusion, improves organ tolerance to prolonged ischemia. The aim of this study was to evaluate the effects of IP on intestinal morphology. Forty rats were subjected to sham surgery (n = 20, group I) or intestinal preconditioning (n = 20, group II) with a cycle of brief ischemia/reperfusion (10-minute occlusion of superior mesenteric artery [SMA], followed by 10-minute reperfusion) before prolonged ischemia produced by SMA occlusion (45 minutes). Five animals in each group were sacrificed 2, 12, 24, and 48 hours after reperfusion. Intestinal samples were processed for light and electron microscopy. A TUNEL assay was performed to detect apoptosis. Statistical analysis used Student t test and Kaplan-Meier survival curves. The overall mortality for the sham-operated group was 15%, while no animals of group II died (NS). Histological evaluation showed early detachment of epithelial cells from villous stroma accompanied by marked congestion and edema. Successive morphological changes were represented by leukocyte infiltration, focal necrosis, and marked villus denudation or loss. Group II animals showed significantly reduced inflammatory infiltrates in the lamina propria and a greater villus height compared to group I. The maximum number of apoptotic nuclei was observed in both groups, Following 2 hours of reperfusion group II animals showed significantly, greater apoptosis at 2 and 12 hours after reperfusion (P <.05). Electron microscopy showed severe mitochondrial and basement membrane damage. The findings from this study confirm that IP preconditioning attenuates morphological alterations that are invariably present after prolonged ischemia and reperfusion.     

Intestinal diamine oxidase levels reflect ischemic injury

Mucosal diamine oxidase (DAO) decreases during intestinal ischemia and may be a useful marker of intestinal ischemic injury. Tissue DAO activity and histologic changes were studied in intestinal segments taken from the midpoint of the small intestine before and 2, 4, and 24 hr after manipulation of the intestinal blood supply in 24 mongrel dogs. Intestinal DAO activity decreased significantly (17 +/- 21% of control value) 24 hr after SMA ligation and was associated with abnormal histology (histology score 7.8 +/- 2.9 at 24 hr vs 0.3 +/- 0.5 at 0 hr). SMA occlusion for 2 hr resulted in a significant decrease in DAO activity (45 +/- 36% of control value) 4 hr after manipulation which returned to normal at 24 hr, as did the histologic injury. Ligation of both the mesenteric arteries and veins resulted in a more rapid decrease in DAO activity. Decreased DAO activity correlated with the extent of histologic injury. Intestinal ischemia is associated with decreased intestinal DAO activity, which is influenced by the mechanism and duration of intestinal ischemia.     

Regulation of intestinal blood flow with increased intraluminal pressure

To better characterize the mechanisms which regulate intestinal blood flow (IBF), we studied the effects of gradual and rapid increases in intraluminal pressure (LP) in anesthetized canines. Polarographic measurements of hydrogen washout allowed repeated assessment of IBF (ml/min X g) in control (CL) and distended (DL) autoperfused small intestinal loops. In group I (n = 7) graded increases in LP (mm Hg) were produced by saline inflation. In group II (n = 4), IBF was measured before and after intraarterial aminophylline (adenosine blockade); LP was then rapidly raised to 24 mm Hg. IBF was unchanged by time (CL 0.64 +/- 0.24) or gradual distension (DL 0.65 +/- 0.28 at mean maximal LP = 26). Aminophylline did not change IBF at LP = 0. Rapid distension after adenosine blockade was accompanied by immediate increases in IBF (0.96 +/- 0.41, P less than 0.05) and decreased resistance (50 +/- 25% control). IBF is maintained despite gradual increases in luminal pressure. Blockade of adenosine, an intestinal vasodilator, does not inhibit this response; hyperemia associated with rapid distension is not impaired. We conclude that autoregulation of IBF during distension is not accomplished by an adenosine mediated metabolic mechanism.     

A comparison between fructose 1,6-diphosphate, glucose, or normal saline infusions and species-specific blood exchange transfusions in the treatment of bowel ischemia

Infusion of fructose 1,6-diphosphate, (FDP), the rate-limiting substrate in anaerobic metabolism, decreases infarction in the ischemic heart. This study evaluates the effect of FDP (5% in H2O), glucose (D5W), or normal saline (N/S) infusions and species-specific blood (SSB) exchange transfusions on mortality rates and bowel infarction in rats with intestinal ischemia. One hundred twenty Sprague-Dawley male rats (50 to 75 gm) were divided into six experimental groups. Group I controls (n = 20) underwent sham laparotomy. Group II (n = 20) underwent superior mesenteric artery (SMA) occlusion for 90 minutes. Group III rats (n = 20) were infused with FDP with SMA occlusion (90 minutes). Group IV rats (n = 20) were infused with D5W with SMA occlusion (90 minutes). Group V rats (n = 20) were infused with N/S with SMA occlusion (90 minutes). Group VI rats (n = 20) received species-specific exchange transfusion after SMA occlusion (90 minutes). A typical rat given 1 ml of D5W/75 gm had a serum glucose of 478 ng/dl with an osmolality of 293 mosm/L. After being given 1 ml of NS/75 gm, rats had a serum glucose level of 170 mg/dl with an osmolality of 291 mos/ml. Control rats had a serum glucose level of 139 mg/dl with an osmolality of 295 mosm/L. Survival at 48 hours without bowel infarction was 20 of 20 (100%) in group I, three of 20 (15%) in group II, 12 of 20 (60%) in group III, 12 of 20 (60%) in group IV, five of 20 (25%) in group V, and six of 20 (30%) in group VI (p less than 0.05 groups III and IV versus group II). FDP and D5W infusions increased survival after bowel ischemia in the rat. The mechanism of action may involve provision of a substrate for anaerobic metabolism to ischemic bowel via collateral pathways, hemodilution, and/or volume expansion.     

不同剂量异丙酚对大鼠小肠缺血再灌注后肺损伤超微结构的影响

目的 探讨不同临床剂量异丙酚对大鼠小肠缺血再灌注后肺损伤肺组织钙离子含量变化和肺组织超微结构改变的影响及其保护作用。方法 雄性SD大鼠40只,随机分为假手术对照组(Ⅰ组)。小肠缺血再灌注组(Ⅱ组)及分别给予异丙酚4mg·kg-1·h-1、8mg·kg-1·h-1、10mg·kg-1·h-1(Ⅳ、Ⅳ、Ⅴ)5组;制作小肠缺血再灌注模型。实验结束即刻取部分肺组织固定于2.5％戊二醛行透射电镜检查肺组织超微结构,部分肺组织用原子吸收分光光度法测钙离子含量。结果IIR后Ⅱ组、Ⅲ组肺组织钙离子含量明显升高,与Ⅰ组、Ⅳ组、Ⅴ组相比均有非常显著差异(P<0.01),Ⅳ组、Ⅴ组与Ⅰ组相比无统计学差异,同时Ⅱ组、Ⅲ组肺组织钙离子含量相比显著差异(P<0.05)。Ⅱ组肺组织超微结构明显受损,异丙酚用药组肺组织超微结构均明显改善,尤其Ⅳ组、Ⅴ组两组除线粒体结构轻微改变外基本接近正常。结论 钙离子在大鼠小肠缺血再灌注后肺损伤中有重要作用,临床剂量异丙酚可明显降低肺组织钙离子含量,并对肺组织超微结构产生保护作用。     

肠型脂肪酸结合蛋白对肠缺血早期诊断的意义

目的　探讨肠型脂肪酸结合蛋白 (IFABP)对肠缺血早期诊断的意义。方法　将SD大鼠随机分成对照组和肠系膜上动脉结扎组 (SMA组 ) ,分别于术前及术后 1,2 ,4h取血 ,检测各时点的血清IFABP、肌酸激酶 (CK )、肌酸激酶BB型同工酶 (CK BB)和乳酸脱氢酶 (LDH )。结果　对照组血清I FABP水平在各时点均无明显差异 (P >0 .0 5 )。SMA组结扎后 1h血清IFABP水平迅速增加 ,与对照组相比 ,差异具显著性 (P <0 .0 1) ;结扎 2h达高峰。血清中CK ,CK BB和LDH活性均随缺血时间的延长而出现升高趋势。与对照组相比 ,各组CK ,CK BB和LDH出现显著性升高的时间依次为缺血后1,2 ,4h(P <0 .0 5 )。结论　IFABP是小肠缺血性疾病的早期、特异、敏感的生化诊断指标。