异氟醚对肺泡Ⅱ型上皮细胞Na~ -K~ -ATP酶活性的影响

目的　通过原代培养的正常及受 (H2 O2 )损伤的肺泡Ⅱ型上皮细胞 ,探讨异氟醚 (Iso)对肺泡Ⅱ型上皮细胞Na K ATP酶活性的影响。方法　肺泡Ⅱ型上皮细胞分离、纯化、培养 2 4h后 ,分为六组 :对照组 (不加任何药物 ) ,0 2 8mmol/LIso组 ,2 8mmol/LIso组 ,75 μmol/LH2 O2 组 ,75 μmol/LH2 O2 0 2 8mmol/LIso组和 75 μmol/LH2 O2 2 8mmol/LIso组 ,继续培养 3h。分别测定肺泡Ⅱ型上皮细胞Na K ATP酶活性以及培养液中乳酸脱氢酶 (LDH)活性和丙二醛 (MDA)含量。结果　Iso降低正常肺泡Ⅱ型上皮细胞Na K ATP酶活性并加重H2 O2 引起的肺泡Ⅱ型上皮细胞Na K ATP酶活性的降低 ;Iso对正常培养的肺泡Ⅱ型上皮细胞培养液中LDH活性和MDA含量无明显影响 ,但 2 8mmol/LIso可使受H2 O2 损伤的肺泡Ⅱ型上皮细胞培养液中LDH活性和MDA含量增加。结论　Iso可以降低肺泡Ⅱ型上皮细胞Na K ATP酶活性 ,尤其是在过氧化环境中可加重肺泡Ⅱ型上皮细胞的损伤     

异丙酚对大鼠脑突触体Na^＋,K^＋—ATP酶活性的影响

目的;了解异丙酚是否通过影响脑突触体Ｎａ＾＋,Ｋ＾＋－ＡＴＰ酶活性产生中枢抑制效应。方法：ＳＤ大鼠３０只,随机分为三组,分别腹腔注射异丙酚５０ｍｇ／ｋｇ,１００ｍｇ／ｋｇ和生理盐水１０ｍｌ／ｋｇ。结果：ｉｐ异丙酚５０ｍｇ／ｋｇ能明显抑制海马,脑干突触体的Ｎａ＾＋,Ｋ＾＋－ＡＴＰ酶活性,ｉｐ异丙酚１００ｍｇ／ｋｇ能使大脑皮层,脑干及海马突触体的Ｎａ＾＋,Ｋ＾＋－ＡＴＰ酶活性明显降低。     

异氟醚对肺泡Ⅱ型细胞表面活性物质相关蛋白A的影响

目的 通过原代培养的正常及受H2O2损伤的肺泡Ⅱ型上皮细胞（ATⅡcell）,探讨异氟醚（Iso）对肺泡Ⅱ型上皮细胞表面性物质相关蛋白A（SP-A）的影响。方法 肺泡Ⅱ型上皮细胞培养32小时后,被分为六组;对照组（不加任何药物）、0.28mmol/L Iso组、2.8mmol/L Iso组、75μmol/L H2O2组、75μmol/L H2O2 0.28mmol/L Iso组和75μmol/L H2O2 2.8mmol/L Iso组,继续培养3小时。通过酶联免疫吸附法（ELISA）检测Ⅱ型上皮细胞内和培养液中SP-A含量。结果 Iso降低正常肺泡Ⅱ型上皮细胞内和培养液中SP-A含量;经H2O2作用后,SP-A含量亦显著减少,异氟醚增强H2O2的作用。结论 Iso可降低肺泡Ⅱ型上皮细胞合成SP-A的功能,尤其是在过氧化环境中。     

安氟醚,异氟醚对肝酶水平的影响

以氧化亚氮吸入麻醉为对照，对血清肝酶值的变化为依据，估价安氟醚，异醚对肝酶的影响。４６例成人（均无肝胆疾患，肝酶血清均在正常范围，不包括肝胆手术）分为安氟醚组，异氟醚组和氧化亚氮组，在麻醉前及手术后，１，４，１０ｄ抽静脉血检测ＧＰＴ，ＧＯＴ和ＬＤＨ值，结果：安氟醚，异氟醚术后转氨酶均较术前有所增加，安氟醚组对照组比较无显著性差异（Ｐ＞０．１以上）；异氟醚组与对照组相比，术后４ｄ，１０ｄ，ＧＰＴ有显     

Na^＋、K^＋—ATP酶及麻醉药对其影响

Na^ 、K^-ATP酶广泛分布于各类细胞质膜上，形成和维持了Na^ 、K^ 在膜内外正常的浓度差，产生并维持细胞膜电位，维持神经细胞的兴奋性和传导性。麻醉药对Na^ 、K^ －ATP酶具有抑制作用。本文综述了Na^ 、K^ -ATP酶的分子结构、分布、生理功能及麻醉药对其影响。     

安氟醚和异氟醚对大鼠中央杏仁核神经元自发放电活动的影响

目的 评价安氟醚（Enf)和异氟醚（Iso）对大鼠中央杏仁核（Ce)神经元自发放电活动的影响。方法 用SD大鼠，30-60d龄，雌雄不拘，断头，迅速取出全脑，置于4℃人工脑脊液（ACSF）中，通入95%O2和5%的CO2混合气，制备下丘脑的薄片，将95%O2和5%的CO2混合气体经过不同麻醉气体挥气罐，安氟醚（1.5%,3.0%,4.5%)和异氟醚（1.1%,2.2%,3.3%）分别通入ACSF溶液，并灌流含Ce脑薄片标本，应用膜片钳全细胞记录技术，观察给药前、给药期间和冲洗后Ce内神经元自发放电频率的变化。结果 1.5%-4.5%Enf和1。1%-3.3%Iso具有明显的浓度依赖性抑制Ce神经元的自发放电活动作用，3.0%Enf和2.2%Iso对Ce神经元自发放电活动的抑制效应用正常ACSF冲洗5min可逐渐恢复至给药前水平。结论 Enf和Iso对大鼠神经元自发放电活动要生产明显可逆性的抑制作用，表明Ce是Enf和Iso在中枢神经系统的作用部位。     

七氟醚及异氟醚在碱石灰中稳定性的观察

为分析七氟醚和异氟醚在碱石灰中的化学稳定性。作者观察了不同条件下七氟醚、异氟醚被碱石灰的吸收和分解产物,报告如下。实验方法反应物及反应条件 140ml容积玻璃瓶15只,分为Ⅰ、Ⅱ、Ⅲ组,每组(为A、B、C、D、E瓶)5只,分别装入上海五四化学试剂厂生产的碱石灰20g及脱脂棉球一个,Ⅰ、Ⅱ两组各瓶内喷入蒸馏水1.2ml,用覆有多层尼龙薄膜的胶塞密封抽去瓶中空气,分别注入液态异氟醚5ml。     

Effects of hydrochlorothiazide on Na-K-ATPase activity along the rat nephron

Na-K-ATPase activity was determined in seven nephron segments of five-week-old, spontaneously hypertensive rats (SHR) with or without continuous hydrochlorothiazide (HCTZ) treatment for seven days. For comparison, the effects of HCTZ treatment on Na-K-ATPase activity in the nephron segments of age-matched normotensive Wistar-Kyoto rats (WKY) were also determined. Na-K-ATPase activity in proximal convoluted tubule (PCT), medullary thick ascending limb (MTAL), cortical thick ascending limb (CTAL), distal convoluted tubule (DCT) and cortical collecting duct (CCD) was significantly lower in HCTZ-treated SHR compared to control (untreated) SHR. However, there was no significant difference in Na-K-ATPase activity in proximal straight tubule (PST) and medullary collecting duct (MCD) between HCTZ-treated and control SHR. HCTZ treatment also produced a significant decrease in blood pressure (BP) and creatinine clearance (CCr) in SHR. On the other hand, HCTZ treatment did not produce a significant change in Na-K-ATPase activity in PCT, PST, MTAL, CTAL and MCD, in BP or in CCr in WKY. However, HCTZ treatment produced a decrease in the enzyme activity in the DCT and an increase in the enzyme activity in the CCD in WKY. The decrease in Na-K-ATPase activity in almost all nephron segments from SHR may be due to a significant decrease in CCr produced by HCTZ. On the other hand, a decrease in Na-K-ATPase activity in the DCT with an increase in the enzyme activity in the CCD from WKY suggest that renal compensation to the natriuretic effect of HCTZ occurs by an increase in Na+ reabsorption in the CCD.     

Effects of tramadol on minimum alveolar concentration (MAC) of isoflurane in rats

It has been suggested previously that tramadol increases central nervous system activity and 'lightens' anaesthesia with volatile agents. We assessed the effects of tramadol on the minimum alveolar concentration (MAC) of isoflurane in 56 Wistar rats, instrumented chronically with an arterial and central venous catheter. The MAC of isoflurane was determined using the tail clamp method under three conditions: (1) after injection of saline (control); (2) after administration of tramadol 10 mg kg-1 i.v.; and (3) after administration of morphine 1 mg kg-1 i.v. The studies were repeated after treatment with the antagonists naloxone or yohimbine. Tramadol and morphine both reduced the MAC of isoflurane from mean 1.38 (SEM 0.05)% to 1.22 (0.06)% and 1.17 (0.06)%, respectively (P < 0.05). Concomitant administration of yohimbine did not abolish this reduction in MAC. In contrast, after pretreatment with naloxone, tramadol (1.47 (0.04)%) or morphine (1.38 (0.07)%) did not cause a reduction in the MAC of isoflurane compared with controls (1.39 (0.06)%). We conclude that tramadol and morphine reduced the MAC of isoflurane to a small but significant extent. For both drugs, this effect was related to their action at opioid receptors.      

Differential effects of isoflurane and i.v. anaesthetic agents on metabolism of alveolar type II cells

Alveolar type II (ATII) cells perform many important functions within the lung, including surfactant metabolism. We have investigated the effects of isoflurane and different i.v. anaesthetics on cell metabolism in primary cultures of rat ATII cells. Biosynthesis of phosphatidylcholine, the main phospholipid component of surfactant, was decreased in cells exposed to isoflurane in a dose- and time-related manner. This effect was fully reversible within 2 h after isoflurane removal. Lactate dehydrogenase (LDH) release, an index of cell damage, was increased with isoflurane exposure (1%) over a long incubation period (8-12 h). Enhanced lactate production, reflecting an increase in glycolytic metabolism, was also observed in isoflurane exposed cells. In contrast, metabolism of ATII cells was moderately affected by i.v. anaesthetics. Our data suggest differential metabolism of alveolar homeostasis depending on the anaesthetic agent used.      

重组人硫氧化还原蛋白对原代培养肝细胞的影响

目的探讨重组人硫氧化还原蛋白(rhTrx)对原代培养肝细胞生存生长的影响。方法逆转录聚合酶链反应法扩增出hTrx cDNA,并在原核表达系统中表达。IgM还原实验和胰岛素还原实验测定rhTrx的生物学活性。3H胸腺嘧啶核苷(TdR)掺入试验和细胞乳酸脱氢酶(LDH)释放试验检测rhTrx对SD大鼠原代培养肝细胞生存生长的影响。结果克隆出hTrx开放阅读框cDNA并获得高效表达,可溶性目的蛋白回收率为23．20％,蛋白纯度为96．30％。IgM还原和胰岛素还原实验均显示制备的rhTrx具有较好的生物学活性(t=7．5860,P<0．01)。加入rhTrx培养的肝细胞生长旺盛,并维持了良好的细胞形态。rhTrx可促进原代培养肝细胞的DNA合成,并以剂量依赖方式明显抑制乙醇造成的肝细胞损害。结论制备出具有生物学活性的rhTrx,hTrx对原代培养肝细胞的生存具有促进作用。     

胸肺顺应性对异氟醚肺泡浓度的影响

目的　观察异氟醚麻醉时不同胸肺顺应性 ( CT)对异氟醚肺泡浓度 ( FA)的影响。方法　60例非开胸手术病人分为 3组 ,每组 2 0例 ;A组 CT>61ml/ cm H2 O,B组 CT为 4 1～ 60 ml/ cm H2 O,C组 CT<4 0 ml/ cm H2 O。记录在氧流量为 1L / min,异氟醚挥发浓度为 1.5 vol%时的 FA 的变化 ,观察时间为 2 0分钟。结果　 C组的 FA 在所观察的各个时间点 ,都明显高于 A、B两组 ( P<0 .0 5或 P<0 .0 1)。结论　在异氟醚麻醉期间 CT良好者 ,FA 上升较慢 ,而 CT差者 ,FA 上升较快。可能与年龄及肺部病变有关。     

异氟醚对肝脏部分切除术病人肺泡巨噬细胞促炎性细胞因子mRNA表达的影响

目的 观察异氟醚麻醉中人肺泡巨噬细胞IL-8、IL-1β基因表达的变化,以探讨异氟醚对肺炎性反应的影响。方法24例肝脏部分切除手术病人随机分为异氟醚全麻观察组（n=12）和硬膜外+全麻对照组（n=12）。两组病人均快速诱导,气管内插管,麻醉维持用药均包括异丙酚4～6mg·kg-1·h-1、芬太尼和维库溴铵。观察组吸入异氟醚,使呼气末异氟醚浓度保持在1.0％,对照组在诱导后经硬膜外注入1.0％利多卡因+0.2％丁卡因混合液5ml/h。在气管插管后即刻和4h用纤维支气管镜进行支气管肺泡灌洗,从灌洗液中收获肺泡巨噬细胞提取RNA,逆转录合成cDNA,PCR后电泳扫描求积,检测肺泡巨噬细胞IL-8、IL-1βmRNA的表达。结果 麻醉维持4h后比气管插管后即刻IL8-、IL-1βmRNA的表达增加,观察组比对照组IL-8、IL-1βmRNA的表达更强（P<0.05）。结论 异氟醚能增强肝脏部分切除病人肺泡巨噬细胞促炎性细胞因子mRNA的表达,即在转录水平上,异氟醚能增强肺部的炎性反应。     

异氟醚对眼部血液动力学的影响

目的 研究异氟醚对眼部血液动力学的影响。方法 选择无明显眼部疾病的成年非头颈手术患者１５例,静脉注射异丙酚、阿曲库铵快速诱导麻醉,插入喉罩,吸入异氟醚维持麻醉,采用彩色多普勒成像仪（ＣＤＩ）预测麻醉前、异氟醚１ＭＡＣ和１．５ＭＡＣ３０ｍｉｎ后的双眼动脉（ＯＡ）、视网膜中央动脉（ＣＲＡ）和睫状后动脉（ＰＣＡ）的收缩期峰流速（ＰＳＶ）、舒张期末流速（ＥＤＶ）、平均流速（Ｔｍａｘ）和阻力指数（ＲＩ）及血     

Corresponding minimum alveolar concentrations of isoflurane and isoflurane/nitrous oxide have divergent effects on thalamic nociceptive signalling

BACKGROUND: Suppression of nociceptive signalling in the thalamus is consideredto contribute significantly to the anaesthetic state. Assumingadditivity of anaesthetic mixtures, our study assessed the effectsof corresponding minimum alveolar concentrations (MACs) of isofluraneand isoflurane/nitrous oxide on thalamic nociceptive signalling. METHODS: Nociceptive response activity (elicited by controlled radiantheat stimuli applied to cutaneous receptive fields) of singlethalamic neurons was compared in rats anaesthetized at 1.1 and1.4 MAC isoflurane with that at 1.1 and 1.4 MAC isoflurane/nitrousoxide. RESULTS: Under baseline anaesthesia (0.9 MAC isoflurane), noxious stimulationelicited excitatory responses in all neurons (n = 19). Theseresponses were uniformly suppressed at 1.1 and 1.4 MAC isoflurane.In contrast, at 1.1 and 1.4 MAC isoflurane/nitrous oxide, excitatoryresponses no different to baseline were still present in 64and 37% of the neurons, respectively. CONCLUSIONS: These data demonstrate a pronounced nitrous oxide-induced responsevariability. It appears that, with respect to thalamic transferof nociceptive information, the interaction of isoflurane andnitrous oxide may not be compatible with the concept of additivityand that the antinociceptive potency of nitrous oxide is considerablyless than previously reported.     

Comparison of minimum alveolar concentration between intravenous isoflurane lipid emulsion and inhaled isoflurane in dogs

BACKGROUND: As in inhaled isoflurane anesthesia, when isoflurane lipid emulsion (ILE; 8%, vol/vol) is intravenously administered, the primary elimination route is through the lungs. This study was designed to determine the minimum alveolar concentration (MAC) and the time course of washout of isoflurane for intravenously infused ILE by monitoring end-tidal isoflurane concentration. METHODS: Twelve healthy adult mongrel dogs were assigned randomly to an intravenous anesthesia group with 8% ILE or to an inhalation anesthesia group with isoflurane vapor. An up-and-down method and stimulation of tail clamping were used to determine MAC of 8% ILE by intravenous injection in the intravenous anesthesia group and MAC by the inhaled approach in the inhalation anesthesia group, respectively. Isoflurane concentration and partial pressure in end-tidal gas, femoral arterial blood, and jugular venous blood were measured simultaneously just before each tail clamping and during washout. RESULTS: The induction time in the intravenous anesthesia group (105 +/- 24 s) was shorter than that in the inhalation anesthesia group (378 +/- 102 s; P < 0.01). MAC of 8% ILE by intravenous injection (1.12 +/- 0.18%) was significantly less than MAC by the inhaled approach (1.38 +/- 0.16%; P < 0.05). No significant difference was found between the two groups in the time course of washout of isoflurane. CONCLUSION: The MAC of intravenous anesthesia with 8% ILE was less than that of inhalation anesthesia with isoflurane vapor in dogs.     

硬膜外利多卡因对异氟醚和地氟醚MAC的影响

目的 本研究以BIS>50作为指标来确定异氟醚和地氟醚的ED50值(MACBIS50),观察硬膜外利多卡因对异氟醚和地氟醚达到满意麻醉深度时用药量的影响。方法 48例患者随机分为两组:异氟醚组和地氟醚组,每组又随机分全麻复合硬膜外组和单纯全麻组(每组12例)。患者术前阿托品肌肉注射,全麻复合硬膜外组给予1.6％利多卡因10ml。全麻诱导采用咪达唑仑、芬太尼、异丙酚和维库溴铵,诱导插管后吸入异氟醚和地氟醚,待呼气末浓度(ET％)达到预定值并且稳定10 min后,记录相应的BIS值。采用上下波动法分别计算异氟醚和地氟醚MACBIS50,BIS值和呼气末浓度进行直线回归分析。结果MACBIS50全麻复合硬膜外组(异氟醚组0.77％、地氟醚组3.87％)和单纯全麻组(异氟醚组1.16％、地氟醚组5.18％)比较显著降低(P<0.01)。四组BIS和ET％均呈直线相关。结论硬膜外利多卡因可显著降低异氟醚(34％)和地氟醚(53％)维持足够麻醉深度的呼气末浓度,并保持BIS值和呼气末浓度的直线相关性。