山茛菪碱佳苏仑在小儿全麻术后催醒效果比较

目的:探讨山莨菪碱(654-2)用于小儿非气管插奎麻术后催醒的临床效果.方法:60例患儿,随机分为山莨菪碱组(A)佳苏仑(B),各30例.所有患儿均用氯胺酮+异丙酚麻醉.A术毕静注654-20.2mg/kg,B静注佳苏仑1mg/kg.结果:A用药后10min、20min、30min的苏醒率为26.7%、90%及100%;B分别是30%、96.7%和100%;两组患儿催醒后心率均快于用药前,P>0.05无统计学差异,B苏醒期有一例出现烦躁.观察结果表明654-2和佳苏仑一样具有较好的催醒作用.结论:654-2用于小儿全麻术后催醒,效果确切,无明显不良反应,是可推广的催醒方法.     

瑞马唑仑复合丙泊酚对无痛胃镜检查患者膈肌运动的影响

目的 探讨超声监测下瑞马唑仑复合丙泊酚对胃镜检查患者膈肌运动的影响。方法选择2021年7—10月行无痛胃镜检查患者210例,男96例,女114例,年龄18～64岁,BMI 18～25 kg/m²,ASAⅠ或Ⅱ级。采用随机数字表法将患者分为两组：瑞马唑仑复合丙泊酚组(R组)和丙泊酚组(P组),每组105例。两组分别于入室吸氧5 min后缓慢静脉注射布托啡诺0.01 mg/kg, 1 min后R组静脉注射瑞马唑仑0.2 mg/kg和丙泊酚0.5 mg/kg, P组静脉注射丙泊酚2 mg/kg,给药完成后即刻评估改良警觉/镇静(MOAA/S)评分,之后每30秒进行一次评估,直至MOAA/S评分≤3分时开始进镜操作。若进镜失败或给药2 min后MOAA/S评分仍≥4分,则追加丙泊酚0.5 mg/kg,直至MOAA/S评分≤3分,每次追加药物间隔时间≥1 min。记录注药前1 min(T₁)、操作开始即刻(T₂)、操作开始后1 min(T₃)、苏醒(T₄,Steward评分≥4分)时的H...     

依托咪酯与雷米芬太尼在全身麻醉诱导时的相互作用

目的用等辐射分析法研究全身麻醉诱导时依托咪酯、雷米芬太尼之间的相互作用。方法择期腹部手术患者75例随机均分为依托咪酯组(E组)、雷米芬太尼组(R组)和复合组(ER组)。各组再分成5个亚组(E1～E5、R1～R5、ER1～ER5组)。麻醉诱导前给药,E1～E5组分别给予依托咪酯0.040、0.060、0.085、0.115、0.155 mg/kg,R1～R5组分别给予雷米芬太尼5.400、7.105、8.850、11.200、15.540μg/kg,ER1～ER5组分别给予依托咪酯及雷米芬太尼0.021 mg/kg+2.600μg/kg、0.030 mg/kg+3.500μg/kg、0.045 mg/kg+4.200μg/kg、0.060 mg/kg+5.500μg/kg、0.080 mg/kg+7.600μg/kg。监测给药前(T1)及给药后1min(T2)、2min(T3)、3min(T4)、5 min(T5)的SBP、DBP、HR、SpO2、听觉诱发电位指数(AAI)的变化。口令法判断患者是否进入催眠状态。点斜法计算各自药物催眠末点的半数有效量(ED50)及复合后两种药物的ED50,以等辐射分析法分析两药在催眠末点的相互作用。结果在催眠末点,依托咪酯ED50为0.084 mg/kg(95%可信限0.070～0.103μg/kg);雷米芬太尼ED50为8.100μg/kg(95%可信限7.901～8.435μg/kg);ER组依托咪酯和雷米芬太尼ED50分别为0.038 mg/kg和3.900μg/kg(95%可信限0.032～0.043μg/kg和3.760～4.200μg/kg)。两药在催眠作用上呈现相加。E1～E5组、R1～R5组、ER1～ER5组给药前后血流动力学变化无统计学意义。E4、ER4组T3、T4时、E5组T2、T3时、ER5组T2～T4时AAI显著低于T1时(P0.05)。结论依托咪酯、雷米芬太尼两药在催眠作用上呈现相加,复合用药血流动力学稳定。     

纳络酮在临床麻醉中的应用体会

<正> 纳络酮是静脉复合麻醉中用于催醒的常用药物。我院在1998年6月～2001年7月对20例全麻病人进行纳络酮催醒,现将临床观察及应用体会总结如下。 1 材料与方法 20例患者中男性14例,女性6例,年龄在20～70岁之间。ASAH～Ⅲ级,手术时间90～220min,术前30min肌注阿托品0.5mg,安定10mg。麻醉诱导以2.5％硫贲妥钠4～8mg/kg,氟芬合剂50:1的1单元,琥珀胆碱1～1.5mg/kg,术中间断辅以芬太尼等,全麻维持以普鲁卡因。手术结束停止全麻维持药及一切麻醉辅助药后,病人经按压眶上神经、吸痰刺激、大声呼唤而无反应的,给予纳络酮0.4mg静注。 2 结果 纳络酮使用后清醒者19例(指令睁眼及运动肢体、呼吸恢     

106例先天性巨结肠根治术的麻醉体会

先天性巨结肠根治术106例,年龄3个月～4岁,体重3.5～15kg,手术时间为160～235min,平均185min。术前插胃管,肌注东莨菪碱0.006～0.01mg/kg、胃复安0.1mg/kg。入室后先用基础麻醉氯胺酮5～10mg/kg、利多卡因3～5mg/kg混合肌注。58例全麻缓慢静注r-OH50～100mg/kg进行全麻诱导气管插管,术中每隔30～60min静注氯胺酮利多卡因合剂(两药各取100mg,稀释至10ml,下称KL)0.1～0.2ml/kg,必要时静注芬太尼2～5μg/kg或安定0.25～0.5mg/kg维持全麻。48例为骶麻组行骶管穿刺置管后首量注入0.5％～1.5％利多卡因5～7mg/kg,术中视情况骶管分次追加首量的1/3～1/2,同时按<0.1ml·kg~(-1)的剂量静注KL合剂,必要时静注辅助用药芬太     

氯胺酮预先给药对慢性炎性痛大鼠急性吗啡耐受的影响

目的 探讨氯胺酮预先给药对慢性炎性痛大鼠急性吗啡耐受的影响.方法 健康成年雄性SD大鼠24只,体重180～200 g,随机分为3组(n=8):吗啡组(M组)、氯胺酮组(K组)和氯胺酮+吗啡组(KM组).于左后足底皮下注射完全弗氏佐剂0.125 ml制备慢性炎性痛模型.注射完全弗氏佐剂后3 d,M组腹腔注射吗啡5 mg/kg,K组腹腔注射氯胺酮10 mg/kg,KM组腹腔注射氯胺酮10mg/kg,10 min后腹腔注射吗啡5 mg/kg,1次/d,连续3 d.于制模前(基础状态)、注射氯胺酮前(T1)、注射氯胺酮后15 min(T2)、30 min(T3)、60 min(T4)及120 min(T5)时测定机械痛阈和热痛阈.结果 与基础值比较,各组T1时机械痛阈及热痛阈均降低(P<0.01).第1次注射情况:与11时比较,M组和KM组T2-5时机械痛阈及热痛阈升高(P<0.05或0.01).第2次注射情况:与T1时比较,M组T2时机械痛阈升高(P<0.05),KM组T3-5时机械痛阈和热痛阈升高(P<0.05或0.01).第3次注射情况:与T1时比较,KM组T4时热痛周升高(P<0.05);与M组第3次注射时比较,KM组T3,5时机械痛阈及T3-5时热痛阈升高(P<0.05).结论 氯胺酮10 mg/kg预先给药可减轻慢性炎性痛大鼠急性吗啡耐受.     

不同剂量艾司氯胺酮联合丙泊酚在体外受精-胚胎移植取卵术中的临床应用效果

目的观察不同剂量艾司氯胺酮联合丙泊酚在体外受精-胚胎移植取卵术中的应用效果并筛选出其适宜剂量。方法 120例择期行体外受精-胚胎移植取卵术的患者, 按随机数字表法分为3组(每组40例):艾司氯胺酮0.3 mg/kg组(S1组)、艾司氯胺酮0.4 mg/kg组(S2组)、艾司氯胺酮0.5 mg/kg组(S3组)。在其他麻醉相同基础上, 3组患者术前1 min静脉注射相应剂量的艾司氯胺酮和丙泊酚1.0～1.5 mg/kg。记录3组患者麻醉前(T0)、麻醉诱导后1 min(T1)、取卵开始后5 min(T2)、苏醒时(T3)、苏醒后10 min(T4)的心率、平均动脉压(MAP)和脉搏血氧饱和度(SpO2), 丙泊酚用量及追加次数, 苏醒时间, 苏醒后清醒镇静(OAA/S)评分, 苏醒后5 min、10 min、30 min时视觉模拟评分法(VAS)疼痛评分, 苏醒后30 min内不良反应(幻觉、眩晕、呼吸抑制、恶心呕吐)发生情况。结果与T0时比较, S1组、S2组T1～T3时心率、MAP降低(均P<0.05)。与S3组比较, S1组T1～T3时心率、MAP较低(均P<0.05)...     

芬太尼与舒芬太尼鼻腔给药用于无痛肠镜的效果比较

目的 探讨舒芬太尼与芬太尼鼻腔给药用于无痛肠镜诊疗的可行性.方法 80例ASA Ⅰ或Ⅱ级,年龄20～59岁,体重50～100 kg,随机分为四组,每组20例.舒芬太尼或芬太尼均稀释至2 ml:Ⅰ绢经鼻滴入芬太尼1 μg/kg;Ⅱ组静注芬太尼1 μg/kg;Ⅲ组静注舒芬太尼0.1 μg/kg;Ⅳ组经鼻滴入舒芬太尼0.1 μg/kg.患者用药2 min后均静注利多卡因50 mg、丙泊酚1～3 mg/kg,直至患者意识消失、睫毛反射消失即可置入纤维结肠镜检查和治疗,丙泊酚50 μg·kg-1·min-1持续输注维持麻醉.术中酌情追加丙泊酚0.5～1.0 mg/kg.记录用药前(T0)、用药后1 min(T1)、2 min(T2)、静脉推注利多卡因及丙泊酚后1 min(T3)、2 min(T4)、3 min(T5)、4 min(T6)及清醒时(T7)的MAP、HR、SpO2、丙泊酚诱导量、总量、术中镇静评分(OAA/S评分法)、肢动反应、诊疗时间、清醒时间、术后恶心、呕吐、嗜睡等发生情况.结果 MAP四组在T2～T7时均低于T0时(P＜0.05),组间比较差异无统计学意义;SpO2在T4、T5时Ⅱ组、Ⅲ组低于Ⅰ组、IV组(P＜0.05),Ⅰ组与Ⅳ组比较差异无统计学意义,Ⅱ组T2～T6时低于T0时、Ⅲ组T3～T6时低于T0时(P＜0.05);丙泊酚的诱导量Ⅱ组高于Ⅰ、Ⅲ、Ⅳ三组(P＜0.05),Ⅰ组、Ⅱ组与Ⅳ组差异无统计学意义.结论 0.1 μg/kg舒芬太尼或1 μg/kg芬太尼鼻腔给药配伍静脉丙泊酚用于无痛肠镜诊疗是安全有效的.     

米非司酮单次和多次给药在Beagle犬体内的药代动力学研究

目的研究米非司酮单次和多次给药在Beagle(比格)犬体内的药动学特征。方法选用雌性8～12kg大小比格犬,根据给药次数分为单次给药组和多次给药组,单次给药采用静脉和灌胃两种方式给药,单次灌胃给药又分为低、中、高3个剂量组,分别是1、3、10mg/kg米非司酮,多次给药采用口服灌胃法给药。每组各3只比格犬。单次给药组:给药前和给药后15、30min,1、2、4、8、12、24、48、72、96h采集血浆样本。多次给药组:分别于第1、3、5、7、9、11、13、15天灌胃10mg/kg米非司酮,给药前、后2h取血,第15天给药前及给药后15、30min,1、2、4、8、12、24、48、72、96h取血。用LC-MS/MS法检测各组血浆中米非司酮的浓度,并采用Phoenix WinNonlin软件处理各组血药浓度测定数据,采用非房室模型估算药代动力学参数,绘制药-时曲线,计算主要药代动力学参数。结果单次灌胃给药1 mg/kg组的t_(1/2)值和MRT与3 mg/kg组和10mg/kg组相比较,差异具有统计学意义(P0.05),3mg/kg组和10mg/kg之间差异无统计学意义(P0.05);AUC_(last)、AUC_(Inf)值的增长比值与给药剂量不成比例,呈现非线性药代动力学特征;单次灌胃给药3个剂量组的tmax值相比,差异无统计学意义(P0.05)。10mg/kg组生物利用度为52.6%。单次灌胃10mg给药组和多次给药组的t_(max)、C_(max)、AUC_(last)、AUC_(Inf)、MRT等主要药动学参数相比较,差异无统计学意义(P0.05);多次灌胃给米非司酮10mg/kg后,比格犬体内的血药浓度保持稳定。结论米非司酮单次与多次给药后的主要药动学参数差异不显著,呈现非线性药代动力学特征,药物在体内有蓄积。     

等辐射分析法研究全麻诱导时异丙酚与氯胺酮的相互作用

目的 以等辐射分析法研究全身麻醉诱导时异丙酚、氯胺酮之间的相互作用。方法75例择期上腹部手术病人随机分成三组:异丙酚(P)组、氯胺酮(K)组、异丙酚复合氯胺酮(C)组,每组25例再各分成5个亚组(P1～P5,K1～K5,C1～C5)。麻醉诱导前各亚组给予不同剂量的异丙酚及氯胺酮。监测给药前、给药后1、2、3、5min的收缩压(SBP)、舒张压(DBP)、心率(HR)、脉搏血氧饱和度(SpO_2)、脑电双频指数(BIS)等指标。病人对口令失去反应即进入催眠状态;已催眠的病人被给予一定强度电刺激,失去反应者即进入麻醉状态。给药2min后,开始评估。以等辐射分析法分析二者之间的相互作用。结果 在催眠、麻醉末点:P组ED_(50)值分别为1.15mg/kg(95％可信限0.95～1.40)、1.89mg/kg(95％可信限1.60～2.22);K组ED_(50)值分别为0.40mg/kg(95％可信限0.34 ～0.47)、0.72mg/kg(95％可信限0.61～0.86);C组ED_(50)值分别为0.65/0.22mg/kg(95％可信限0.55/0.18～0.78/0.26)、1.19/0.40mg/kg(95％可信限0.95/0.32～1.48/0.49)。在催眠和麻醉末点,C组ED_(50)偏离相加线无统计学意义(P>0.05)。C组的SBP、DBP在给药前后无显著变化(P>0.05)。结论 经等辐射分析法分析后判定异丙酚、氯胺酮(剂量比3/1)在麻醉和催眠作用上呈现相加,复合用药血液动力学稳定     

氯胺酮对大鼠肾脏缺血再灌注损伤的影响

目的 探讨氯胺酮对大鼠肾脏缺血再灌注损伤的影响.方法 健康雄性Wistar大鼠24只,随机分为4组(n=6):假手术组(S组)、缺血再灌注组(IR组)、氯胺酮2 ms/kg组(K_1组)及氯胺酮10 mg/kg组(K_2组).采用无创动脉夹夹闭左肾动脉45 min,再灌注6 h,制备大鼠肾脏缺血再灌注模型.K_(1,2)组于再灌注前5 min分别经尾静脉注射氯胺酮2、10 mg/kg.于再灌注6 h时取右心耳血样2 ml,测定血清肌酐(Cr)及尿素氮(BUN)的浓度;光镜下观察肾组织病理学结果 ;采用免疫组织化学法测定肾组织Fas或Caspase-3表达水平;采用TUNEL法检测肾小管上皮细胞凋亡情况,并计算凋亡指数(AI).结果 与S组比较,其余3组血清Cr、BUN的浓度升高,肾组织Fas、Caspase-3的表达上调,AI升高(P<0.01);与IR组比较,K_(1,2)组血清Cr、BUN的浓度降低,肾组织Fus、Caspase-3的表达下调,AI降低(P<0.01);与K_1组比较,K_2组血清Cr、BUN浓度降低,肾组织Fas、Caspase-3的表达下调,AI降低(P<0.01).K_2组肾组织病理损伤较K_1组明显减轻.结论 氯胺酮可减轻肾脏缺血再灌注损伤,且呈剂量依赖性,可能与其抑制肾小管上皮细胞凋亡有关.     

The status of biochemical parameters in varying degrees of vitamin D deficiency

Vitamin D (Vit D) is an essential element for the regulation of serum calcium, phosphate, and alkaline phosphatase (Alk Ph). Because the Vit D serum level is not usually measured directly, Vit D deficiency is diagnosed indirectly by changes in serum calcium, phosphate, and Alk Ph leves. The current study assessed the status of these biochemical parameters in subjects with different degrees of Vit D deficiency. We selected 1210 subjects, between 20 and 69 years old, randomly from the Tehran population. Subjects with diseases or medications that modified bone metabolism were excluded from the study. Serum 25(OH) D, calcium, phosphate, Alk Ph, and parathyroid hormone (PTH) levels were measured and the status of these biochemical parameters was compared in subjects with different degrees of Vit D deficiency. Vit D deficiency was diagnosed in 79.6% of the subjects. Different degrees of Vit D deficiency were classified as follows: group 1, severe; group 2, moderate; and group 3, mild. Serum PTH levels in the Vit D-deficient groups were significantly higher than that in group 4 (normal Vit D). Serum calcium and phosphate levels in groups 1 and 2 were significantly lower than those in groups 3 and 4. No significant difference was seen in serum Alk Ph in the groups with different degrees of Vit D deficiency. The sensivity for at least one biochemical variable (calcium, phosphorus, or Alk Ph) for the detection of severe, moderate, and mild Vit D deficiency was 24.2%, 13.8%, and 6%, respectively. When the serum 25(OH) D level was reduced to less than 25 nmol/l (groups 1 and 2), the effects of Vit D deficiency on calcium and phosphate levels were obvious. Therefore, the usual biochemical parameters (calcium, phosphate, Alk Ph) alone do not have sufficient sensitivity to detect mild deficiency of Vit D.     

VENTILATORY DEPRESSION OF THE NEWBORN OF WOMEN RECEIVING PETHIDINE OR PENTAZOCINE: A double-blind comparative trial

Forty-two women at term received pethidine 100 mg and 43 receivedpentazocine 45 mg, both given in a double-blind randomized manner.There was no difference in analgesic effect between the groups,but twelve patients were judged to need more than one injectionof pentazocine, compared with seven in the pethidine group.The Apgar scores at 1 and 5 min were significantly less in thepethidine group. Four neonates in the pethidine group and twoin the pentazocine group were severely depressed and receivednalozone between 5 and 15 min after birth. The remainder ofthe infants received naloxone 200 µg i.m. 15 min afterbirth. From 5 min after birth, end-expiratory carbon dioxideconcentrations and from 15 min transcutaneous Po₂ were recorded.A significantly smaller end-tidal carbon dioxide concentrationwas measured when more than one injection of pentazocine hadbeen given. Repeated doses of pethidine, on the other hand,resulted in a greater end-tidal carbon dioxide concentration.Vigorous ventilation was even more pronounced when naloxonewas given indicating an analeptic effect when two drugs withantagonistic activity are combined. At no time was transcutaneousPo₂ less than 6.1 kPa. We conclude that both pethidine and pentazocineproduce adequate pain relief during labour, but more than oneinjection of pethidine is associated with greater neonatal depression.     

早期应用维生素E对急性胰腺炎大鼠胰腺细胞凋亡和胰腺组织病变的影响

目的:探讨早期应用维生素E(Vit.E)对急性胰腺炎(AP)大鼠胰腺细胞凋亡和胰腺组织病变的影响.方法:将SD大鼠72只随机分为对照组、AP组和Vit.E治疗组,每组24只.经十二指肠行胆胰管逆行加压注射4%的牛磺胆酸钠,诱导大鼠AP模型.于术后3 h、6 h、12 h和24 h采取断颈方法分批处死动物,应用末端脱氧核苷酸转换酶(TdT)介导的原位末端标记(TUNEL)法检测胰腺细胞凋亡情况,观察各组胰腺组织的病理切片并进行组织病理学评分.结果:AP组和Vit.E治疗组术后胰腺凋亡细胞明显增多,两组在3 h和6 h的凋亡指数均无明显差异(P>0.05),而Vit.E治疗组在12 h和24 h的凋亡指数显著高于对应时相的AP组(12 h,P<0.05;24 h,P<0.01);与AP组比较,Vit.E治疗组胰腺组织病变较轻,12 h和24 h的胰腺组织病理学评分明显低于AP组(12 h,P<0.05;24 h,P<0.01).结论:早期应用抗氧化剂Vit.E能够有效地减轻AP胰腺病变的严重程度,而胰腺细胞凋亡可能是介导此过程的一个重要病理、生理改变.     

加味玉屏风散与流感疫苗预防流感的黏膜免疫效应与机制研究

目的：研究维生素C（Vit C）玉屏风散合剂和流感疫苗预防流感的免疫效应和机制,探索中西医结合预防流行性感冒的优化方案。方法选取BALB/c小鼠36只,随机分为对照组、Vit C玉屏风散组和流感疫苗组,分别给予Vit C玉屏风散合剂连续灌胃14 d,流感病毒亚单位疫苗肌肉注射免疫小鼠,而对照组不做任何处理,模仿人体生理状态;上述动物连续喂养14 d后取血清、支气管肺泡灌洗液（BALF）和肠灌洗液;ELISA法检测肺肠灌洗液中SIgA和IgG的含量,以及外周血Th1细胞因子（IL-2、IFN-γ和TNF-α）和Th2细胞因子（IL-4、IL-6和TGF-β）含量。结果 VitC玉屏风散上调支气管肺泡灌洗液SIgA和IgG水平（SIgA：t =1.68,P ＞0.05;IgG：t =-0.85,P ＞0.05）,对血液Th1和Th2细胞因子水平无显著影响（t 分别为0.51、0.58、1.55、1.51、0.72和1.21;P均＞0.05）,细胞因子呈Th1优势反应（Th1/Th2=1.19）;流感疫苗上调血液中和IgG抗体水平（Z =0.20,P ＞0.05）,上调血液IFN-γ、TNF-α、IL-6和TGF-β水平（t 分别为1.78、0.95、2.05和0.71;P均＞0.05）可显著提高血液IL-2和IL-4水平（t分别为2.53和2.29;P均＜0.05）,且Th1漂移更加明显（Th1/Th2=1.35）。结论 VitC玉屏风散可直接激活黏膜免疫防御机制,促进呼吸道保护性抗体SIgA和IgG的形成,抵御病毒入侵;流感疫苗主要激活系统免疫,上调系统免疫水平,对入侵体内的流感病毒发挥细胞免疫和体液免疫作用。二者可以优势互补,通过不同的机制在防治流行性感冒的不同阶段发挥作用。     

Vitamin D and HRT: No benefit additional to that of HRT alone in prevention of bone loss in early postmenopausal women. A 2.5-year randomized placebo-controlled study

The study was designed to examine the effect of hormone replacement therapy (HRT) and low-dose vitamin D (Vit D) supplementation on the prevention of bone loss in non-osteoporotic early postmenopausal women and to determine whether Vit D supplementation can give additional benefit to an already optimized estrogen regimen. The effects of HRT and Vit D on bone mineral density (BMD) were studied in postmenopausal women in a 2.5-year randomized placebo-controlled study. The study population was a subgroup of the Kuopio Osteoporosis Risk Factor and Prevention Study (OSTPRE) (n=13100). A total of 464 early postmenopausal women were randomized to four groups: (1) HRT (a sequential combination of 2 mg estradiol valerate and 1 mg cyproterone acetate (E₂Val/CPA); (2) vitamin D₃ (cholecalciferol, 300 IU/day); (3) HRT+Vit D; and (4) placebo (calcium lactate; 93 mg Ca²⁺/day). Lumbar (L1–4) and femoral neck BMD were determined by dual-energy X-ray absorptiometry before and after 2.5 years of treatment. After 2.5 years, lumbar BMD had increased by 1.8% in the HRT group (p<0.001) and by 1.4% in the HRT+Vit D group (p=0.002), whereas lumbar BMD had decreased by 3.5% (p<0.001) in the Vit D group and by 3.7% (p<0.001) in the placebo group. The loss of femoral neck BMD was lower in the HRT (–0.3%) and the HRT+Vit D (–0.9%) groups compared with the Vit D (–2.4%) and the placebo groups (–3.7%). This study confirms the beneficial effect of HRT on BMD. It also shows that low-dose vitamin D supplementation has only a minor effect in the prevention of osteoporosis in non-osteoporotic early postmenopausal women and does not give any benefit additional to that of HRT alone.     

Restoration of Cellular Proliferation and Characteristics of Human Tenocytes by Vitamin D

Vitamin D (Vit D) increases calcium absorption in the intestine after binding to the Vit D receptor (VDR). The VDR has also been identified in muscle cells. Vit D supplementation resulted in improved muscle strength. However, there is a paucity of studies of the role of Vit D on tenocytes. We investigated the effects of Vit D on damaged tenocytes. Human tenocytes were treated with dexamethasone (Dex) to induce cell injury. Expression of the tenocyte‐related markers tenomodulin (Tnmd), tenascin C (Tnc), scleraxis (Scx), mohawk (Mkx), and collagen (Col) 1 and 3 were measured. Then, tenocytes were cotreated with Vit D. 1‐α‐Hydroxylase and VDR were explored in tenocytes. With 10 μM Dex, the growth of tenocytes was significantly inhibited, and the gene expression of Tnmd, Tnc, Scx, Mkx, Col 1 and 3 also decreased. When tenocytes were cotreated with Vit D, cell proliferation recovered in a dose‐dependent manner, and the expression of TNMD and Col 1 improved. When studying the mechanisms of the effects of Vit D on tenocytes, reactive oxygen species produced by Dex decreased with Vit D, and the phosphorylation of extracellular signal–regulated kinase and p38 was stimulated by Vit D cotreatment. 1‐α‐Hydroxylase and VDR were found in tenocytes, indicating that the cells have the ability to use an inactive form of Vit D and interact with it. Vit D is known to perform diverse actions and its protective effects on tenocytes suggest its beneficial role in tendon in addition to muscle and bone. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:2241–2248, 2019     

Mechanism of antagonism by physostigmine of acute flunitrazepam intoxication

The effect of physostigmine on the loss of consciousness and respiratory depression induced in rabbits by flunitrazepam, 1 mg/kg, was studied to demonstrate whether the restoration of consciousness and respiration rate results from an increase in central cholinergic activity or from an interference by physostigmine with specific binding of flunitrazepam to its receptors. Physostigmine, 0.1-0.4 mg/kg iv, caused a dose-related reversal of consciousness and respiration rate within 15 min of its injection, which lasted 15-30 min depending on the dose. This was associated with peak inhibition of acetylcholinesterase (AChE) in the frontal cortex and medulla, at 15 min, ranging from 35-51%. The analeptic effect of physostigmine in flunitrazepam-treated rabbits was prevented by pretreatment with scopolamine, 1 mg/kg. The effective dose range for physostigmine, 3-12 mumol/kg, is close to concentrations of this agent that inhibit activity in solubilized preparations of AChE from rabbit cortex, 1-3 X 10(-8) M. However, physostigmine, 10(-9) -10(-4) M, failed to displace 3H flunitrazepam from specific binding sites on membranes prepared from rabbit cerebral cortex. It is concluded that physostigmine antagonizes the somnolence and respiratory depression induced by benzodiazepines by restoring cholinergic transmission to normal levels. The effective dose range of physostigmine is small, and serious side effects from overdose can occur as a result of excess cholinergic activity at neuromuscular synapses.     

Effect of prolonged whole-body hyperthermia on adult male rat testes and the protective role of vitamin C and E: A histological and biochemical study

Hyperthermia (HT) is a significant risk factor for male infertility. Most researchers investigated the effect of localized and short-term HT on male fertility. This study aimed to assess the harmful impacts of prolonged and generalized HT on testicular histology and ultrastructure in rats. The possible protective effects of vitamin E (Vit E), Vit C, and their combination were also investigated. Thirty male adult Wister rats were used (5 groups). 1- control, 2- HT, 3- Vit C, 4- Vit E, and 5- Vit C + Vit E. Rats in groups 2–5 were subjected to HT (41°C), 1 hr daily for 2 weeks. HT-induced a significant decrease in body weight gain, food and water intake, and serum testosterone. HT showed a damaging effect on the testicular and coda epididymis tissue. HT significantly (p ≤ .05) produced oxidative stress (decreased serum catalase (145.49 ± 8.98), glutathione peroxidase (20.27 ± 4.46), superoxide dismutase (2.68 ± 0.54), and reduced glutathione (5.18 ± 0.33), and increased malondialdehyde (9.46 ± 1.55). Vit E alone and combined with Vit C, significantly protected the gonads against the deleterious effects of HT. The results recommended that prolonged HT of the whole body is harmful to male fertility. Prophylactic therapy with Vit E could help decrease the HT-induced male gonadal harm.