交替拟合残差算法与HPLC-DAD结合快速测定复合麻醉剂

将交替拟合残差算法与HPLC-DAD(高效液相色谱-二极管阵列检测)相结合,用于复合麻醉剂中盐酸普鲁卡因和盐酸利多卡因的同时直接快速测定,两组样本中盐酸利多卡因的回收率范围分别为96.2%~101.6%和100.3%~102.3%,盐酸普鲁卡因的回收率范围分别为93.7%~110.4%和97.3%~107.9%.研究表明,交替拟合残差算法可以很好地解决HPLC中色谱和光谱的重叠问题.     

单扫描示波极谱法测定利多卡因的研究

利多卡因与亚硝酸钠在中性介质中发生反应，其亚硝化衍生物具有良好的电活性．在pH9．15的B．R．缓冲溶液中，于-0．48V(vs．SCE)处产生灵敏的极谱还原峰，峰电流与利多卡因浓度在0．04-0．8mg／L范围内有良好的线性关系，检测下限为0．02mg/L．用此方法测定盐酸利多卡因针剂，结果满意．     

不同麻醉药物在气道表面麻醉时对气管插管及拔管反应的影响分析

目的探讨不同麻醉药物行气道表面麻醉时对气管插管及拔管反应的影响.方法选取收治的80例择期行下腹部剖腹手术患者为研究对象,随机分为2%利多卡因组(L组,n=20)、0.75%丁卡因组(T组,n=20)、0.75%罗哌卡因组(R组,n=20)、对照组(C组,n=20),静脉诱导后分别用5 m L上述麻醉药物行气道表面麻醉,其中对照组用5 m L生理盐水.观察记录各组麻醉诱导前、插管即刻、插管后3 min、拔管即刻及拔管后3 min的平均动脉压(MAP)、收缩压(SBP)和心率(HR)情况;记录患者麻醉苏醒期呛咳评分及术后患者不良记忆情况.结果插管后4组患者HR,SBP及MAP较插管前显著升高(P0.05);与C组比较,插管后各组患者HR,SBP,MAP指标显著偏低(P0.05),其中R组插管后上述指标较L组、T组显著偏高(P0.05);拔管时C组HR,SBP,MAP较T组、R组显著偏高(P0.05),T组上述指标较L组低(P0.05);T组、R组呛咳评分及拔管时不良回忆评分较L组、C组低(P0.05).结论与2%利多卡因和7.5%罗哌卡因相比,0.75%丁卡因更能有效地抑制插管反应.     

流动注射化学发光测定盐酸利多卡因

酸性介质中盐酸利多卡因被质子化后与AuCl4^-形成离子缔合物．当该缔合物进入鲁米诺的逆胶束“水池”中时，离解出来的AuCl4^-与鲁米诺产生化学发光．据此建立了测定盐酸利多卡因的新方法．在优化的实验条件下。测定盐酸利多卡因的线性范围为0．5～30μg／mL，检出限(3d)为81ng／mL，对浓度为1μg／mL的盐酸利多卡因进行11次平行测定．其相对标准偏差为2．64％．将本法用于制剂中盐酸利多卡因的测定。结果令人满意．     

Relationship between action potential, contraction-relaxation pattern, and intracellular Ca2+ transient in cardiomyocytes of dogs with chronic heart failure

Abnormalities of contractile function have been identified in cardiomyocytes isolated from failed human hearts and from hearts of animals with experimentally induced heart failure (HF). The mechanism(s) responsible for these functional abnormalities are not fully understood. In the present study, we examined the relationship between action potential duration, pattern of contraction and relaxation, and associated intracellular Ca²⁺ transients in single cardiomyocytes isolated from the left ventricle (LV) of dogs (n = 7) with HF produced by multiple sequential intracoronary microembolizations. Comparisons were made with LV cardiomyocytes isolated from normal dogs. Action potentials were measured in isolated LV cardiomyocytes by perforated patch clamp, Ca²⁺ transients by fluo 3 probe fluorescence, and cardiomyocyte contraction and relaxation by edge movement detector. HF cardiomyocytes exhibited an abnormal pattern of contraction and relaxation characterized by an attenuated initial twitch (spike) followed by a sustained contracture ('dome') of 1 to 8 s in duration and subsequent delayed relaxation. This pattern was more prominent at low stimulation rates (58% at 0.2 Hz, n = 211, 21% at 0.5 Hz, n = 185). Measurements of Ca²⁺ transients in HF cardiomyocytes at 0.2 Hz manifested a similar spike and dome configuration. The dome phase of both the contraction/relaxation pattern and Ca²⁺ transients seen in HF cardiomyocytes coincided with a sustained plateau of the action potential. Shortening of the action potential duration by administration of saxitoxin (100 nM) or lidocaine (30 μM) reduced the duration of the dome phase of both the contraction/relaxation profile as well as that of the Ca²⁺ transient profile. An increase of stimulation rate up to 1 Hz caused shortening of the action potential and disappearance of the spike-dome profile in the majority of HF cardiomyocytes. In HF cardiomyocytes, the action potential and Ca²⁺ transient duration were not significantly different from those measured in normal cells. However, the contraction-relaxation cycle was significantly longer in HF cells (314 ± 67 ms, n = 21, vs. 221 ± 38 ms, n = 46, mean ± SD), indicating impaired excitation-contraction uncou pling in HF cardiomyocytes. The results show that, in cardiomyocytes isolated from dogs with HF, contractile abnormalities and abnormalities of intracellular Ca²⁺ transients at low stimulation rates are characterized by a spike-dome configuration. This abnormal pattern appears to result from prolongation of the action potential. Received 22 January 1998; received after revision 16 March 1998; accepted 27 March 1998     

利多卡因对人角膜上皮细胞的毒性作用及其机理研究

利用不同浓度利多卡因（ｌｉｄｏｃａｉｎｅ）处理体外培养的人角膜上皮（ＨＣＥＰ）细胞系细胞,利用光镜观察、ＭＴＴ、荧光染色、ＤＮＡ电泳、ＴＵＮＥＬ、流式细胞仪和透射电镜方法研究了利多卡因对 ＨＣＥＰ细胞的毒性作用及其机理。光镜观察和 ＭＴＴ检测结果显示,质量浓度 １２５～１０００ｇ／Ｌ的利多卡因对 ＨＣＥＰ细胞具有显著的毒性作用,并具有浓度和时间依赖性;ＡＯ／ＥＢ荧光双染色结果显示,质量浓度 ０６２５～１００００ｇ／Ｌ的利多卡因可引起 ＨＣＥＰ细胞的质膜通透性显著提高,细胞凋亡率也具有浓度和时间依赖性;ＤＮＡ电泳和 ＴＵＮＥＬ检测结果显示,利多卡因能引起 ＨＣＥＰ细胞发生 ＤＮＡ断片化;ＴＥＭ观察结果显示,利多卡因能引起 ＨＣＥＰ细胞的超微结构出现了凋亡细胞的形态结构特征,如胞质空泡化、染色质浓缩、线粒体膨胀且嵴的结构紊乱、出现凋亡小体等;ＡｎｎｅｘｉｎＶ／ＰＩ染色的流式细胞仪检测结果显示,利多卡因能引起 ＨＣＥＰ细胞质膜中的磷脂酰丝氨酸（ＰＳ）发生外翻变化;ＥＬＩＳＡ检测结果显示,利多卡因还能引起 ＨＣＥＰ细胞中胱冬肽酶3、8、9、10表达量的增加,表明利多卡因确能引起 ＨＣＥＰ细胞发生细胞凋亡,而不是细胞坏死。由此可见,利多卡因在质量浓度大于 0.625ｇ／Ｌ时对 ＨＣＥＰ细胞具有显著的细胞毒性,并具有浓度和时间依赖性,且其毒性作用的发挥是通过诱导细胞凋亡实现的,在眼科临床应用中具有很大的毒副作用,应谨慎使用。     

舒泰、速眠新Ⅱ 和利多卡因复合麻醉在比格犬开颅手术中的应用

摘要:目的 本实验采用舒泰、速眠新Ⅱ 全身麻醉并配合利多卡因局部浸润麻醉方法,研究其在比格犬开颅手术中的麻醉效果。 方法 麻醉前 15 min 皮下注射阿托品(0. 1 mg / kg) ,麻醉采用静脉注射舒泰( 2 mg / kg) ,同时肌肉注射速眠新Ⅱ (0. 02 mL / kg) ,术部皮下注射 0. 5%利多卡因溶液( 0. 1 mL / kg) 。 检测指标包括麻醉镇痛评分,麻醉前后动物心率、呼吸和体温变化。 结果 1. 利多卡因可以显著增加麻醉镇痛效果;2. 阿托品使犬心率显著增加;3. 复合麻醉方法对犬呼吸和体温有一定影响,但在正常范围内。 结论 此复合麻醉方法安全性较高及麻醉镇痛效果好,可以满足犬开颅手术对于麻醉效果的要求,但对犬的心率影响较大,因此对心率要求较高的实验需谨慎选择。     

正交试验法优化利多卡因传递体

筛选利多卡因传递体得到制备药物的最佳配比.为利用排列整齐的水平-因素指标对利多卡因传递体试验进行整体设计、综合比较、统计分析,实现通过少数的实验次数找到较好的生产条件,以达到最高生产工艺效果.采用正交试验法优化利多卡因传递体配比的药物量,以包封率和载药量作为考察指标.采用L9(34)正交试验优化利多卡因传递体的处方.这样能对该实验各关键因素变化范围内均衡抽样,使每次试验都具有较强的代表性.由于正交表具备均衡分散的特点,保证了全面实验的某些要求,往往能够较好或更好地达到研究目的.试验结果表明,利多卡因传递体的最佳处方是A2B3C1D2组合,即卵磷脂:胆固醇为2:1;卵磷脂:利多卡因为3:1;甲醇:氯仿为1:1;超声时间为10 min.用此处方配比得到的利多卡因传递体的平均粒径为(81.1±3.1)nm.包封率为(80.95±0.5)%.载药量为(1.87±0.03)%.由此,经过正交试验法优选利多卡因传递体处方在配比上得到的药物质量最佳,载药量适宜大小适中、稳定性好,能够为以后的利多卡因传递体透皮给药提供实验依据.     

毛细管电泳-联吡啶钌电化学发光测定利多卡因

基于利多卡因对联吡啶钌在铂电极上的电致发光信号有增敏作用,建立了一种测定利多卡因的毛细管电泳-电化学发光分析方法.讨论了磷酸盐缓冲液pH值、浓度、分离电压、检测电位等实验参数对利多卡因分离检测的影响.在优化的实验条件下,利多卡因在1.5～740μmol/L内呈良好线性,检出限为0.1μmol/L.应用此法测定了尿液中利多卡因的含量,回收率为90%～93.5%.