L-肉碱对奥硝唑所致弱精子症大鼠的治疗作用

目的:探讨L-肉碱(LC)对奥硝唑(ORN)所致的弱精子症雄性大鼠的治疗作用。方法:性成熟雄性SD大鼠(200～230g)40只,随机均分为5组,连续灌胃20d,1次/d,每次1ml。A组(对照组):0.5%的羧甲基纤维素钠(溶剂);B组:ORN[400mg/(kg.d)];C组:ORN[400mg/(kg.d)]+LC[100mg/(kg.d)];D组:ORN[800mg/(kg.d)];E组:ORN[800mg/(kg.d)]+LC[100mg/(kg.d)]。将各组半数大鼠末次给药24h后,麻醉处死,取附睾,进行精子活力检测,并对附睾尾精子进行计数,剩余大鼠进行交配实验。结果:①与A组相比,B组,D组附睾头和附睾尾精子活力显著降低(P<0.05);精子数目显著减少(P<0.05)。②与B组相比,C组精子活力明显升高(P<0.05),精子数目明显增多(P<0.05),与A组比较无显著差异(P>0.05)。③E组大鼠的精子活力没有显著的提高,精子数目无明显增多,并且与D组相比没有差别(P>0.05)。结论:LC治疗后能提高ORN所致弱精子症大鼠的精子活力,增加精子密度。     

L-肉碱治疗附睾结节伴弱精子症初步观察

目的 :评价L 肉碱治疗附睾结节伴弱精子症患者的疗效。　方法 :2 0 0 3年 5月～ 2 0 0 4年 7月至我院男科门诊就诊的 35例附睾结节伴弱精子症患者 ,年龄 2 5～ 39岁 ,平均 31岁。口服L 肉碱口服溶液 ,1.0 g/次 ,2次 /d ,共3个月。分别于治疗前及治疗 3个月末 ,采用DNA荧光染色精子动 (静 )态图像分析系统进行精液参数分析。　结果 :完成治疗的 32例患者中 ,除 4例精液质量未见明显改善外 ,其余 2 8例精液质量均明显改善。其中 ,除精子密度治疗前后差异无显著性外 (P >0 .0 5 ) ,前向精子活动率、总活动率、曲线运动速度、直线运动速度以及平均轨迹速度等主要精液参数指标 ,在L 肉碱治疗 3个月后均有显著改善 (P均 <0 .0 1)。治疗期间及治疗后随访 2个月内有 4例配偶怀孕 ,其中 1例已正常分娩。　结论 :L 肉碱对附睾结节伴弱精子症具有较好的疗效。     

弱精子症大鼠模型的建立及左旋肉碱对其改善作用的相关研究

目的 研究弱精子症大鼠模型的建立及左旋肉碱(L-肉碱)与精子质量的关系.方法 24只雄性SD大鼠随机均分成3组,分别连续灌胃20d,A组(对照组):0.5%羟甲基纤维素钠(溶剂);B组:400mg/kg奥硝唑悬液:C组:400mg/kg奥硝唑悬液+100mg/kg左旋肉碱.末次给药24h后,麻醉处死所有大鼠,分别检测各组精子密度、活力、形态正常率以及附睾总L-肉碱和游离L-肉碱浓度.结果 A组、B组及C组的精子密度差异无统计学意义(P＞0.05);A组、C组精子活力、精子形态正常率及附睾总L-肉碱、游离L-肉碱浓度均明显高于B组(P＜0.05),A组与C组精子活力、精子形态正常率及附睾总L-肉碱、游离L-肉碱浓度比较,差异均无统计学意义.精子活力与附睾总L-肉碱、游离L-广肉碱浓度呈正相关(r=0.645,P＜0.05:r=0.676,P＜0.05),精子形态与附睾总L-肉碱、游离L-肉碱浓度呈正相关(r=0.557,P＜0.05;r=0.583,P＜0.05),均相关性其具有统计学意义.结论 奥硝唑可以降低大鼠精子活力、精子形态正常率,以及附睾L-肉碱水平,附睾L-肉碱浓度与精子活力、精子形态正常率呈正相关,L-肉碱对精子质量有改善作用.     

L-肉碱在奥硝唑所致大鼠睾丸和附睾损伤中的保护作用

目的:探讨L-肉碱(LC)在奥硝唑(ORN)所致大鼠附睾和睾丸损伤中的的保护作用。方法:40只雄性SD大鼠(200～230g)随机均分为5组:①A组:给予0.5%的羧甲基纤维素钠(溶剂)灌胃;②B组:每天给予400mg/kgORN灌胃;③C组:每天给予800mg/kgORN灌胃;④D组:每天给予[ORN(400mg/kg)+LC(100mg/kg)]灌胃;⑤E组:每天给予[ORN(800mg/kg)+LC(100mg/kg)]灌胃。上述各组均连续灌胃20d,末次给药24h后,所有大鼠麻醉后处死,分别取睾丸、附睾,进行称重和HE染色,计算睾丸、附睾系数并观察睾丸和附睾病理组织学改变。结果:①与A组相比,B组睾丸、附睾系数明显降低(P<0.05);而C组睾丸、附睾系数为极显著性降低(P<0.01);D组与A组相比无差异,E组与A组相比有极显著性差异(P<0.01);②HE染色显示,与A组相比,B组睾丸生精小管内各级生精细胞排列基本整齐,部分生精小管管腔内有脱落的生精细胞,附睾管腔中精子数目下降,有时可见散在的生精细胞;C组大鼠睾丸生精小管管腔内均可见坏死脱落的生精细胞,附睾管腔中精子数目明显减少,且有较多的非精子细胞成分。D组睾丸生精小管无明显改变,附睾管腔中精子数目也未见明显下降;E组睾丸生精小管管腔内精子数目减少,可见坏死脱落的生精细胞,附睾腔中精子数目明显减少,并伴有较多的非精子细胞成分。结论:奥硝唑(ORN)可导致雄性大鼠附睾和睾丸病理组织学改变,LC对ORN引起大鼠附睾和睾丸损伤具有一定的保护作用。     

硫辛酸对奥硝唑所致少弱精子症大鼠精子发生的保护作用研究

目的:研究硫辛酸(LA)对奥硝唑(ORN)所致少弱精子症模型雄性大鼠生精功能的保护作用。方法:取70只雄性SD大鼠,随机分成7组,每组10只,分别为:A组(溶剂对照组):1 ml 0.5%羧甲基纤维素钠(CMC-Na)+1 ml橄榄油;B组(低剂量ORN造模组):400 mg/kg ORN+1 ml橄榄油;C组(低剂量ORN+低剂量LA治疗组):400 mg/kg ORN+50 mg/kg LA;D组(低剂量ORN+高剂量LA治疗组):400 mg/kg ORN+100 mg/kg LA;E组(高剂量ORN造模组):800 mg/kg ORN+1 ml橄榄油;F组(高剂量ORN+低剂量LA治疗组):800 mg/kg ORN+50 mg/kg LA;G组(高剂量ORN+高剂量LA治疗组):800 mg/kg ORN+100 mg/kg LA。连续给药20 d,处死大鼠,称量大鼠体重、睾丸、附睾、精囊重量,计算脏器指数,检测附睾精子计数及活力,睾丸、附睾做HE染色观察组织形态学改变。结果:与A组相比,E组大鼠体重增量、睾丸、附睾脏器指数明显减少[(117.67±11.53)g vs(88.11±12.65)g;(1.06±0.12)%vs(0.65±0.13)%;(0.21±0.03)%vs(0.17±0.01)%,P均0.01];与E组相比,F组大鼠附睾脏器指数明显增加[(0.17±0.01)%vs(0.20±0.02)%,P0.01],G组大鼠体重增量、睾丸、附睾脏器指数明显增加[(88.11±12.65)g vs(102.70±16.10)g,P0.05;(0.65±0.13)%vs(0.95±0.06)%,P0.01;(0.17±0.01)%vs(0.19±0.02)%,P0.05],精囊脏器指数各组之间并无明显差异。与A组相比,B组大鼠精子活力明显降低[(74.12±8.73)%vs(40.25±6.08)%,P0.01],E组大鼠精子计数与活力明显降低[(38.59±6.40)×105/100 mg vs(18.67±4.59)×105/100 mg;(74.12±8.73)%vs(27.58±8.43)%,P均0.01];与B组相比,C、D组大鼠精子活力明显增加[(40.25±6.08)%vs(58.13±7.62)%;(40.25±6.08)%vs(76.04±8.44)%,P均0.01];与E组相比,F、G组大鼠精子计数及活力明显增加[(18.67±4.59)×10~5/100 mg vs(25.63±9.66)×10~5/100 mg,P0.05;(18.67±4.59)×10~5/100 mg vs(29.92±4.15)×10~5/100 mg,P0.01;(27.58±8.43)%vs(36.56±11.08)%,P0.05;(27.58±8.43)%vs(45.05±9.59)%,P0.01]。A、B、C、D组大鼠睾丸、附睾组织形态学无明显改变。E组大鼠睾丸与A组相比,生精小管腔内可见坏死脱落的生精细胞,生精细胞层次不清,排列紊乱;附睾管腔中精子数目明显减少,并伴有较多非细胞成分存在。F、G组大鼠睾丸生精小管内精子数目增加,但仍可见到生精小管内有生精细胞脱落,生精细胞层次不清晰,排列紊乱,但较E组有明显改善;F、G组大鼠附睾管腔中精子数目明显减少,可见散在、脱落的生精细胞,但较E组有明显改善。结论:LA能够改善ORN对大鼠造成的生殖系统损伤,提高精子质量,对生殖系统有较好的保护作用。     

弱精子症动物模型中尿纤溶酶原激活因子的含量及表达情况研究

目的:利用奥硝唑所致弱精子症动物模型,采用免疫组化方法和RT-PCR技术,了解尿纤溶酶原激活因子(uPA)在弱精子症动物模型中的含量及表达情况,初步探讨奥硝唑所致弱精子症动物模型的机制及uPA作为预防或治疗弱精子症药物的可能性。方法:48只雄性SD大鼠随机分为1d用药组,5d用药组,10d用药组,15d用药组,20d用药组和对照组,每组8只,用药组每天给予奥硝唑200mg/kg,对照组给予0.5%羧甲基维素钠连续灌胃,用药组分别在给药第1、5、10、15、20d后24h内,麻醉处死动物取附睾和睾丸。低渗肿胀试验检测精子细胞膜完整性,免疫组化方法动态观察睾丸与附睾组织中uPA蛋白表达情况,RT-PCR检测睾丸组织中uPAmRNA含量。结果:奥硝唑持续给药构建弱精子症时,精子膜完整性下降发生在给药的第10d,并一直维持低值。与建立弱精子症模型同步的uPA在睾丸和附睾组织蛋白表达及mRNA含量下降在用药15d,下降趋势上是平行的,而显效性稍滞后。用药15d组与用药20d组uPA蛋白表达、mRNA水平分别与对照组比较有统计学意义(P<0.05)。结论:精子细胞膜受损、运动能力下降与uPA表达及含量下降平行,奥硝唑所致弱精子症模型形成可能是由于uPA含量及表达下降所致。弱精子症形成原因较复杂,uPA含量及表达的下降可认为是弱精子症形成因素之一,检测uPA含量可能有助于弱精子症的诊断和预防。     

还少胶囊对奥硝唑诱导的弱精子症模型大鼠生殖功能损伤的保护机制研究

目的:探讨还少胶囊对奥硝唑(ORN)诱导的弱精子症模型大鼠生殖功能损伤可能的保护机制。方法:将SD雄性大鼠随机分为4组,每组10只,分别是空白对照组、模型组、还少胶囊组和左卡尼汀组,除空白对照组外,其余3组采用ORN 400 mg/(kg·d)灌胃大鼠28 d,制成弱精子症大鼠模型。并同时连续给药28 d后,处死大鼠,检测大鼠附睾中左卡尼汀的含量,精子浓度、活率,附睾组织中有机阳离子转运子2(OCTN2)mRNA的表达,并观察大鼠睾丸组织病理结构。结果:还少胶囊组、阳性对照药左卡尼汀组与模型组相比,附睾左卡尼汀的含量均可明显提高(6 366.5、6 934.7 mg/L vs 2 880.3 mg/L,P<0.01);改善精子浓度[(46.19±14.23)、(42.25±6.11)×10~6/ml vs(34.58±10.25)×10~6/ml,P<0.01]、活率[(61.34±7.98)%、(61.34±7.98)%vs(42.59±7.54)%,P<0.01];上调附睾OCTN2 mRNA的表达量(27.26、27.15 vs 26.07,P<0.01);同时还少胶囊组能保护ORN造模导致的睾丸生精细胞的病理损伤,使生精细胞在生精小管形态、排列方式、生精细胞的活跃程度上与空白对照组更加接近。结论:还少胶囊对ORN诱导的弱精子症大鼠模型生殖功能损伤具有保护作用,能提高模型大鼠的精子浓度与活率,其机制可能与上调附睾OCTN2 mRNA的表达量、提高附睾左卡尼汀的含量有关。     

弱精子症相关基因与蛋白研究进展

男性不育病因复杂,其中弱精子症是导致男性不育的常见原因之一。然而,弱精子症的发病机制仍然不明确。近年来对弱精子症的研究取得了一定进展,一些基因(如tejin-2、DNAI1、DNAH5、DNAH11、AKAP4、SEPT4和Smcp)和蛋白(如精子蛋白ACTB、ANXA5、PRM1、PRM2、SABP等和精原蛋白Tf、PSA、PAP、Fractalkine等)被证实与弱精子症的发生有关,这些分子标记物的发现将为阐述弱精子症的分子机制提供基础,同时可能成为弱精子症诊断和治疗的靶标。     

中西医结合治疗少弱精子症45例临床观察

不育已经成为影响社会总体生活质量及社会和谐不可忽视的问题,笔者在近2年期间采用中西医结合方法治疗少弱精子症45例,取得满意疗效,现报道如下.     

L-肉碱对糖尿病大鼠生精细胞凋亡及附睾精子数量和活动率的影响

目的:探讨L-肉碱(LC)对糖尿病(DM)大鼠生精细胞凋亡及附睾精子数量和活动率的影响。方法:24只雄性SD大鼠随机均分为3组,一组作为对照组,剩余两组分别注射链脲佐菌素(STZ,65 mg/kg)建立DM模型。建模成功后,各组大鼠分别给予如下灌胃剂量:对照组:生理盐水;DM模型组:生理盐水;LC组:300 mg/kgLC溶液,连续灌胃6周。末次给药24 h后,麻醉处死所有大鼠,分别进行附睾精子计数并检测精子活动率,流式细胞术检测各组大鼠睾丸生精细胞凋亡情况。结果:用LC治疗后的大鼠附睾头、尾精子活动率(%)分别为53.7±1.8和60.3±1.6,显著高于DM模型大鼠(分别为32.2±2.0和40.5±1.4,P<0.05),但低于对照组大鼠精子活动率63.1±2.4和68.9±1.3。与对照组附睾尾精子相对计数[(37.8±1.1)×106/100 mg]相比,DM组显著减少[(25.5±1.1)×106/100 mg],且具有统计学差异(P<0.05);LC治疗后大鼠附睾尾精子相对计数[(32.0±1.5)×106/100 mg]比DM组显著增加(P<0.05),但仍低于对照组。与对照组生精细胞凋亡率[(3.7±1.3)%]相比,DM组生精细胞凋亡率[(52.5±4.4)%]显著上升(P<0.05);经LC治疗后,LC组大鼠生精细胞凋亡率为(35.3±3.5)%,比DM组显著降低(P<0.05),但仍显著高于对照组。结论:LC(300 mg/kg)灌胃DM大鼠6周,可以减少DM大鼠生精细胞凋亡,增加附睾精子数量,提高精子活动率。     

L-carnitine reduces susceptibility to bupivacaine-induced cardiotoxicity: an experimental study in rats

Background

The primary aim of this study was to evaluate the effect of acute administration of L-carnitine 100 mg·kg^?1 iv on susceptibility to bupivacaine-induced cardiotoxicity in rats.

Methods

In the first of two experiments, L-carnitine 100 mg·kg^?1 iv (n = 10) or saline iv (n = 10) was administered to anesthetized and mechanically ventilated Sprague-Dawley rats following which an infusion of bupivacaine 2.0 mg·kg^?1·min^?1 iv was given until asystole occurred. The primary outcome was the probability of survival. Secondary outcomes included times to asystole, first dysrhythmia, and to 50% reductions in heart rate (HR) and mean arterial pressure (MAP). To determine whether the same dose of L-carnitine is effective in treating established bupivacaine cardiotoxicity, we also conducted a second experiment in which bupivacaine 20 mg·kg^?1 iv was infused over 20 sec. Animals (n = 10 per group) received one of four iv treatments: 30% lipid emulsion 4.0 mL·kg^?1, L-carnitine 100 mg·kg^?1, 30% lipid emulsion plus L-carnitine, or saline. The primary outcome was the return of spontaneous circulation (ROSC) during resuscitation.

Results

In the first study, L-carnitine 100 mg·kg^?1 increased the probability of survival during bupivacaine infusion (hazard ratio, 12.0; 95% confidence interval, 3.5 to 41.5; P < 0.001). In L-carnitine-treated animals, the times to asystole, first dysrhythmia, and to 50% reductions in HR and MAP increased by 33% (P < 0.001), 65% (P < 0.001), 71% (P < 0.001), and 63% (P < 0.001), respectively. In the second study, no animal in the control or L-carnitine alone groups achieved ROSC when compared with the lipid emulsion groups (P < 0.01).

Conclusion

These findings suggest that acute administration of L-carnitine 100 mg·kg^?1 decreases susceptibility to bupivacaine cardiotoxicity, but is ineffective during resuscitation from bupivacaine-induced cardiac arrest.

     

强精煎对少弱精子症抗氧化作用及其调控能量代谢的实验研究

目的:探讨强精煎对大鼠少弱精子症抗氧化作用及其调控能量代谢作用机制。方法:将100只SPF级雄性SD大鼠随机分为正常组、模型组、黄精赞育胶囊组、左卡尼汀口服溶液组、强精煎组,每组20只。通过奥硝唑(ORN)建立大鼠少弱精子症模型,强精煎组、黄精赞育胶囊组、左卡尼汀组均在灌胃ORN[800 mg/(kg·d),160 mg/ml]的同时分别灌胃强精煎配方颗粒[10 g生药量/(kg·d),浓度为1.4 g生药量/ml]、黄精赞育胶囊[200 mg/(kg·d),20 mg/ml]、左卡尼汀口服溶液[100 mg/(kg·d),7.5 mg/ml],每只大鼠灌胃剂量为4 ml/d,1次/d。模型组灌胃等剂量ORN,正常组大鼠灌胃生理盐水,连续给药4周。观察药物对大鼠附睾精子浓度和活动率的影响,检测附睾组织SOD、MDA、GSH-Px、α葡糖苷酶、果糖、LDH等指标,并采用实时荧光定量PCR法(q PCR)检测大鼠附睾组织核因子NF-E2相关因子(Nrf2)和琥珀酸脱氢酶(SDH)mRNA水平。结果:1模型组、正常组、强精煎组、黄精赞育胶囊组和左卡尼汀口服溶液组精子浓度分别(35.34±4.22)、(53.05±4.55)、(50.25±5.08)、(48.12±5.56)、(47.14±4.87)×106/ml;活动率分别为(40.04±7.05)%、(70.20±8.54)%、(66.34±7.58)%、(62.46±7.12)%、(63.23±6.34)%,模型组大鼠附睾精子浓度及活动率明显低于正常组(P0.05),而强精煎组、黄精赞育胶囊组和左卡尼汀口服溶液组精子浓度和活动率则明显高于模型组(P0.05);2超微结构显示模型组附睾管壁变薄,管腔内精子明显减少,不能充满管腔,排列紊乱,附睾管腔间间隙增大;与模型组相比,强精煎组、黄精赞育胶囊组和左卡尼汀口服溶液组附睾管壁较厚,精子充满管腔,排列较为规则,呈团簇样,管腔间隙较紧密,均与正常组类似。3模型组、正常组、强精煎组、黄精赞育胶囊组和左卡尼汀口服溶液组SOD、GSH-Px、MDA水平分别为(84.12±23.25)、(110.04±19.56)、(120.56±23.68)、(115.34±21.35)、(116.67±22.67)nmol/mg,(10.56±3.02)、(17.25±3.56)、(16.34±3.12)、(15.23±3.67)、(15.35±3.45)nmol/mg,(14.04±2.06)、(8.87±1.35)、(8.45±1.56)、(8.33±1.54)、(8.05±1.78)nmol/mg。模型组SOD和GSH-Px含量明显低于正常组(P0.05),而MDA含量则明显高于正常组(P0.05);与模型组相比,黄精赞育胶囊组、强精煎组和左卡尼汀口服溶液组SOD、GSH-Px明显高于模型组(P0.05),而MDA含量明显低于模型组(P0.05)。4模型组、正常组、强精煎组、黄精赞育胶囊组和左卡尼汀口服溶液组果糖、LDH、α葡糖苷酶水平分别为(100.22±12.12)、(128.12±13.45)、(130.23±13.67)、(124.16±14.02)、(123.34±15.08)mg/(ml·g),(322±46.13)、(428±35.12)、(455±51.50)、(419±43.14)、(430±31.80)U/(ml·g),(10.48±2.33)、(15.34±3.12)、(18.56±4.67)、(17.64±4.08)、(16.85±5.55)U/(ml·g)。与正常组相比,模型组α葡糖苷酶、LDH、果糖浓度明显下降(P0.05);与模型组相比,黄精赞育胶囊组、强精煎组和左卡尼汀口服溶液组α葡糖苷酶、LDH、果糖浓度明显升高(P0.05)。5q PCR结果显示,模型组Nrf2 mRNA比正常组明显下降(P0.05);与模型组比较,黄精赞育胶囊组、强精煎组和左卡尼汀口服溶液组Nrf2 mRNA明显升高(P0.05),也高于正常组(P0.05)。q PCR结果显示,模型组SDH mRNA明显低于正常组(P0.05);与模型组比较,黄精赞育胶囊组、强精煎组和左卡尼汀口服溶液组SDH mRNA明显升高(P0.05),也高于正常组(P0.05),并且强精煎组表达量明显高于黄精赞育胶囊组(P0.05)。结论:ORN可诱导大鼠产生少弱精子症,并且与氧化过度和能量代谢障碍密切相关。强精煎可以改善甚至逆转ORN诱导产生的少弱精子症。强精煎可以改善ORN诱导的附睾和睾丸的超微结构。抗氧化作用和改善能量代谢很可能是强精煎治疗少弱精子症的机制。     

Effects of Ureaplasma urealyticum infection on the male reproductive system in experimental rats

To study the effects of Ureaplasma urealyticum (Uu) infection on the male reproductive system, the mechanism of infertility induced by Uu infection was investigated in experimental rats. Male Sprague–Dowley rats were infected with Uu4 (serotype 4) through repeated natural sexual intercourse for 8 weeks to establish infection. After 8 weeks, the blood samples of the animals were collected and analysed for cytokine production, and the animals were microdissected for the analysis of the reproductive system. Morphological study showed that spermatozoa exhibited curling and breaks in the rats infected at different dosages. Of the infected rats, 27.5% had both soft and hard calculi in the urinary tract, compared with 12% in the control groups. Uu infection resulted in a decline of sperm quality, eventually leading to the death of the spermatozoa. In the infected animals, the serum interleukin 6 and interleukin 8 levels increased significantly (P < 0.05), while tumour necrosis factor‐alpha and interferon‐gamma showed only modest changes. Our observations showed that Uu infection has an impact on sperm morphology, leading to the death of the spermatozoa. It is plausible that the morphological alterations of spermatozoa induced by Uu infection are one of the possible factors that contribute to male infertility.     

左卡尼汀联合西地那非对雄性糖尿病大鼠生殖内分泌功能的保护作用

目的:初步探讨左卡尼汀与西地那非片在保护糖尿病(DM)大鼠生殖内分泌功能中的作用。方法:40只体重为200～230 g的雄性SD大鼠随机均分为5组:A组为正常对照组,B组为DM大鼠模型组,C组为DM大鼠给予西地那非[5 mg/(kg.d)]治疗组,D组为DM大鼠给予左卡尼汀[300 mg/(kg.d)]治疗组,E组为DM大鼠给予左卡尼汀[300 mg/(kg.d)]联合西地那非[5 mg/(kg.d)]治疗组。各组大鼠治疗6周后分别进行血睾酮(T)、卵泡刺激素(FSH)、黄体生成素(LH)的检测。结果:糖尿病大鼠治疗6周后,血清T,FSH、LH含量,A组:T为(25.25±2.67)nmol/L,FSH为(5.78±0.61)IU/L,LH为(625.21±43.45)ng/L;B组:T为(9.63±1.71)nmol/L,FSH为(1.98±0.42)IU/L,LH为(479.89±27.62)ng/L:C组:T为(18.98±3.07)nmol/L,FSH为(5.08±0.33)IU/L,LH为(586.57±31.72)ng/L;D组:T为(16.18±2.65)nmol/L,FSH为(4.63±0.30)IU/L;LH为(540.78±25.52)ng/L;E组:T为(23.65±2.66)nmol/L,FSH为(5.59±0.48)IU/L,LH为(621.53±36.40)ng/L。各组血清T,FSH、LH含量之间比较,B组均显著低于A、C、D、E组(P均<0.01);C、D组均显著低于A、E组(P均<0.05),而C、D组之间比较,差异均无显著性(P>0.05);E组与A组比较,差异也均无显著性(P>0.05)。结论:西地那非片与左卡尼汀灌胃6周后均可增加DM大鼠血清T、FSH、LH的水平,而两者联合用药时,T、FSH、LH增加水平比单独用药更明显,显示联合用药在保护雄性DM大鼠生殖内分泌功能方面效果更佳。     

An experimental study on the development of myleran-induced oligodactyly in rats

The same type of preaxial oligodactyly appeared in all new born rats when a Wistar rat was treated with myleran on the 12th day of gestation in this experiment. In order to clarify the mechanism of this type of oligodactyly, the development of digital formation and the extent and location of the tissue damage in the hand plate were examined histologically. The preaxial ectoderm of the hand plate was specifically damaged in the early stage of gestation from the 12th and a half to the 13th day. On the other hand, the mesoderm of the hand plate was diffusely damaged at the same time. Condensation of mesodermal cell never occurred in the preaxial part of the mesoderm corresponding to the damaged ectoderm. The finding obtained in this study strongly indicate that disorder of ectoderm-mesoderm interaction may play a role in the development of the oligodactyly produced by myleran.     

An experimental study on fracture healing in paraplegic rats

Fracture healing in denervated limbs was studied using paraplegic rats of Wistar stain. Femoral fractures were made at the same time as spinal cord injury or at regular intervals after spinal cord injury, for roentgenological and histological observation. In the former, proliferation and differentiation of osteogenic cells derived from the periosteum was almost the same as controls, with earlier bone union than controls. In the latter, with longer intervals between spinal cord injury and fracture, osteogenic cells were less proliferated and differentiated resulting in scant callus or delayed union. The environment of paralytic limbs was evidently altered substantially from 2 to 3 weeks after spinal cord injury, because thereafter fracture healing seemed to become poor. Circulatory disturbance plays a major role in fracture healing in paralytic limbs. Although healing is accelerated by increased circulatory volume at the acute phase of spinal cord injury, this potentiality is gradually decreased because of the regressive degeneration of long-term vasomotor nerve insufficiency.     

The effect of twisting on single and double based perforator flap viability: An experimental study in rats

In this study, the histological and vital effects of rotation on multiple and single based perforator flaps were evaluated. A 6 cm × 6 cm abdominal perforator flap model was used on 80 male rats; half of these received a single‐pedicled flap, and the other half double‐pedicled. The flaps of control subgroups were raised and sutured without rotation. In rotation subgroups 90‐, 180‐, 270‐degree rotations were performed, and rotation effects on flap viability and histological changes were analyzed. Among single‐ and double‐pedicled perforator flaps, respectively, mean survival area was 12.59 cm² and 27.84 cm² in non‐rotated subgroups, 12.49 cm² and 17.06 cm² in 90‐degree rotation subgroups, 5.96 cm² and 9.96 cm² in 180‐degree rotation subgroups, and 1.45 cm² and 1.70 cm² in 270‐degree rotation subgroups. While survival areas of double‐ and single‐pedicled perforator flaps with the same rotation degree showed no statistically significant difference, non‐rotated double‐pedicled perforator flaps had a statistically larger survival area compared to single‐pedicled perforator flap (P = 0.001). In the single‐pedicled flap group, there were no statistical differences between survival flap areas of the non‐rotated subgroup and the 90‐ and 180‐degree rotation subgroups (P > 0.05), but the non‐rotated subgroup had a statistically larger survival area compared to the 270‐degree rotation subgroup (P = 0.003). In double‐pedicled perforator flap group, the control subgroup had a statistically larger flap survival area compared to 90‐degree, 180‐degree, and 270‐degree rotation subgroups (P = 0.004, P = 0.002, P = 0.001). Degenerative histological changes gradually increased in correlation with the rotation angle in both single‐ and double‐pedicled groups. When double‐ and single‐pedicled groups were compared; degenerative histology score displayed no statistical difference between control subgroups and rotated subgroups (P > 0.05). In this rat abdominal propeller perforator flap model, we found that double perforators without pedicle rotation could support larger flap survival when compared to the single pedicle. However, double perforators did not cause an increase of survival area when pedicles were rotated. In the single‐pedicled perforator flap, the flap survival area did not significantly decrease until 180‐degree pedicle rotation. In the double‐pedicled perforator flap, the flap survival area decreased when the degree of rotation increased. The degenerative changes increased in correlation with the rotation degree in both single‐ and double‐pedicled perforator flaps. © 2014 Wiley Periodicals, Inc. Microsurgery 34:464–469, 2014.     

Influence of hepatic artery ligation on survival: An experimental study in rats

Interruption of the arterial blood supply to the liver has been used clinically for more than 15 years in patients with nonresectable liver tumors. The induced effect of hepatic artery occlusion on blood flow and metabolism has been studied extensively, whereas survival time has hardly been examined. Evidence of prolongation of survival after hepatic artery ligation, although not properly statistically analyzed, has been found in previous series of experimental animals, but the effect has not been established clinically. In this experimental study of rats with adenocarcinoma in the liver, a statistically significant prolongation of survival time was observed for the animals subjected to hepatic artery ligation when compared with untreated control animals. A statistically significant increase in body weight developed in all ligated animals during the experimental period, whereas the untreated control animals showed a statistically significant decrease in body weight.     

智能体温单信息系统的实验研究

目的检验智能体温单系统的时间效率和准确度,为进一步提高临床护理自动化水平奠定基础。方法根据病历规范设计智能体温单系统,并设计6名虚拟住院患者连续3d的体温单项目信息。实验室条件下,两年级各10名本科护生分别采用传统手工法(下称手工法)和智能系统法(下称智能法)采集信息并绘制体温单,记录操作时间和出错情况。结果两法所生成的体温单视觉效果差异明显;手工法和智能法绘制体温单绘制总时间,出错、不规范及涂改次数比较,差异有统计学意义(均P0.01);出错内容包括体温、脉搏、呼吸、血压、大便、物理降温、出入量、文字标记、体温单换页及术后天数记录等;两年级手工法出错率、不规范率及涂改率比较,差异有统计学意义(均P0.01)。结论智能体温单系统可显著缩短操作时间,有效减少差错,对减轻护理负荷及提高体温单质量具有重要作用。