高压氧干预对大鼠肾缺血再灌注损伤保护作用的实验研究

目的探讨高压氧(HBO)对大鼠肾缺血再灌注损伤(IRI)的作用及其机制。 方法建立大鼠肾IRI模型,54只Wistar大鼠分为假手术组、肾IRI组和HBO治疗组,每组18只。各组分别于再灌注后1,3,5 h（每个时间点6只）采血测定血浆肿瘤坏死因子（TNF-α）、丙二醛（MDA）的水平及肾功能［肌酐(SCr）、尿素氮（BUN)］;同时肾组织HE染色后光镜观察病理变化。 结果(1)肾IRI组血浆TNF-α、MDA和SCr、BUN的水平明显高于假手术组(P<0.05);与肾IRI组相比,HBO治疗组血浆TNF-α、MDA和SCr、BUN的水平显著降低(P<0.05)。(2)假手术组各时间点肾小球、肾小管上皮细胞结构正常;肾IRI组随时间延长,肾小球毛细血管、肾小管上皮细胞损伤逐渐加重;HBO治疗后肾损伤的程度明显减轻,再灌注后1 h和3 h肾损伤减轻的程度明显优于再灌注后5 h。 结论TNF-α和MDA促进了肾IRI的发生发展。HBO通过减少TNF-α的生成和防止组织脂质过氧化,明显减轻了肾IRI,保护了肾功能。HBO早期干预更有利于防治肾IRI。     

高压氧干预对急性有机磷中毒大鼠脑组织中缺氧诱导因子-1α表达的影响

目的观察急性有机磷中毒大鼠脑组织缺氧诱导因子-1α(HIF-1α)表达的变化，探讨高压氧（HBO）对急性有机磷中毒脑损伤的作用及其机制。 方法健康雄性SD大鼠60只，按随机数字表法分为健康对照组、中毒组、常规治疗组和HBO治疗组，健康对照组6只大鼠，其余每组18只，建立大鼠急性有机磷中毒脑损伤模型，均造模成功。常规治疗组给予长托宁和氯解磷定治疗1次，HBO治疗组在给予常规治疗后即行HBO治疗1次。中毒组、常规治疗组和HBO治疗组分别于造模成功后1、3和7h（每个时间点6只）下腔静脉采血检测丙二醛（MDA）的含量，荧光定量PCR检测脑组织HIF-1α mRNA的表达，免疫组织化学法检测脑组织HIF-1α蛋白的表达，同时行HE染色观察脑组织病理改变。 结果①HE染色显示，治疗后HBO治疗组的脑组织病理损伤形态学表现较中毒组有所减轻；②与健康对照组比较，中毒组常规治疗组和HBO治疗组各时间点脑组织HIF-1α蛋白表达明显增高（P<0.05），各时间点脑组织HIF-1α mRNA相对表达量亦明显增高（P<0.05）；③造模成功后1、3和7h，HBO治疗组各时间点的脑组织HIF-1α的表达分别为（226.57±57.49）、（205.91±30.36）、（187.67±29.25），明显低于较中毒组脑组织HIF-1α的表达［（1305.67±167.17）、（2667.83±367.79）、（1709.24±199.07）］，且血清MDA含量［（7.74±0.14）、（7.40±0.13）和（6.10±0.08）nmol/ml］亦较中毒组的血清MDA含量［（9.48±0.05）、（11.56±0.13）和（12.26±0.14）nmol/ml］明显下降，组间差异均有统计学意义（P<0.05）；而HBO治疗组治疗后1h和3h时间点的上述指标低于同时间点常规治疗组，组间差异亦有统计学意义（P<0.05）；④线性相关分析表明，HIF-1α mRNA相对表达量与血清MDA含量具有显著的正相关性（r=0.909，P=0.000）。 结论HIF-1α参与了急性有机磷中毒性脑损伤的病理生理过程，HBO对急性有机磷中毒性脑损伤早期的保护作用优于常规治疗组，其作用机制与抗氧化损伤和抑制HIF-1α的表达有关。     

高压氧对缺血再灌注小鼠脑组织MMP-9﹑MMP-2mRNA的表达及血脑屏障通透性的影响

目的探讨高压氧（HBO）对缺血再灌注小鼠脑组织中基质金属蛋白酶（MMPs）MMP-9、MMP-2 mRNA的表达及血脑屏障通透性的影响。 方法复制清醒小鼠脑缺血再灌注模型，并于再灌注期间行0.25 MPa HBO治疗5次，在处死动物前1h经尾静脉注射2%伊文蓝（EB）,采用逆转录多聚酶链反应（RT-PCR）方法及比色法分别检测脑组织中MMP-9、MMP-2 mRNA的表达及EB的含量。 结果脑缺血再灌注组MMP-9、MMP-2 mRNA的表达及EB的含量明显高于假手术组，差异有统计学意义（P<0.01），高压氧组与假手术组比较，脑组织中MMP-9、MMP-2 mRNA的表达及EB的含量相近（P&rt;0.05），HBO+脑缺血再灌注组脑组织中基质金属蛋白酶MMP-9、MMP-2 mRNA的表达及EB的含量明显低于脑缺血再灌注组，差异有统计学意义（P<0.01）。 结论高压氧可明显减少脑缺血再灌注脑组织中基质金属白蛋酶MMP-9、MMP-2的表达，具有降低血脑屏障通透性的作用。     

电针对局灶脑缺血再灌注大鼠大脑皮质基质细胞衍生因子-1α表达的影响及其促进脑内血管再生的作用

目的探讨电针促进局灶性脑缺血再灌注大鼠脑内缺血区血管再生的作用机制。 方法选择Sprague-Dawley大鼠84只,分为对照组、模型组和模型电针组。采用线栓法制备局灶性脑缺血再灌注模型并按局灶性脑缺血1h再灌注后观察时间点,将模型组和模型电针组分为第1,3,7,14和21天5个亚组。取双侧合谷穴（LI4）为电针刺激穴位。再灌注第3,7,14天,采用逆转录聚合酶链反应法检测基质细胞衍生因子-1α（SDF-1α）mRNA的表达;再灌注后各时间点,采用免疫组织化学法检测SDF-1α蛋白的表达,CD34标记微血管并计数。 结果与对照组各时间点比较,模型组、模型电针组缺血区大脑皮质SDF-1α蛋白表达增加（P<0.05）;与模型组比较,再灌注第3,7,14天,模型电针组缺血区大脑皮质SDF-1α mRNA表达增加（P<0.05）。再灌注第1天,模型电针组缺血区大脑皮质SDF-1α蛋白表达增强,微血管计数增加,但与模型组比较,差异无统计学意义（P&rt;0.05）。再灌注第3,7,14,21天,模型电针组缺血区大脑皮质SDF-1α蛋白表达明显增强,微血管计数明显增加（P<0.05）。 结论电针可能通过上调局灶性脑缺血再灌注大鼠缺血区大脑皮质SDF-1α mRNA 及蛋白质的表达而促进缺血区大脑皮质血管再生。     

穴位电针刺激对局灶性脑缺血再灌注大鼠基质细胞衍生因子/CXC类趋化因子受体4信号轴的影响

目的探讨穴位电针刺激对局灶性脑缺血再灌注大鼠基质细胞衍生因子（SDF-1α）/CXC类趋化因子受体4（CXCR4）信号轴的影响。 方法选取SD大鼠98只,按照随机数字表法将其分为对照组（8只）、模型组（50只）和电针组（40只）,根据造模后观察时间点的不同,将模型组和电针组大鼠细分为第1、3、7、14、21天5个亚组。采用线栓法对模型组和电针组大鼠进行造模,制备大鼠局灶性脑缺血再灌注模型,在电针组大鼠双侧合谷穴采用电针刺激,对照组和模型组不作特殊处理。采用免疫组化法检测模型组与电针组大鼠CXCR4阳性细胞的数目,第3、7、14天时采用逆转录聚合酶反应法（RT-PCR）检测模型组和电针组大鼠SDF-1α mRNA及CXCR4 mRNA的表达量。 结果造模后,模型组大鼠缺血区大脑皮质SDF-1α mRNA的表达水平随再灌注时间延长呈单峰样增加,造模后3d（0.971±0.058）明显升高,7d（1.057±0.054）达峰值,随后逐渐下降（P<0.05）。造模后3d、7d、14d,电针组大鼠SDF-1α mRNA表达亦呈单峰样变化,造模后7d达峰值（P<0.05）,且电针组大鼠SDF-1α mRNA水平较模型组同时间点高（P<0.05）。模型组与电针组造模后7d、14d的CXCR4 mRNA相对值均高于组内造模后3d（P<0.05）,造模后14d时的CXCR4 mRNA相对值亦高于组内造模后7d（P<0.05）,与模型组同时间点比较,电针组大鼠CXCR4 mRNA相对值均较高,差异有统计学意义（P<0.05）。模型组大鼠CXCR4阳性细胞于造模后1d［（5.60±1.18）个/HP］开始增加,7d［（18.93±1.38）个/HP］达峰值,14d［（8.20±1.08）个/HP］开始回落,21d［（5.80±1.01）个/HP］的表达量仍然较高（P<0.05）。电针组大鼠CXCR4阳性细胞计数的变化趋势与模型组相似,但电针组的增加趋势更加明显（P<0.05）。 结论穴位电针刺激可激活局灶性脑缺血再灌注大鼠缺血区大脑皮质的SDF-1α/CXCR4信号轴,促进血管新生。     

高压氧对局灶性脑缺血再灌注大鼠脑组织小窝蛋白-2表达及血脑屏障通透性的影响

目的研究高压氧（HBO）对局灶性脑缺血再灌注（I/R）大鼠脑组织小窝蛋白-2（caveolin-2）、基质金属蛋白酶-9（MMP-9）表达及血脑屏障(BBB)通透性的影响。 方法将雄性Wistar大鼠370只分成假手术组80只、I/R组130只、HBO组80只、HBO+I/R组80只。采用线栓法建立大鼠局灶性脑缺血再灌注模型。HBO组和HBO+ I/R组于再灌注0,2,9,21,45,69 h进入HBO舱,经0.25 MPa HBO治疗5次。采用比色法、免疫组化法及Western blot法检测BBB的通透性、caveolin-2及MMP-9的表达。 结果第4,12,24,48,72小时脑组织伊文思兰（EB）的含量与0 h组相比明显增加,再灌注后4 h脑组织EB的含量最高。HBO+I/R组脑组织EB的含量明显低于I/R组。HBO组与假手术组相比脑组织EB的含量无明显变化。脑缺血再灌注第24,48,72小时caveolin-2、MMP-9表达明显高于0 h组。HBO+I/R组与I/R组相比脑组织caveolin-2、MMP-9表达显著减低。HBO组脑组织caveolin-2、MMP-9表达与假手术组相比无明显变化。 结论HBO降低脑缺血再灌注时增高的脑微血管内皮细胞caveolin-2和MMP-9的表达,从而降低BBB通透性。     

高压氧联合细胞周期特异性药物对结肠腺癌Lovo细胞的杀伤作用

目的探讨高压氧(HBO)联合细胞周期特异性药物氟尿嘧啶对结肠腺癌Lovo细胞的杀伤作用。 方法0.20 MPa HBO暴露后联合应用不同浓度氟尿嘧啶处理结肠腺癌Lovo细胞。流式细胞仪检测细胞周期,四甲基偶氮唑盐（MTT）法观察其对结肠腺癌细胞增殖的抑制作用。 结果①HBO暴露后Lovo细胞S期细胞积聚较对照组明显增多（P<0.01）,HBO暴露后24 h组Lovo细胞S期积聚明显高于HBO暴露后12 h组和48 h组（P<0.01）;②0.20 MPa HBO暴露后24 h联合应用低浓度氟尿嘧啶（≤8 μM）作用Lovo细胞12 h后,HBO联合氟尿嘧啶组癌细胞增殖的抑制程度与氟尿嘧啶组比较,差异有统计学意义(P<0.05);药物作用48 h后,HBO联合氟尿嘧啶组与氟尿嘧啶组比较,差异有统计学意义 (P<0.01);③中浓度和高浓度（16、32和64 μM）的氟尿嘧啶作用于Lovo细胞12 h,HBO联合氟尿嘧啶组与氟尿嘧啶组之间差异无统计学意义 (P&rt;0.05);药物作用48 h后,HBO联合氟尿嘧啶组与氟尿嘧啶组比较差异有统计学意义 (P<0.05)。 结论0.20 MPa HBO暴露可提高细胞周期特异性药物氟尿嘧啶对Lovo细胞的杀伤作用,尤其增强低浓度氟尿嘧啶对结肠腺癌细胞的杀伤作用。     

不同时间窗高压氧治疗对脊髓损伤患者疗效的影响

目的观察不同时间窗高压氧治疗对脊髓损伤（SCI）患者疗效的影响。 方法共选取284例SCI患者,将其随机分为高压氧治疗组（HBO组）及对照组。2组均给予常规处理（包括脱水剂、神经营养药物、康复训练、针灸以及对症支持治疗等）,HBO组患者在此基础上于不同时间窗（SCI发生8 h以内、8 h~1 d、1 d~1周、1周以上）分别辅以HBO治疗。于治疗前、治疗3个月后分别采用美国脊髓损伤协会(ASIA)评分及Barthel指数对患者脊髓功能及日常生活活动（ADL）能力进行评定。 结果在SCI发生8 h内开始治疗,2组患者脊髓感觉、运动功能及ADL能力均较治疗前显著改善（P<0.01）,2组间疗效差异无统计学意义（P&rt;0.05）;在SCI发病24 h内或1周内开始治疗,2组患者脊髓功能、ADL能力亦较治疗前获得一定程度改善（P<0.05）,但均明显不及发病8 h内开始治疗的患者（P<0.05）;且此时HBO组疗效显著优于对照组（P<0.05）;在SCI发病1周后开始治疗,发现2组患者脊髓功能及ADL能力均无明显改善（P＞0.05）。 结论于SCI发病早期（<8 h）辅以HBO治疗,能显著改善患者脊髓功能及ADL能力,其疗效明显优于其它时间窗治疗。     

高压氧辅助治疗对脑卒中后抑郁患者血清细胞因子及抑郁状态的影响及其临床意义

目的探讨高压氧(HBO)治疗对脑卒中后抑郁(PSD)患者血清细胞因子［肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）］和抑郁状态的影响及其临床意义。 方法将60例PSD患者随机分为高压氧治疗组(HBO组)30例和常规治疗组(常规组)30例,常规组仅给予临床常规治疗,HBO组在常规治疗的基础上加用HBO治疗。应用双抗体夹心酶联免疫吸附法（ELISA）检测HBO组和常规组治疗前、后血清TNF-α及IL-1β的水平。于治疗前与治疗30 d后,采用汉密尔顿抑郁量表(HAMD)、中国卒中量表(CSS)、改良Barthel指数（MBI）评定2组的疗效。 结果治疗前,脑卒中后重度抑郁患者的血清TNF-α、IL-1β水平显著高于轻、中度抑郁的患者(P<0.01),中度抑郁患者血清TNF-α、IL-1β水平与轻度抑郁患者比较,差异有统计学意义(P<0.01)。HBO组血清TNF-α及IL-1β的水平与常规组比较,差异无统计学意义(P&rt;0.05)。治疗30 d后,HBO组和常规组血清TNF-α及IL-1β浓度均有下降(P<0.05),且HBO组低于常规组(P<0.01);HBO组和常规组HAMD、CSS、MBI评分较治疗前均显著下降(P<0.01),且HBO组各项评分明显优于常规组(P<0.05)。 结论细胞因子TNF-α、IL-1β参与了PSD的发生和发展,细胞因子的血清水平可在一定程度上反映PSD的严重程度;HBO辅助治疗能够明显降低PSD患者血清TNF-α和IL-1β的水平,显著改善患者的抑郁状态。HBO可能通过减轻脑梗死急性期继发的炎性损伤发挥治疗作用。     

不同时间窗电针结合经颅磁刺激对脑梗死大鼠B细胞淋巴瘤/白血病-2基因及脑源性

目的观察大鼠脑缺血/再灌注后不同时间窗介入电针及经颅磁刺激（TMS）对其B细胞淋巴瘤/白血病-2基因（Bcl-2）和脑源性神经营养因子（BDNF）表达的影响。 方法将100只SD大鼠随机分为正常组、假手术组、治疗组及模型组,每组又根据术后干预时间点不同细分为术后6 h、12 h、24 h、48 h及72 h共5个亚组。采用线栓法将治疗组及模型组大鼠制成左侧大脑中动脉栓塞/再灌注（MCAO/R）模型。治疗组各亚组大鼠分别于脑缺血/再灌注后第6,12,24,48及72小时给予电针及TMS治疗,而正常组、假手术组及模型组各亚组均于上述相同时间点给予假电针及假TMS治疗。各组大鼠均于治疗后第14天时取脑,采用实时荧光定量PCR技术检测脑梗死灶Bcl-2及BDNF mRNA表达情况。 结果各组大鼠梗死侧脑标本中均检测到BDNF及Bcl-2 mRNA阳性表达,治疗组各亚组Bcl-2及BDNF mRNA表达均显著高于模型组各亚组水平（P<0.05）;对治疗组各亚组进行组内比较发现,该组各亚组间BDNF及Bcl-2 mRNA（除术后12 h与术后72 h亚组外）组间差异均具有统计学意义（P<0.05）,其中以术后48 h亚组BDNF及术后24 h亚组Bcl-2 mRNA表达水平相对较高。 结论于脑缺血/再灌注后24~48 h期间介入电针及TMS治疗,能显著促进脑梗死大鼠BDNF及Bcl-2表达,对保护受损神经细胞、促进神经功能恢复具有重要意义。     

急性肾功能损伤与衰竭生物标志物

急性肾功能损伤（ARI）与急性肾功能衰竭（ARF）是加强医疗病房（ICU）的常见疾病．ICU中80％的ARF由急性肾小管损伤所致，而非肾小球或间质性病变引起。其死亡率较高，寻找敏感性和特异性较好的ARI或ARF生物标志物，对早期诊断、治疗和改善预后有着重要意义。本文介绍和评估了ARI或 ARF生物标志物的研究现状。并展望了其未来的前景。[第一段]     

Biomarkers of acute renal injury and renal failure

Acute renal failure (ARF) is a frequent problem in the intensive care unit and is associated with a high mortality. Early recognition could help clinical management, but current indices lack sufficient predictive value for ARF. Therefore, there might be a need for biomarkers in detecting renal tubular injury and/or dysfunction at an early stage before a decline in glomerular filtration rate is noted by an increased serum creatinine. A MEDLINE/PubMed search was performed, including all articles about biomarkers for ARF. All publication types, human and animal studies, or subsets were searched in English language. An extraction of relevant articles was made for the purpose of this narrative review. These biomarkers include tubular enzymes (alpha- and pi-glutathione S-transferase, N-acetyl-glucosaminidase, alkaline phosphatase, gamma-glutamyl transpeptidase, Ala-(Leu-Gly)-aminopeptidase, and fructose-1,6-biphosphatase), low-molecular weight urinary proteins (alpha1- and beta2-microglobulin, retinol-binding protein, adenosine deaminase-binding protein, and cystatin C), Na+/H+ exchanger, neutrophil gelatinase-associated lipocalin, cysteine-rich protein 61, kidney injury molecule 1, urinary interleukins/adhesion molecules, and markers of glomerular filtration such as proatrial natriuretic peptide (1-98) and cystatin C. These biomarkers, detected in urine or serum shortly after tubular injury, have been suggested to contribute to prediction of ARF and need for renal replacement therapy. However, excretion of these biomarkers may also increase after reversible and mild dysfunction and may not necessarily be associated with persistent or irreversible damage. Large prospective studies in human are needed to demonstrate an improved outcome of biomarker-driven management of the patient at risk for ARF.     

Epidemiology of renal recovery after acute renal failure

PURPOSE OF REVIEW: Recovery of renal function after acute renal failure is an important clinical determinant of patient morbidity. Herein, the epidemiology of renal recovery after acute renal failure will be described, along with potential predictive factors and interventions. RECENT FINDINGS: Renal recovery has been variably defined, most often as recovery to independence from renal replacement therapy. A recent consensus definition for acute renal failure has been published and included provisions for defining renal recovery. Renal recovery to renal replacement therapy independence occurs in the majority by hospital discharge and peaks by 90 days. All of older age, female sex, co-morbid illnesses, especially chronic kidney disease, and late initiation of renal replacement therapy or conventional intermittent renal replacement therapy have been coupled with non-recovery. Analysis of the literature suggests several interventions may influence recovery. SUMMARY: The prognosis is generally good for recovery after acute renal failure. Most patients will be independent of renal replacement therapy by 90 days. Additional research is necessary, however, to understand recovery rates not only to independence from renal replacement therapy, but also to complete and partial recovery. Future studies need to consider the health economic implications for survival and non-recovery. Finally, questions on the role of various interventions require characterization in randomized controlled trials to determine how they may influence renal prognosis.     

Ultrasonographic determination of renal mass and renal volume.

Volumes and surface areas of 45 kidneys were determined ultrasonographically in vivo before autopsy and in a water bath phantom after autopsy by means of both the ellipsoid and the stepped section methods. Comparison of results revealed that renal volume may be determined by the simplest method, the ellipsoid method, with sufficient accuracy for clinical use. Results also revealed that renal mass expressed in grams may be directly obtained from renal volume expressed in milliliters, but mass in grams was found to correlate better with renal surface area than with renal volume. A formula relating renal mass to both volume and surface area was developed from regression analysis of the data and was found to provide a more precise estimate of renal mass than does mass computed from either volume or surface area alone.     

Preservation of renal function in chronic renal failure.

Mechanisms of progression of chronic renal failure (CRF) have been well documented in the rat but may not be relevant in man. Factors which may modify clinical CRF include underlying disease, diet, hypertension, intercurrent events, and adverse or beneficial effects of drug therapy. It has been argued that progression in many forms of renal disease is inexorable below a certain level of renal function. In other diseases, eg primary malignant hypertension, analgesic nephropathy, function frequently improves in both the short and long term with appropriate management. Thus knowledge of the nature of the underlying disease is essential in assessing progression. The value of diet in preserving renal function has been debated, particularly the relative roles of protein and phosphate control. In our own unit, a prospective randomized study showed a benefit of protein restriction. Development of accelerated hypertension is an important cause of progression of renal disease and clinical and experimental evidence supports the view that non-accelerated hypertension is also a factor in progression, amenable to treatment. Various intercurrent events may accelerate progression and function may be lost permanently following sepsis, urinary tract obstruction, renal arterial or venous obstruction, hypotension and in some cases pregnancy. Numerous drugs can have deleterious effects on the kidney. The possibility that converting enzyme inhibitors might preserve renal function is attracting attention but in view of their side effects their place in therapy should be determined by prospective controlled studies in which the above factors are carefully considered.     

Ruptured renal angiomyolipoma presenting as renal colic

The case of a patient with acute onset of flank pain and hematuria is presented. Initial therapy was directed toward relief of pain believed to be caused by renal colic. It was not until the patient developed atypical features that the true diagnosis, ruptured renal angiomyolipoma, was discovered. The case and discussion emphasize the need to carefully consider a complete differential diagnosis when evaluating patients with flank pain and hematuria who have atypical clinical features or an atypical course.     

肾血管平滑肌脂肪瘤和肾癌的螺旋CT诊断

目的 分析探讨肾血管平滑肌脂肪瘤和肾癌的螺旋CT征象.方法 回顾性分析205例临床肾肿瘤病例的螺旋CT征象.其中肾血管平滑肌脂肪瘤63例,肾癌142例(小肾癌21例),增强扫描146例.结果 肾血管平滑肌脂肪瘤特征性的病理表现为内含脂肪,强化较均匀;肾癌平扫大部分呈混杂密度,不均匀强化;小肾癌病例强化后大部分呈快进快出表现.结论 肾血管平滑肌脂肪瘤和肾癌螺旋CT表现具有一定特征性,增强扫描至关重要.