不同剂量阿仑膦酸钠对磨损颗粒诱导假体周围骨溶解的影响

目的观察不同剂量阿仑膦酸钠对磨损颗粒诱导假体周围骨溶解的影响，确定其合适剂量.方法雄性SD大鼠24只，经膝关节将钛合金假体及混合磨损颗粒植入胫骨近端（双侧），随机分为对照组和实验Ⅰ、Ⅱ、Ⅲ组，每组6只，术后对照组每日空腹生理盐水2ml灌胃；实验Ⅰ、Ⅱ、Ⅲ组每日空腹阿仑膦酸钠灌胃，剂量分别为0．01、0．1、1mg／（kg·d），持续6周.术后12周处死取材，进行组织学观察及组织形态计量学测定.结果对照组和实验Ⅰ组假体柄周围纤维界膜厚，细胞成分多，与纤维界膜连接处新生骨边缘呈虫蚀状，新生骨对假体的支撑作用较差；实验Ⅱ、Ⅲ组假体柄周围纤维界膜较薄，新生骨与假体间可见有直接接触，对假体有良好的支撑作用.假体周围界膜厚度及面积的形态计量学检测并经统计学分析显示：对照组与实验Ⅰ组、实验Ⅱ与Ⅲ组间差异无显著性（P〉0．05），对照组和实验Ⅰ组分别与实验Ⅱ组和实验Ⅲ组间差异有显著性（P〈0．05）.结论以阿仑膦酸钠预防磨损颗粒诱导的假体周围骨溶解时，最适合剂量为0．1mg／（kg·d）.     

阿仑膦酸钠对人工关节假体周围骨长入的影响

目的观察阿仑膦酸钠对人工关节假体周围骨长入的影响。方法SD雄性大鼠16只,双侧胫骨上端经膝关节植入定制钛合金假体,随机分成对照组和实验组,对照组术后每日空腹生理盐水灌胃;实验组术后每日空腹阿仑膦酸钠灌胃,剂量0.1 mg/(kg.d),持续6周。术后12周处死取材,进行组织学观察及组织形态计量学测定。结果组织学观察发现,对照组假体周围由新生骨、类骨质和纤维界膜构成。纤维界膜较厚,与新生骨或类骨质间界限清晰。实验组假体周围纤维界膜薄且稀少,新生骨与假体界面多为直接接触,有些部位新生骨与假体界面完全整合。组织形态计量学测定发现,对照组假体周围界膜的厚度和面积均明显大于实验组,差异有显著性(P<0.05)。结论阿仑膦酸钠经胃肠给药可能对钛合金人工关节假体周围骨长入有一定的促进作用。     

阿仑膦酸钠对骨质疏松性大鼠钛合金假体骨整合影响的实验研究

[目的]观察阿仑磷酸钠对骨质疏松大鼠假体骨整合的影响。[方法]SD雌性大鼠39只,双侧胫骨结节处垂直骨面置入定制钛合金假体,随机分为正常组、对照组、治疗组(每组13只),正常组不做任何处理;对照组和治疗组8周后行双侧切除卵巢建立骨质疏松模型。骨质疏松模型建成后,对照组术后每周空腹生理盐水灌胃;治疗组术后每周空腹阿仑膦酸钠灌胃,剂量1 mg/(kg/周),持续8周。灌胃结束后处死取材,进行组织学观察及组织形态计量学测定。[结果]组织学观察发现,正常组假体周围纤维界膜薄且稀少,新生骨与假体界面为直接接触,大部位新生骨与假体界面完全整合。对照组假体周围由新生骨、类骨质和纤维界膜构成。纤维界膜较厚,与新生骨或类骨质间界限清晰。治疗组假体周围纤维界膜薄且稀少,新生骨与假体界面多为直接接触,有些部位新生骨与假体界面完全整合。组织形态计量学测定发现,治疗组假体周围界膜的厚度和面积均明显大于对照组,差异有统计学意义(P<0.05)。[结论]阿仑膦酸钠经胃肠给药对骨质疏松大鼠假体骨整合有一定的促进作用。     

阿仑膦酸钠预防磨损颗粒诱导假体周围骨溶解的作用机制

目的 目的是利用阿仑膦酸钠来研究其对人工关节假体周围骨溶解的影响及其作用机制。方法 体重300～350g的雄性SD大鼠24只，经膝关节将特制的钛合金假体及混合磨损颗粒植入胫骨近端（双侧），随机分为实验组和对照组，每组12只，术后分别每日空腹阿仑膦酸钠（0.1mg／kg体重）灌胃和生理盐水2ml灌胃，共6周。术后12周处死取材，进行组织学观察及组织形态计量学测定，并采用ELISA法及半定量RT—PCR检测假体周围组织中TNF-α的的含量及OPGL／OPG含量的比率。结果 组织学观察发现，对照组假体柄周围纤维界膜厚、细胞成分多。可分3层：紧贴假体处为疏松结缔组织，稍外为致密纤维结缔组织。最外层含有单核细胞、巨噬细胞及异物巨细胞。与纤维界膜连接处新生骨边缘呈虫蚀状，新生骨与假体接触少。对假体的支撑作用差。实验组假体周围纤维界膜较薄、细胞成分少，多为成纤维细胞。新生骨与假体间呈点状接触。对假体有明显的支撑作用。形态计量学检测发现，两组间假体周围界膜厚度及面积差异有统计学意义；ELISA和半定量RT—PCR检测假体周围组织中TNF-α及OPGL／OPG发现。两组间差异有统计学意义。结论 阿仑膦酸钠不仅可直接作用于假体周围组织的中破骨细胞。同时可通过调节假体周围组织分泌TNF-α、OPGL、OPG等的含量来调节破骨细胞的分化、成熟及增殖。     

阿仑膦酸钠对假体周围骨溶解中OPG及RANKL的影响

目的 探讨阿仑膦酸钠对聚乙烯颗粒诱导假体周围骨溶解中OPG及RANKL影响.方法 将钛金属棒植入新西兰大白兔左侧股骨内,每2周向左膝关节内注射聚乙烯颗粒,使用随机数字表随机分成实验组和对照组,各6只.实验组给予阿仑膦酸钠灌胃,而对照组给予等量的0.9％的氯化钠溶液灌胃.12周后处死动物,取出假体周围界膜组织,用ELIS...     

载阿仑膦酸钠骨水泥抑制钛磨屑诱导的假体周围骨溶解

目的 比较载阿仑膦酸钠丙烯酸骨水泥与皮下注射阿仑膦酸钠抑制钛磨眉诱导的骨溶解的效果.方法 48只成年雄性新西兰兔随机均分为无钛磨屑且无阿仑膦酸钠组(A组),有钛磨屑注射且无阿仑膦酸钠组(B组),钛磨屑分别注射0.1%、0.5%、1.0%载阿仑膦酸钠丙烯酸骨水泥组(C、I)、E组),钛磨屑注射且皮下手射阿仑膦酸钠组(F组),每组8只.将载阿仑膦酸钠骨水泥植入兔股骨远端.制备磨屑诱导骨溶解动物模型.术后8周对股骨行组织形态学分析、骨密度(bone mineral density,BMD)测定及界面力学测试结果 B组假体周围可见明显的骨溶解,而C、D、E、F组骨溶解明显少于B组.B组假体周围BMD和骨-骨水泥界面抗剪强度分别较A组下降17%和56%;D组假体周围BMD和界面抗剪强度较B组分别增加29%和62%;E组假体周围BMD和界画抗剪强度较B组分别增加37%和29%;F组假体周围BMD和界面抗剪强度较B组分别增加51%和69%;C组、D组、E组分别与F组比较,假体周围BMD和界面抗剪强度的差异均无统计学意义.结论 载阿仑瞵酸钠丙烯酸骨水泥与皮下注射阿仑瞵酸钠均可在一定程度上抑制磨屑诱导的骨吸收,增强界画抗剪强度.     

唑来膦酸钠防治假体周围骨溶解的实验研究

目的:观察唑来膦酸钠对磨损颗粒诱导的大鼠假体周围骨溶解的影响及其作用机制。方法:选用30只成年雄性SD大鼠,体重250～300 g,随机分3组,每组10只,分别为空白对照组、模型对照组和唑来磷酸钠组。空白对照组不作任何处理;模型对照组及唑来磷酸钠组行右侧股骨植入聚乙烯颗粒和钛棒制备聚乙烯颗粒诱导假体周围骨溶解大鼠模型,术后唑来膦酸钠组每周皮下注射唑来磷酸钠0.1 mg/kg,连续用药8周后取血、处死并采集右侧股骨标本。测定各组股骨骨密度(BMD)、IL-1β、IL-6、TNF-α及血清TRAP5b、CTX-Ⅰ的含量。结果:与模型对照组比较:唑来膦酸钠组大鼠股骨骨密度增高,IL-1β、IL-6、TNF-α含量均下降;唑来膦酸钠组大鼠血清TRACP5b、CTX-Ⅰ水平降低。结论:唑来膦酸钠组能够有效抑制聚乙烯颗粒诱导的大鼠假体周围骨溶解,可能是通过抑制破骨细胞的活性及IL-1β、IL-6、TNF-α等细胞因子的表达实现,为临床防治人工关节假体周围骨溶解提供理论基础。     

药物抑制磨损颗粒所致骨溶解的动物实验研究

[目的]探讨药物预防人工关节磨损颗粒致假体周围骨溶解及无菌性松动的可能性.[方法]成年新西兰兔双侧股骨髁和胫骨平台横向钻4 mm×8 mm孔洞,不同部位分别植入CoCr合金(平均5.38 μm)、Ti合金(平均3.21 μm)及超高分子聚乙烯(UHMWPE)颗粒(12～200 μm)各1 mg,植入组配相同者为1组,共4组,每组3只.随机确定给药组,分别经口饲给予非选择性COX阻断剂-消炎痛0.5 mg/kg体重、钙通道阻滞剂-尼群地平0.1 mg/kg体重以及破骨细胞抑制剂-阿仑膦酸钠0.1 mg/kg体重,生理盐水为空白对照,2次/d,双盲实验.术后12周处死取材,脱钙切片,组织学观察、计算机图像分析测量并计算BA/TTA比值.[结果]CoCr合金和Ti合金颗粒各组切片中少见颗粒,正常松质骨表现.空白对照组双折光性UHMWPE颗粒周围大量炎性纤维组织细胞反应;消炎痛与尼群地平组相似,组织细胞反应相对空白对照组稍弱,偶见增生纤维组织中骨样组织存在.阿仑膦酸钠组UHMWPE颗粒包埋于骨组织中,组织细胞反应及纤维组织增生少见,间有髓样组织.UHMWPE颗粒阿仑膦酸钠组BA/TTA比值明显高于空白对照组(P<0.01),消炎痛和尼群地平组之间及其与空白对照组之间则无显著性差异(P>0.05).[结论]药物抑制或预防磨损颗粒性骨溶解及假体无菌性松动具有一定的可行性,其中阿仑膦酸钠的作用较为肯定,值得进一步作体内外相关研究及临床验证.     

阿仑膦酸钠和鲑鱼降钙素对骨质疏松骨床中假体骨整合影响的对比研究

目的探讨阿仑膦酸钠(ALO)和鲑鱼降钙素(CT)两种药物促进假体骨整合作用效果的差异,为临床药物的选择应用提供参考。方法将40只雌性SD大鼠随机分为四组(A,B,C,D组),每组10只。切除B、C、D组大鼠卵巢建立骨质疏松(OP)模型(骨密度降幅20%),A组行假手术做为对照。随后在大鼠的胫骨平台植入羟基磷灰石假体,术后C、D组分别给予皮下注射CT(5IU/kg/d)和口服ALO(7mg/kg/w)各12周,A、B组做药物干预的对照组。所有大鼠在处死前,行体内荧光染色。处死后取带假体的胫骨制备成薄片,运用骨组织计量学检测手段,观察假体周围的骨量和测量假体的骨结合率。结果(1)ALO和CT两者均能促进假体周围成骨,增加骨量,显著提高骨-假体界面骨结合率至63.7%和45.7%,较OVX组骨整合比率分别提高近1～2倍,但阿仑膦酸钠促进假体周围成骨与促进骨整合较鲑鱼降钙素作用更为显著(P0.05),骨结合率增加18%;(2)阿仑膦酸钠和鲑鱼降钙素组大鼠腰椎BMD均提高,分别从(0.081±0.009)g/cm2和(0.078±0.009)g/cm2提至(0.116±0.008)g/cm2和(0.109±0.010)g/cm2。而且,阿仑膦酸钠的效果较降钙素更为明显。结论骨质疏松条件下,全身给予阿仑膦酸钠和鲑鱼降钙素均可增强假体周围成骨及骨量,有效促进假体的骨整合,但与鲑鱼降钙素相比,阿仑膦酸钠作用更为明显。     

阿伦膦酸钠防治人工关节松动的实验研究

目的：评价二膦酸盐阿伦膦酸钠在防治人工关节松动中的作用。方法：36只SD大鼠右膝置入自制人工关节假体,建立人工关节松动的动物模型,分成3组：阴性对照组,阳性对照组和实验组。阴性对照组关节腔内注射磷酸缓冲液与鼠血清混合液,阳性对照组关节腔内注射10^10/ml关节磨屑（超高分子聚乙烯颗粒）,实验组关节腔内注射10^10/ml关节磨屑同时用阿伦膦酸钠灌胃（每日1mg/kg）。术后12周,处死各组动物行组织切片对比观察假体周围骨溶解情况。体外分离培养人外周血单个核细胞并分成5组,A组为单核细胞组,B组为单核细胞和关节磨屑混合培养组,C组为单核细胞和关节磨屑混合培养加入10^-4mol/L阿伦膦酸钠,D组单核细胞和关节磨屑混合培养加入10^-5mol/L阿伦膦酸钠,E组为单核细胞和关节磨屑混合培养加入10^-6mol/L阿伦膦酸钠,检测各组单个核细胞分泌溶骨因子的情况。结果：关节磨屑可引起假体周围骨溶解,刺激单个核细胞分泌溶骨因子,阿伦膦酸钠可阻止这种作用。结论：阿伦膦酸钠可有效防止关节磨屑诱导的人工关节松动,有望用于临床。     

Burdened by training not by anaesthesia

Editor—Larsson and colleagues¹ have investigated importantbut often ignored aspects of anaesthetic practice. However,they imply that specialist anaesthetists experience reducedlevels of stress when compared with trainees because they havedeveloped successful coping mechanisms over the years. Thisconclusion cannot be drawn because the specialists' attitudesto work were identified at a particular time and cannot showa progression in learned coping abilities. To demonstrate thedevelopment of these skills, the specialists would have hadto be interviewed     

Treatment of hemospermia caused by dilated seminal vesicles by direct drug injection guided by ultrasonography

Bilateral seminal vesicle puncture and injection of drugs with ultrasound guidance were performed in patients with hemospermia resistant to conservative therapy and with dilated seminal vesicles. Of 7 patients 6 had resolution of hemospermia for 2 to 3 months and then relapse. No side effect was noted.     

Amplification by hyperoxia of coronary vasodilation induced by propofol

We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia. IMPLICATIONS: Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.     

Tracheal constriction by morphine and by fentanyl in man

The effects of morphine and fentanyl on tracheal smooth muscle tone were studied in 38 patients during induction of anesthesia. Endotracheal tube cuff pressure was used to measure tracheal tone. Anesthesia was maintained with nitrous oxide, 70 per cent in oxygen, and pancuronium and ventilation was controlled with a respirator. Morphine, 0.5 mg/kg, produced a biphasic response, initially causing tracheal dilatation and then tracheal constriction. Ten minutes after morphine injection, cuff pressure increased to significantly (21 +/- 8 per cent) above control. Morphine-induced tracheal constriction could be completely blocked by the prior administration of atropine, 0.5 mg. Fentanyl, 0.006 mg/kg, also produced significant tracheal constriction, cuff pressures increasing to 44 +/- 11 per cent above control at 10 min. Fentanyl-induced tracheal constriction could be blocked by pretreatment with droperidol, 0.25 mg/kg. At equianalgesic doses, morphine and fentanyl produced similar tracheal constriction.     

Reversal by nalbuphine of respiratory depression caused by fentanyl

In 60 ASA class I or II patients given intravenous fentanyl for elective operations in doses large enough to produce postoperative respiratory depression, the intravenous administration of 20 mg nalbuphine resulted in prompt reversal of respiratory depression without loss of analgesia.     

Lavage by laparoscopy fares better than lavage by laparotomy

Background: Although carbon dioxide (CO2) pneumoperitoneum is proposed increasingly for treatment of secondary peritonitis, associated deleterious effects have been reported in experimental models, with the hypothesis that increased intraperitoneal pressure might facilitate bacterial translocation. The purpose of this study was to compare the outcome (and qualitative microbiologic analysis) from peritonitis in rats after lavage by laparoscopy with the outcome after lavage by laparotomy. Methods: After determination of the standard innoculum for this study in 30 animals, 120 male Wistar rats received 1 ml of Escherichi coli 106 colony-forming unit (CFU), Bacteroides fragilis 107 CFU, Enterococcus faecalis 107 CFU in a sterile rat feces-barium sulfate suspension adjuvant, were anesthetized with intramuscular ketamine, and then underwent peritoneal lavage by either laparotomy (n = 60) or laparoscopy (n = 60). The duration of peritonitis defined two groups: group A: duration less than 3 h (n = 20) and group B: duration 3 h or more (n = 40). Both groups underwent successive lavage with 10-ml aliquots (total, 50 ml) of 0.9% saline solution at 37°C. Five 2-ml samples of liquid lavage were drawn for culture and microbiologic analysis. Blood (0.2 ml) and peritoneal liquid lavage samples were incubated 48 h at 37°C and cultured. Results: All the animals survived. Mean duration of peritoneal lavage was 13.2 min (range, 6-25 min) for laparoscopy and 9.7 min (range, 6-15 min) and for laparotomy. The difference was not statistically significant. The mean duration of operation was significantly longer with laparoscopy than with laparotomy: 44.5 min (range, 35-62 min) and 25 min (range, 16-40 min), respectively (p = 0.0001). The collected lavage volumes were not statistically different: 48.5 ml (range, 40-54 ml) and 46.7 ml (range, 37-56 ml), respectively. No statistically significant differences were found between the laparoscopy and laparotomy groups in terms of E. coli bacteremia, irrespective of peritonitis duration. The rates of positive blood culture for B. fragilis and E. faecalis were signficantly lower after laparoscopy than after laparotomy, both in the overall group (p = 0.025 and p = 0.045, respectively) and when duration of peritonitis exceeded 3 h (p = 0.001 and p = 0.044, respectively). Conclusions: In this animal model of secondary peritonitis, lavage by laparoscopy was associated with less bacteremia for B. fragilis and E. faecalis than peritoneal lavage by laparotomy.