肾盂灌注冲洗对肾脏功能和结构的影响

目的：探讨经皮肾镜碎石术肾盂灌注冲洗压对肾脏结构和功能的影响。方法：建立20头活体猪高压肾盂冲洗模型,建立24F肾造瘘通道,分别在0mmHg（作自身对照,只造瘘不灌注）、150mmHg、200mmHg、250mmHg、300mmHg压力下各冲洗30分钟。术中取肾组织送病理检查,监测肾单位光镜和电镜下的形态学改变;术后5天留取尿标本,应用免疫比浊测定法（ITM）检测尿微量白蛋白（ALB）和β2-微球蛋白（β2-MG）;并于术后第5天再次取肾组织行病理检查观察肾单位的形态学改变。结果：所有灌注组术后都出现尿蛋白的增高,术后第1天和术前相比,都有显著差异（P〈0.01）。形态学观察：当肾盂灌注冲洗压在150-200mmHg时,光镜下观察见肾小囊腔轻度扩张,压力超过250mmHg,肾小囊腔见红细胞和蛋白渗出物,肾小管扩张。电镜下见肾近曲小管上皮细胞内空泡形成,微绒毛排列杂乱、稀疏、部分微绒毛脱落。结论：肾盂灌注冲洗安全压不应超过200mmHg。     

肾盂灌注冲洗并发全身炎症反应综合征猪模型的建立

目的:建立一种肾镜下肾盂灌注冲洗并发全身炎症反应综合征(SIRS)的猪模型。方法:家猪10头,随机分为假手术组和模型组,每组按时间点分为基础状态(Basic)、术后0h、术后6h、术后12h和术后24h 5个亚组。猪肾穿刺造瘘,利用自体盲肠内容物加入肾盂冲洗液中,模拟经皮肾镜取石术(PCNL)持续肾盂灌注冲洗1h。每个时间点观测肛温(T)、呼吸(RR)、心率(HR);采血行血细胞计数分析(WBC、RBC、PLT)、肾功能(Cr、BUN、β2-MG)测定、血清IL-6、IL-10、TNF-α含量测定;用光镜和电镜观察肾脏组织病理变化。结果:模型组在术后6 h-24 h各项指标与假手术组相比变化明显,差异有统计学意义(P<0.05或<0.01)。模型组肾脏组织光镜和电镜下观察病理切片均较假手术组有明显的形态学改变。结论:本模型较好地模拟了临床病人PCNL并发SIRS的病理生理过程,为进一步研究其发病机制和预防治疗具有重要意义。     

棕熊肾脏的解剖学及光电镜观察

本文观察了棕熊肾脏的大体解剖和光、电镜下的组织结构。棕熊的肾脏为分叶肾,每个肾叶为多面锥体形。光镜下H—E染色切片标本可见肾实质有皮质和髓质两部分。皮质可见清晰的皮质迷路和髓放线结构。肾小体可分出血管极和尿极。血管球由毛细血管缠绕形成,外包有肾小囊。近曲小管管腔面可见刷状缘。在透射电镜下可见到摅过屏障由有孔内皮、基膜及足细胞的次级突起构成。电镜下还可看到近曲小管游离面紧密排列的微绒毛和基底面的质膜内褶结构。     

牛磺酸对大鼠肢体缺血/再灌注后肺组织损伤的保护作用

目的:观察大鼠肢体缺血再灌注(LIR)后肺组织形态学的变化及牛磺酸对其影响.方法:Wistar大鼠随机分为3组,对照组(control)、缺血/再灌注组(LIR)、牛磺酸 缺血/再灌注组(Tau LIR),各组动物通过大体、光镜和透射电镜观察肺组织形态学变化,并测定肺系数和肺通透指数及肺组织活性氧和MDA含量.结果:大鼠LIR后肺组织出现以肺泡毛细血管膜通透性增加为特征的组织细胞损伤,光镜下显示毛细血管扩张充血、血管周围间隙增大、肺泡腔中有大量蛋白渗出物,电镜下可见肺泡上皮细胞之间、毛细血管内皮之间的紧密连接松解;肺系数和肺通透指数升高;肺组织活性氧及MDA含量增加.提前给予外源性牛磺酸可使肺组织损伤变化减轻.结论:牛磺酸对大鼠LIR后肺损伤有保护作用,其保护机理之一与其抗氧化,保护细胞之间的紧密连接有关.     

经皮肾造瘘术治疗尿脓毒血症患者感染状态的监测与护理

目的探讨尿脓毒血症需行经皮肾造瘘术患者的护理要点。方法回顾性分析58例行经皮肾造瘘术治疗的尿脓毒血症患者,给予心理护理、及穿刺前后病情动态观察、体温监测、早期液体复苏及血管活性药物应用的护理、控制感染的护理以及经皮肾造瘘术后护理。结果57例患者成功行经皮肾造瘘术,1例患者因穿刺失败改行输尿管内支架管置入术;1例患者因并发DIC抢救无效死亡,3例患者因无法解除梗阻需长期留置引流管,余患者均解除梗阻后康复出院。结论经皮肾造瘘术治疗梗阻引起的尿脓毒血症安全有效,医护人员密切合作是挽救尿脓毒血症患者生命的基础。专科护理人员应熟知病情变化,缓解患者的紧张情绪,取得满意的治疗效果。     

肾实质切开取石的术后护理

我院外科自 1 986年 9月至 2 0 0 2年 1 2月 ,对经中西医久治不愈的 2 0 0例复杂性肾结石 ,采用肾实质切开术治疗。其中肾背侧实质切开取石 1 5 3例 ,肾下极切开取石 2 0例 ,肾下极切开取石并肾部分切除 2 7例。 2 0 0例均获良好效果并保存了患肾 ,无 1例发生出血、尿瘘、感染等并发症 ,现将术后护理介绍如下。1　一般护理　　肾脏是一质脆、血液循环极为丰富的器官。肾实质切开取石术中在肾盂内留置有肾盂造瘘管 ,肾切开处放置有一多孔橡胶引流管和烟卷引流 ,因此患者术终回病房后 ,应将各引流管接于无菌袋中 ,严防脱落与扭曲 ,并须保持各…     

兔肾皮质-D氨基酸氧化酶和α-羟酸氧化酶的铈法定位及能谱分析

用铈作捕捉剂,在光镜和电镜下进行兔肾皮质的D-氨基酸氧化酶和α-羟酸氧化酶活性定位。光镜下用Ce-DAB法可显示这两种氧化酶的定位;电镜下,这两种酶主要定位在肾近端小管微绒毛和过氧物酶体上,用能谱仪对这些酶反应产物进行X射线微区元素分析显示铈峰,表明酶的铈法反应具特异性。     

终板造瘘对动脉瘤性蛛网膜下腔出血后慢性脑积水的影响

目的:探讨终板造瘘对动脉瘤性蛛网膜下腔出血后慢性脑积水的影响。方法:回顾性分析201例动脉瘤性蛛网膜下腔出血患者的临床资料,将所有患者按动脉瘤夹闭术中是否进行终板造瘘分为两组,随访6个月以上,评价其慢性脑积水的发生率。结果:所有患者慢性脑积水的总发生率为17.4%,终板造瘘组慢性脑积水的发生率7.8%,而单独夹闭组慢性脑积水的发生率为28.1%,显著高于终板造瘘组(P0.05)。在FisherⅠ-Ⅱ级中,终板造瘘组与单独夹闭组慢性脑积水的发生率分别为5.0%、7.7%,两组比较无统计学差异(P0.05);FisherⅢ-Ⅳ级中,终板造瘘组与单独夹闭组慢性脑积水的发生率分别为10.8%、40.3%,单独夹闭组显著高于终板造瘘组(P0.05);而Hunt-HessⅠ-Ⅱ级中,终板造瘘组与单独夹闭组慢性脑积水的发生率分别为7.0%、9.4%,两组比较无统计学差异(P0.05),Hunt-HessⅢ-Ⅳ级中终板造瘘与单独夹闭组慢性脑积水的发生率分别为11.3%、46.5%,单独夹闭组显著高于终板造瘘组(P0.05)。结论:终板造瘘可明显降低Hunt-HessⅢ-Ⅳ级、FisherⅢ、Ⅳ级动脉瘤性蛛网膜下腔出血后患者慢性脑积水的发生率,而对Hunt-HessⅠ-Ⅱ级、FisherⅠ-Ⅱ级的动脉瘤性蛛网膜下腔出血后患者慢性脑积水的发生率影响不明显。     

亲属活体供肾的病理改变及其临床相关性

目的 探讨亲属活体供肾的病理改变与类型,分析供肾病理改变与供体临床预后的相关性.方法 2007 年5 月至2008 年7 月完成59 例亲属活体供肾肾移植,供肾灌注后用Trucut 肾活检针(18 G)行肾下极穿刺活检,常规行光镜检查和免疫组化检查.供体术后观察血清肌酐、尿常规和尿生化等.结果 55 岁以下供者肾脏出现...     

大鼠经皮肾穿刺造瘘模型的建立

目的:建立大鼠经皮肾穿刺造瘘模型,探讨血清胱抑素C在急性机械性肾损伤中的作用.方法:健康雄性Wistar大鼠共34只,其中10只行数字减影肾动脉造影(DSA),其余24只随机分为甲、乙、丙三组,每组8只,甲组(对照组)不穿刺不灌注,乙组(穿刺灌注组)以穿刺孔径1.6 mm、灌注压力80 cmH2O(1 cmH2O=0.098 kPa)行肾脏穿刺灌注;丙组(单肾组)术前行一侧肾脏切除后以1.6 mm穿刺孔径、80 cmH2O灌注压力行手术.于术后2 h、12 h、24 h分别采血测定血清Cys C、BUN、SCr变化情况,术后取肾组织行病理检查.结果:大鼠行数字减影肾动脉造影,肾脏血管走形分布及集合系统形态结构显示清晰;同对照组相比,丙组术后2 h Cys C与术前相比有统计学意义(P＜0.05);术后12 b、24 h血清Cys C、BUN、SCr与术前相比变化均有统计学意义(术后12 h P＜0.05;术后24 h P＜0.01).结论:以大鼠建立经皮肾穿刺造瘘模型,可反映肾脏损伤情况;评价急性肾机械性损伤时,与SCr、BUN相比,Cys C灵敏性更高.     

Nucleolar organizing regions in renal cell carcinoma, renal oncocytoma and renal adenoma

Nucleolar organizing regions (NORs), as demonstrated by the silver-colloid staining technique, have been counted in 75 renal cell carcinomas (20 grade 1, 22 grade 2, 17 grade 3 and 16 sarcomatoid), eight renal oncocytomas and nine renal adenomas. Mean NOR counts were 3.27, 6.28, 9.24 and 8.12, respectively, for grades 1, 2, 3 and sarcomatoid tumours, 3.09 for renal oncocytomas and 2.63 for renal adenomas. Analysis of data using the unpaired Student's t-test showed significant difference between NOR counts of grade 1, 2 and 3/sarcomatoid renal cell carcinoma, and grades 2, 3 and sarcomatoid renal cell carcinomas when compared to renal oncocytomas and adenomas. The association between type and grade of tumour, NOR value and tumour proliferation is discussed.     

The renal cortical fibroblast in renal tubulointerstitial fibrosis

Renal cortical fibroblasts have key roles in mediating intercellular communication with neighboring/infiltrating cells and extracellular matrix (ECM) and maintenance of renal tissue architecture. They express a variety of cytokines, chemokines, growth factors and cell adhesion molecules, playing an active role in paracrine and autocrine interactions and regulating both fibrogenesis and the interstitial inflammatory response. They additionally have an endocrine function in the production of epoetin. Tubulointerstitial fibrosis, the common pathological consequence of renal injury, is characterized by the accumulation of extracellular matrix largely due to excessive production in parallel with reduced degradation, and activated fibroblasts characterized by a myofibroblastic phenotype. Fibroblasts in the kidney may derive from resident fibroblasts, from the circulating fibroblast population or from haemopoetic progenitor or stromal cells derived from the bone marrow. Cells exhibiting a myofibroblastic phenotype may derive from these sources and from tubular cells undergoing epithelial to mesenchymal transformation in response to renal injury. The number of interstitial myofibroblasts correlates closely with tubulointerstitial fibrosis and progressive renal failure. Hence inhibiting myofibroblast formation may be an effective strategy in attenuating the development of renal failure in kidney disease of diverse etiology.     

Involvement of angiotensin-mediated renal vasoconstriction in renal hypertension

Systematic arterial blood pressure and renal vascular resistance were found to be significantly greater in morphine, chloraloseurethane anesthetized renal hypertensive dogs than in similarly treated normotensive dogs. A lower dose infusion of the angiotensin antagonist 1-sar-8-ala-angiotensin II in the concentration of 20 mμg/ml into the renal artery decreased renal vascular resistance in the hypertensive, but not in the normotensive animals. The subsequent administration of a higher dose (approximately 50 mμg/ml) of 1-sar-8-ala-angiotensin II produced a decrease in renal vascular resistance in the normotensives, but a still greater effect in the hypertensives. Systemic blood pressure was significantly decreased with the higher dose in the hypertensive, but not in the normotensive group. The results indicate the participation of angiotensin-mediated renal vasoconstriction in the increased renal resistance in the hypertensive animals.     

N-acetyl-L-cysteine improves renal medullary hypoperfusion in acute renal failure

This study evaluated the effects of N-acetyl-L-cysteine (NAC), a free radical scavenger, and N(omega)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthesis inhibitor, on the changes in renal function, intrarenal blood flow distribution (laser-Doppler flowmetry), and plasma peroxynitrite levels during the acute renal failure (ARF) produced by inferior vena cava occlusion (IVCO; 45 min) in anesthetized rats. Renal blood flow fell on reperfusion (whole kidney by -45.7%; cortex -58.7%, outer medulla -62.8%, and papilla -47.7%); glomerular filtration rate (GRF) also decreased (-68.6%), whereas fractional sodium excretion (FE(Na%)) and peroxynitrite and NO/NO plasma levels increased (189.5, 46.5, and 390%, respectively) after ischemia. Pretreatment with L-NAME (10 microg. kg(-1). min(-1)) aggravated the fall in renal blood flow seen during reperfusion (-60%). Pretreatment with NAC (150 mg/kg bolus + 715 microg. kg(-1). min(-1) iv) partially prevented those changes in renal function (GFR only fell by -29.2%, and FE(Na%) increased 119.4%) and laser-Doppler blood flow, especially in the outer medulla, where blood flow recovered to near control levels during reperfusion. These beneficial effects seen in rats given NAC seem to be dependent on the presence of NO, because they were abolished in rats pretreated with L-NAME. Also, the antioxidant effects of NAC prevented the increase in plasma peroxynitrite after ischemia. In conclusion, NAC ameliorates the renal failure and the outer medullary vasoconstriction induced by ICVO, effects that seem to be dependent on the presence of NO and the scavenging of peroxynitrite.