内源性硫化氢对实验性肝硬化门静脉高压调节作用

目的:探讨内源性硫化氢在实验性肝硬化门静脉高压中的调节作用。方法:32只雌性SD大鼠随机分为4组:肝硬化组、肝硬化+炔丙基甘氨酸组、正常组和正常+炔丙基甘氨酸组,每组各8只。肝硬化组和肝硬化+炔丙基甘氨酸组大鼠采用四氯化碳复合法制备肝硬化门静脉高压动物模型。肝硬化+炔丙基甘氨酸组及正常+炔丙基甘氨酸组大鼠腹腔内注射炔丙基甘氨酸30 mg/(kg.d),肝硬化组及正常组大鼠每日腹腔内给予等量生理盐水。炔丙基甘氨酸干预1周后,采用门静脉导管法测量各组大鼠门静脉压力,用敏感硫电极法检测大鼠血浆内源性硫化氢含量,用免疫组织化学法检测门静脉胱硫醚-γ-裂解酶表达。结果:炔丙基甘氨酸干预1周后,正常组与正常+炔丙基甘氨酸组门静脉压力比较差异无统计学意义(P0.05),肝硬化组较正常组升高(P0.05),肝硬化+炔丙基甘氨酸组较肝硬化组、正常组均升高(P0.05)。血浆内源性硫化氢含量与门静脉胱硫醚-γ-裂解酶蛋白含量在正常+炔丙基甘氨酸组较正常组降低(P0.05),肝硬化组较正常组降低(P0.05),肝硬化+炔丙基甘氨酸组较肝硬化组及正常组均降低(P0.05)。结论:内源性硫化氢在肝硬化门静脉高压形成过程中发挥保护性调节作用。     

肝硬化大鼠脊髓内一氧化氮合酶阳性神经元的分布

背景肝硬化时可对脊髓等身体其他组织器官产生严重的影响.目的应用四氯化碳损伤大鼠肝脏制备肝硬化大鼠模型,探讨肝硬化大鼠脊髓内一氧化氮合酶分布情况.设计完全随机对照实验.单位首都医科大学解剖教研室.材料实验于2002-03/2003-12在首都医科大学解剖教研室完成.20只Wistar雄性大鼠随机分为肝硬化组和正常组,每组10只.方法肝硬化组经四氯化碳损伤大鼠肝脏制备肝硬化大鼠模型,正常大鼠组不作任何处理.于模型制备后3个月,各组大鼠在麻醉状态下开胸,灌注,固定,取脊髓组织,制备切片,采用还原型烟酰胺腺嘌呤二核苷酸磷酸黄递酶组化法及Leica Q500IW图像分析系统对肝硬化大鼠脊髓一氧化氮合酶阳性细胞进行数量及灰度的测定.主要观察指标[1]两组大鼠一氧化氮合酶阳性神经元灰度值.[2]两组大鼠一氧化氮合酶阳性细胞分布情况.结果20只大鼠均进入结果分析.[1]两组大鼠一氧化氮合酶阳性神经元灰度均为60(P＞0.05).[2]在脊髓灰质区,一氧化氮合酶阳性细胞主要分布在中央管周围即脊髓板层第Ⅹ层和中间外侧核.还原型烟酰胺腺嘌呤二核苷酸磷酸黄递酶组化法呈色为强阳性,细胞形态多为三角形和梭形,胞核不着色,胞质色深.细胞中等大小,以25 μm为主.在脊髓颈、胸、腰各段灰质中间带一氧化氮合酶阳性细胞分布的数量基本相等,没有特异性变化.结论肝硬化大鼠与正常大鼠-氧化氮合酶在脊髓内的表达基本相同.一氧化氮在脊髓节段的分布特性可能说明肝硬化大鼠在低级交感神经的调控上与正常无差异.     

早期营养干预对宫内发育迟缓大鼠小肠发育及黏膜双糖酶活性的影响

目的探讨生后早期营养干预对胎儿宫内发育迟缓(intrauterine growth retardation,IUGR)大鼠小肠发育及小肠黏膜双糖酶活性的影响.方法采用母鼠全程饥饿法建立IUGR大鼠模型.实验分为以下4组①正常对照组(C组);②IUGR模型组(S组);③IUGR低蛋白组(SL组);④IUGR高蛋白组(SH组).各组大鼠分别于出生、第3周(哺乳期)、4周(幼年期)和12周(成年期)各取8只雌鼠处死后测量其小肠长度、质量,测定空肠黏膜双糖酶活性.结果①IUGR大鼠出生时小肠长度、质量均显著小于C组;乳糖酶、麦芽糖酶活性显著高于C组(均P＜0.05).②小肠长度和质量SL组在3、4、12周时均显著低于C组(P＜0.05);而SH组在4、12周时与C组比较均无统计学差异(P＞0.05).③乳糖酶活性3周时SL、SH组显著高于C组(P＜0.05);12周时双糖酶活性各组间无统计学差异(P＞0.05).结论宫内和生后早期营养对IUGR大鼠小肠发育及成年期能否达正常水平有重要的影响.各组IUGR大鼠生后4周恢复正常饮食,其小肠黏膜双糖酶活性在成年期可恢复正常水平.     

热应激对肝硬化内毒素血症大鼠HSP72表达及致炎细胞因子分泌的影响

目的:探讨热应激诱导肝硬化内毒素血症大鼠热休克蛋白72(HSP72)表达及对致炎细胞因子TNF-α分泌的影响.方法:CCl<,4>诱导的肝硬化SD大鼠及正常饮食的SD大鼠先后给予热应激处理及腹膜腔内注入脂多糖(LPS),另外两组肝硬化SD大鼠及正常饮食SD大鼠仅腹腔内注入LPS作为对照.EUSA检测并比较各组大鼠血浆内毒素、HSP72、TNF-α的含量,RT-PCR检测肝组织HS72 mRNA表达,评价HSP72表达对TNF-α分泌的影响.结果:外源给予LPS能加重肝硬化大鼠内毒素血症.热处理及LPS注入后,肝硬化大鼠及正常大鼠血浆及肝组织HSP72表达均较未热处理组增强,而未热处理的两组大鼠LPS注入后血浆TNF-α含量明显高于热处理组.结论:热应激能促进肝硬化内毒素血症大鼠肝组织及血浆HSP72表达,而抑制TNF-α分泌.     

~(18)F-脱氧葡萄糖单光子发射式计算机断层显像对肠辐射损伤检测方法的研究

目的:探讨 18F-脱氧葡萄糖(18F-FDG)单光子发射式计算机断层显像(SPECT-CT)对大鼠肠辐射损伤检测的敏感性.方法:选取20只雄性SD大鼠随机分为两组,即正常组和模型组.模型组大鼠进行60Co一次性全身照射8.0Gy,观察大鼠一般情况;模型组腹泻症状明显时立即做18F-FDG SPECT-CT并检测肠道浓聚影;检测后取出大鼠小肠,4%甲醛固定,常规病理切片,于电子显微镜下观察.结果:(1)6只大鼠照射4 d后出现腹泻,3只5 d后出现腹泻,1只观察7 d未出现腹泻.(2)SPECT-CT显示腹泻大鼠肠道有明显浓聚影,正常组大鼠肠道无明显浓聚影.(3)病理显示:模型组大鼠小肠破坏严重,炎症明显;对照组大鼠小肠无粘连、局部充血,肠壁不增厚,未见溃疡.结论:18F-FDG SPECT-CT作为一种无创性检测方法,能够直观有效地检测大鼠肠辐射损伤.     

糖尿病大鼠骨骼肌细胞膜葡葡糖转运蛋白4含量在不同强度运动状态下的变化

背景:运动能影响骨骼肌细胞膜葡萄糖转运蛋白4含量,但不同强度的运动对骨骼肌细胞膜葡萄糖转运蛋白4含量产生怎样的影响还不被人们所知.目的:拟了解不同强度运动对大鼠骨骼肌细胞膜葡萄糖转运蛋白4含量的影响.设计、时间及地点:随机对照动物实验,于2007-09/10在辽宁师范大学中心实验室完成.材料:健康SD大鼠60只,体质量(200±16)g,雌雄不拘.方法:制备糖尿病大鼠模型.将SD大鼠分为6组:正常对照组、糖尿病对照组和糖尿病4种不同强度运动组(包括15m/min组、20m/min组、25m/min组和30m/min组),每组10只.运动组按上述强度训练50min/d, 6d/周,共6周.主要观察指标:用Western blot免疫印迹法检测骨骼肌细胞膜表面葡萄糖转运蛋白4表达:并观察不同强度运动对各组大鼠体质量、血糖和胰岛素水平的影响.结果:①与糖尿病对照组相比,20m/min和25m/min组股四头肌葡萄糖转运蛋白4含量分别升高44.2%和48.0%(P＜0.01);15m/min和30m/min组股四头肌葡萄糖转运蛋白4含量分别升高17.3%和19.2%(P＜0.05),但各组仍没有恢复到正常对照组水平.②与糖尿病对照组相比,20m/min组大鼠体质量恢复良好(P＜0.05);不同强度运动组大鼠血糖均下降(P＜0.05或P＜0.01),以15m/min组和20m/min组下降显著;15m/min组、20m/min组和25m/min组大鼠胰岛素水平均显著升高(P＜0.01).结论:以20m/min和25m/min的强度运动对SD大鼠股四头肌葡萄糖转运蛋白4含量的升高可能具有最佳的影响效果.     

大鼠放射性肺损伤模型制作及影像学评价

目的研究大鼠放射性肺损伤影像学模型制作方法,评价HRCT对放射性肺损伤的早期诊断价值.方法 30只SD大鼠随机分为对照组和照射组,右肺单分隔15Gy60Co照射建立肺损伤模型.照射后第4、8、16、24周分别行CR和HRCT检查.结果 HRCT显示大白鼠放射性肺损伤,包括肺部毛玻璃改变、斑片状及条索样高密度影,显示病变时间早于CR片,阳性率高于CR(P<0.05).结论 SD大鼠单侧肺单分隔15Gy照射可以制作放射性肺损伤模型.HRCT可以早期诊断放射性肺损伤.     

电针足三里兴奋胆碱能通路对烫伤大鼠胃肠黏膜血流量和肠动力的影响

目的 观察电针足三里穴对烫伤大鼠早期胃和小肠黏膜血流量及小肠动力的影响,探讨其与胆碱能神经通路的关系.方法 Wistar大鼠80只,随机分为假烫组、烫伤组、电针治疗组、非经非穴组、迷走神经切断(迷切)组、迷切后电针组、M受体阻断组、M阻断后电针组,各组又分为2 h和6 h两个亚组,每个时间点组5只.除假烫组外,其余大鼠采用置于100 ℃沸水中15 s造成背部35%总体表面积(TBSA)Ⅲ度烫伤.迷切组或M受体阻断组分别于烫伤后30 min切断双侧膈下迷走神经或腹腔注射阿托品2 mg/kg;电针组针刺双侧足三里,持续1.5 h,强度为2 mA,2～100 Hz.于烫伤后2 h和6 h采用激光多谱勒血流仪测定胃和小肠黏膜血流量,采用葡聚糖蓝推进率测定各组大鼠小肠动力.结果 各烫伤组胃和小肠黏膜血流量及小肠推动率较假烫组均显著降低(P均<0.01);电针治疗组胃和小肠黏膜血流量及小肠推动率伤后2 h和6 h较烫伤组明显增加(P均<0.01);切断迷走神经或阻断M受体可使伤后2 h胃黏膜血流量和小肠推动率较烫伤组降低程度更加明显(P均<0.01);迷切或M受体阻断后电针不能改善肠动力和胃肠黏膜血流.结论 电针足三里穴能明显改善大鼠烫伤早期小肠动力,增加胃肠黏膜血流量;其作用机制可能与激活胆碱能神经通路有关.     

实时三维超声和二维斑点追踪技术评价肝硬化患者右心房功能

目的探讨实时三维超声(RT-3DE)和二维斑点追踪(2D-STI)评价肝硬化患者右心房功能的价值。方法 60例临床确诊的肝硬化患者分为30例肝硬化代偿组(B组)和30例肝硬化失代偿组(C组),与30例健康对照组(A组)应用RT-3DE获得右心房容积指数(RAVI);应用2D-STI获取收缩期、舒张期右心房心肌应变与应变率参数MSs、MSe、MSa、MSRs、MSRe、MSRa。结果与A组相比,B组右心房容积参数RAVImax、RAVImin、RAVIpre、RAVIt、ETV/e′TV增大,C组较B组进一步增大(P0.05);B组RAVIp减小(P0.05),C组较B组进一步减小(P0.05);C组较B组MS、MSR减低(P0.05)。相关分析显示MSe、MSRe与ETV/e′TV呈中度负相关(r=-0.390、-0.373,P0.001)。结论 RT-3DE和2D-STI不仅能够敏感反映肝硬化患者右心房功能的早期改变,而且还可以定量评估肝硬化患者不同阶段右心房形态及功能改变,具有明显的临床意义。     

~(99m)Tc-3PRGD_2在放射性肺炎早期诊断中的研究

目的探讨~(99m)Tc-3PRGD_2诊断早期放射性肺炎的影像学研究方法。方法将20只雌性SD大鼠随机分为正常对照组、30Gy照射对照组,每组各10只。照射后0、10、20、30d时,以20%乌拉坦腹腔麻醉动物,行CT及SPECT扫描,观察影像学变化;并在照射后30d时进行病理组织学检查。结果受照射大鼠肺CT影像在30d时显示放射性肺炎变化明显,SPECT动态扫描图像显示不同组间在照射后10d已出现非常明显的差异;照射后30d时病理组织学检查显示受照射大鼠肺组织改变明显。结论 ~(99m)Tc-3PRGD_2对于早期放射性肺炎的诊断具有潜在价值。     

Gastrointestinal motor alterations induced by precipitated benzodiazepine withdrawal in rats.

The effects of benzodiazepine withdrawal on intestinal motor activity and propulsion were investigated in two groups of diazepam-dependent rats (15 mg/kg/day for 8 days). Withdrawal was precipitated by injection of two benzodiazepine antagonists (Ro 15.1788 and PK 11.95) acting on central and peripheral-type receptors, respectively. Intestinal motor activity was assessed by implanting electrodes for long-term electromyographic recordings. Gastrointestinal transit was evaluated after gavage by a marker (51CrO4Na2) and radioactivity counting. Both RO 15.1788 (15 mg/kg) and PK 11.195 (5 mg/kg) triggered an abstinence syndrome with behavioral and autonomic signs. At the intestinal level, Ro 15.1788 induced a phase of strong irregular spiking activity (173 +/- 63 min) which remained located in the duodenum. In contrast, PK 11.195 induced a period of propagated myoelectric complexes characterized by phases II and III of high amplitude. The cecal frequency was doubled during the 1st hr after withdrawal induced by the two antagonists. Both Ro 15.1788 and PK 11.195 at this dosage had no effect per se on intestinal motility in vehicle-treated rats. In the second group of rats, gastric emptying was enhanced by 49.4 and 45.6% by Ro 15.1788 and PK 11.195, respectively. In contrast, PK 11.195 was able to accelerate the intestinal transit more than did Ro 15.1788 (geometric center, 5.9 +/- 0.43 and 5.3 +/- 0.49, respectively, vs. 4.1 +/- 0.31 in control rats). Our study shows that precipitated benzodiazepine withdrawal in diazepam-dependent rats induces alterations of the intestinal myoelectrical activity leading to an increase of the gastrointestinal transit. Central and peripheral-type receptors are involved in these effects.     

Clonidine delays small intestinal transit in the rat

Subcutaneous clonidine (0.01--1.0 mg/kg) was found to delay small intestinal transit but not gastric emptying in the unanesthetized rat, with a maximal effect seen at 0.1 mg/kg. Gastric emptying was expressed as the percentage of intragastrically administered 51Cr emptied into the small intestine after 45 min. Small intestinal transit was the percentage of the small intestinal length traveled 45 min after oral or duodenal administration of black ink. The depression of small intestinal transit by clonidine to 20 to 30% of control values was blocked by phentolamine and yohimbine, but not by prazosin or phenoxybenzamine, suggesting a presynaptic (alpha-2) agonist action of clonidine. Pretreatment of rats with 6-hydroxydopamine, propranolol, atropine, methysergide, naloxone, mepyramine or metiamide failed to alter the effects of clonidine. These results suggest that an alpha adrenergic receptor, possibly presynaptic, regulates small bowel propulsion in rat without involvement of acetylcholine, norepinephrine, endorphins, histamine or serotonin.     

Epidermal growth factor reduces ischemia-reperfusion injury in rat small intestine

OBJECTIVE: To measure the effect of pre-ischemic administration of intraluminal epidermal growth factor on the changes in intestinal permeability induced by 30 mins of superior mesenteric artery occlusion, followed by 2 hrs of reperfusion. DESIGN: Prospective, randomized, placebo-controlled experimental study. SETTING: University basic science research laboratory. SUBJECTS: Healthy, young, adult, male Sprague-Dawley rats. INTERVENTIONS: A 10-cm segment of small intestine was isolated and studied in situ in rats that were anesthetized with fentanyl and mechanically ventilated. Intestinal ischemia-reperfusion injury was induced by temporary occlusion of the superior mesenteric artery for 30 mins, followed by 2 hrs of reperfusion. Three groups were studied: time controls with a sham operation, saline-treated ischemia-reperfusion, and epidermal growth factor-treated ischemia-reperfusion. Epidermal growth factor, 100 ng/min, was infused intraluminally, beginning 30 mins before and continued until 40 mins after ischemia. MEASUREMENTS AND MAIN RESULTS: Intestinal permeability was measured for each 10-min time period by using chromium-labeled EDTA. Histopathologic injury was assessed by light microscopy. After superior mesenteric artery occlusion, intestinal permeability increased approximately ten-fold and was sustained for 2 hrs of reperfusion in saline-treated rats. Pretreatment with epidermal growth factor significantly reduced the permeability changes during reperfusion by >60% compared with saline-treated animals (p <.05). Histopathologic sections revealed apparently more extensive loss of epithelial cells and mucosal disruption in saline-treated intestine compared with epidermal growth factor-treated intestine. CONCLUSION: Pre-ischemic administration of intraluminal epidermal growth factor significantly protects against intestinal ischemia-reperfusion injury.     

Determination of single and repeated red cell volumes by the indicator dilution method using carbon monoxide as the indicator

The use of radioactive isotopes limits clinical applications of blood volume measurement in the ICU. We measured red cell volumes with carbon monoxide-labeled RBC in six dogs and five human volunteers. The measured values obtained on the dogs were compared with the simultaneous measurements with the 51Cr method; the ratio of the carbon monoxide to 51Cr values ranged from 0.86 to 1.17, and the mean ratio was 1.0 +/- 0.1 (SD), r = .93. We infer from these results that the carbon monoxide method has several advantages over the 51Cr method: a) the short labeling time (about 1 min), b) rapidly decreasing background levels of carbon monoxide with FIO2 1.0, and c) repeatability at intervals of several hours.     

Centrally mediated inhibition of small intestinal transit and motility by morphine in the rat

The effects of morphine treatment on small intestinal propulsion and contractile activity were investigated in unanesthetized rats. Intragastrically, s.c. and i.c.v. administered morphine produced dose-related decreases in the transit of a radioactive marker (51Cr) through the small intestine. Morphine was most potent after i.c.v. administration whereas the intragastric route was the least potent. Intracerebroventricular and s.c. morphine also delayed gastric emptying of [3H]polyethylene glycol placed directly into the stomach. Intragastric morphine at doses up to 500 mg/kg did not alter gastric emptying. The antitransit effects of i.c.v. and s.c. morphine were antagonized by prior treatment with naloxone (2 mg/kg s.c.). Changes in small intestinal motility resulting from morphine treatment were measured directly through chronically implanted silastic cannulas. Two cannulas were implanted in each rat, one into the duodenum and the second in the proximal jejunum. Each cannula was perfused with distilled water at a low flow rate (0.04 ml/min) and increases in intraluminal pressure associated with contractions were recorded as changes in outflow resistance. Morphine treatment decreased the frequency of contractions in both areas of the small intestine. Intracerebroventricular morphine again was the more potent route of administration when compared to s.c. morphine. These data indicate that morphine can act within the central nervous system to alter autonomic outflow to the small intestine. The result is an inhibition of motility which accounts for the antitransit effects of opiate-like compounds in the rat.     

In Vivo Assessment of Pulmonary Vascular Integrity in Experimental Pulmonary Edema

During single pass indicator studies across the lungs [(14)C]urea remains in the vascular compartment, but its molecular size and solubility suggest it might escape abnormally permeable vessels. To test the hypothesis that [(14)C]urea might be used to distinguish pulmonary edema due to acutely increased intravascular pressure from that due to vascular damage by alloxan, we studied [(51)Cr]erythrocytes (r), [(125)I]albumin (a), [(14)C]urea (u), and tritiated water as dilution indicators in the pulmonary circulation of anesthetized dogs. In addition, the adequacy of albumin as an intravascular indicator was evaluated.Indicator curves, blood gases, hematocrit, and vascular pressures were determined during a base-line period and repeated 30 and 60 min after treatment in five groups of dogs: (a) saline control. (b) alloxan edema. (c) epinephrine infusion, (d) volume overload, and (e) left atrial (LA) balloon obstruction.Groups b, d, and e developed a similar degree of edema judging by wet/dry lung weights and histology. Groups a and c did not develop edema. In alloxan edema, differences between the mean transit time volume of u and r (V(v-r)) increased over base line at 30 (P < 0.001) and 60 min (P < 0.02); the differences between the mean transit time volume of a and r (V(e-r)) increased slightly at 30 (P < 0.03) and 60 min (P < 0.02); and V(u-r) significantly exceeded V(a-r) at 30 (mean difference = 9 ml, P < 0.02) and 60 min (mean difference = 11, P < 0.04). In none of the other groups did V(u-r) significantly exceed V(a-r). Thus, comparison of V(u-r) with V(a-r) may permit distinction between "high pressure" and "increased permeability" pulmonary edema.Albumin was not a consistently reliable indicator of intravascular volume as compared with composite red cell and albumin curve.     

多器官功能障碍综合征时肠淋巴细胞再循环的变化

目的观察大鼠肠缺血--再灌注致多器官功能障碍综合征(MODS)后肠淋巴细胞归巢的改变,从肠黏膜免疫角度探讨肠淋巴细胞归巢在MODS中的作用.方法采用随机分组方法,用夹闭肠系膜动脉根部45 min、再灌注6 h制备大鼠MODS模型.MODS 1组大鼠(n=10)于再灌注第5 h从肠系膜淋巴管插管引流肠淋巴液1 h,检测淋巴细胞数及T、B细胞比例,同时取肠、肝、肺、肾组织进行病理组织学观察;对照1组(n=6)大鼠仅单纯施行肠淋巴液引流.MODS 2组大鼠(n=6)于再灌注第3 h从肠系膜淋巴管插管引流肠淋巴液2 h,肠淋巴细胞在体外经51Cr标记后,于第6 h回输入大鼠的体内,1 h后取上述各组织或器官以检测51Cr-淋巴细胞在体内的分布; 对照2组单纯施行肠淋巴液引流及淋巴细胞标记后回输.结果肠缺血-再灌注致MODS时,MODS组大鼠由肠黏膜迁移至血循环肠淋巴细胞总数[(0.28±0.15)×107/h]较对照组[(2.69±0 .61)×107/h]显著降低;而归巢至肠黏膜的肠淋巴细胞增加,派伊尔(Peyer)淋巴结及小肠内所分布的 51Cr-淋巴细胞量分别占总51Cr细胞量为(5.04±1.23)%和(3. 23±1.69)%,显著高于对照组(2.69±2.19)% 和(1.11±0.75)%,P均<0.05,并伴随肠淋巴内毒素含量及肿瘤坏死因子-α(TNF-α)浓度显著增加及重要器官或组织功能损害.结论肠淋巴细胞归巢增加是MODS发病机制的一个重要方面.     

~1H-MRS采用短回波扫描在超急性脑梗死治疗中的应用价值

目的探讨MR波谱采用激励回波采集方法、短回波时间扫描时,MR波谱在超急性脑梗死治疗中的临床应用价值。材料与方法采取溶栓治疗与非溶栓治疗的超急性期脑梗死患者经住院治疗1 w后均行常规磁共振及MR波谱扫描,对病灶中心区、病灶边缘区、病灶周围正常区及对侧镜像区N-乙酰天门冬氨酸(N-acetylpartate,NAA)/总肌酸(肌酸+磷酸肌酸)(Creatine,Cr)、胆碱化合物(Choline,Cho)/Cr、NAA/Cho等比值进行分析。结果 (1)非溶栓组病灶中心区NAA/Cr、NAA/Cho值明显降低,Cho/Cr、肌醇(Myo-inositol,m I)/Cr值高于病灶边缘区,谷氨酸复合物(Glutamine/Glutamate,Glx)/Cr值高于对侧镜像区(P0.05);病灶边缘区NAA/Cr值低于病灶周围正常区,NAA/Cho值低于对侧镜像区(P0.05);病灶中心区NAA/Cho、Cho/Cr及Glx/Cr值与临床美国国立卫生院神经功能缺损评分(National Institutes of Health Stroke Scale,NIHSS)呈明显相关性(r=-0.626、0.629、-0.689,P0.05),病灶边缘区域乳酸(Lactate,Lac)/Cr值与临床NIHSS评分具有明显相关性(r=0.812,P0.05)。(2)溶栓组病灶中心区Cho/Cr值高于病灶边缘区,病灶边缘区NAA/Cr、m I/Cr值低于对侧镜像区,病灶边缘区NAA/Cho值低于病灶周围正常区(P0.05);病灶中心区NAA/Cho、Cho/Cr、m I/Cr及Glx/Cr值与临床NIHSS评分具有明显相关性(r=-0.686、0.791、-0.757、-0.791,P0.05),病灶边缘区Lac/Cr值与临床NIHSS评分具有明显相关性(r=0.735,P0.05)。(3)溶栓组病灶边缘区NAA/Cr、NAA/Cho及m I/Cr值明显高于非溶栓组,病灶中心区、病灶周围正常区Lac/Cr值明显低于非溶栓组,病灶中心区Glx/Cr值明显高于非溶栓组(P0.05)。结论 ~1H-MRS采用短回波时间扫描检测到更多代谢物的变化,能更全面地检测脑梗死临床治疗后受损脑组织的恢复情况,能客观评估诊疗效果及其预后,为临床应用提供客观的影像学依据。     

Cholinergic neurons mediate intestinal propulsion in the rat

Cholinergic influences on intestinal propulsion were determined in vivo in fasted rats by measuring the movement of a nonabsorbable radioactive marker along the intestine following treatment with cholinergic drugs. The marker was instilled directly into the intestine via a previously implanted cannula. The direct effects of cholinergic drugs on intestinal contractions were determined in vitro using isolated segments of duodenum and jejunum. Neostigmine (0.1 mg/kg) produced a marked increase in intestinal transit that was blocked by atropine pretreatment (1.0 mg/kg) but not hexamethonium pretreatment (20 mg/kg). Atropine pretreatment alone significantly delayed transit while hexamethonium treatment alone did not affect intestinal transit. Neostigmine produced a concentration-dependent (0.3-30 microM) increase in contractions in both duodenal and jejunal segments in vitro. Prior incubation of the tissues with atropine (10(-7) M) blocked the neostigmine-induced contractions while prior incubation with hexamethonium (10(-6) M) did not. Contractions produced by substance P were not affected by atropine or hexamethonium. These data indicate that enhancement of cholinergic neurotransmission by neostigmine treatment increased intestinal propulsion and that this effect was mediated at muscarinic cholinergic receptors. Furthermore, inhibition of ongoing cholinergic transmission by atropine treatment reduced intestinal propulsion. The increase in transit produced by neostigmine may result from a stimulation of intestinal contractions. Cholinergic neurons are important mediators of intestinal propulsion in the rat as in other species.     

Ischemic preconditioning protects against gut dysfunction and mucosal injury after ischemia/reperfusion injury

Mesenteric ischemia/reperfusion (IR) damages the gastrointestinal epithelia and impairs gut function. Ischemic preconditioning (IPC) has been shown to protect organs against IR injury. We hypothesized that IPC protects the gut from IR injury. Rats were randomized to a sham group, a sham early IPC + IR group (sham IPC + SMA occlusion for 30 min and 6 h of reperfusion), an early IPC + IR group (IPC, three cycles of SMA occlusion for 4 min and reperfusion for 10 min) followed immediately by SMA occlusion for 30 min and 6 h of reperfusion), a sham 24-h group, a sham late IPC + IR group (sham IPC followed by additional reperfusion for 24 h + SMA occlusion for 30 min and 6 h of reperfusion), and a late IPC + IR group (IPC protocol followed by additional reperfusion for 24 h, and then SMA occlusion for 30 min followed by 6 h of reperfusion). At 6 h, transit was determined and expressed as the mean geometric center. Ileum was harvested for assessment of mucosal injury and myeloperoxidase (MPO) activity. Tissue water was determined using the wet-to-dry weight ratio to assess gut edema. Early IPC + IR significantly improved transit (3.9 +/- 0.2), decreased MPO levels (3 +/- 2), and lessened mucosal injury (1.2 +/- 0.3) compared with animals subjected to sham early IPC + IR (transit, 2.9 +/- 0.2; MPO levels, 9 +/- 1; mucosal injury, 3.0 +/- 0.6). Late IPC + IR also improved transit (6.0 +/- 0.4) and decreased MPO levels (1 +/- 1) compared with sham late IPC + IR (transit, 4.4 +/- 0.2; MPO levels, 8 +/- 1), however, there was no difference in the mucosal protection between late IPC + IR (1 +/- 0.3) and sham late IPC + IR (1 +/- 1). Our results suggest that early and late IPC improves intestinal dysfunction, decreases inflammation, and provides mucosal protection in the intestine after IR. Our results show that IR-induced gut dysfunction can be improved by IPC. Both phases of IPC can potentially be useful in the clinical setting of surgical patient care.