七氟烷与异氟烷吸入麻醉对肝肾功能影响的比较

手术中应用的麻醉剂的类型可以分为吸入型麻醉剂和液体型麻醉剂,常用的吸入型麻醉剂有一氧化二氮、七氟烷、地氟醚、异氟烷等;液体麻醉剂通常可通过静脉注射管直接注入血液,然后流入大脑,主要有巴比妥酸盐、丙泊酚、氯胺酮、依托咪酯等[1].各种麻醉剂大部分通过肝肾代谢,大多能促使氧自由基、过氧化质脂生成增多[2],对肝肾具有一定的损害[3].本研究主要比较七氟烷与异氟烷吸入麻醉对肝、肾功能影响.现报告如下.     

七氟烷用于神经外科麻醉的评价

七氟烷是一种新型的吸入麻醉剂,吸入和诱导迅速,可控性佳。近年来在我国麻醉临床中逐渐普及。本文对其应用于神经外科手术麻醉的优劣进行综述。希望对神经外科麻醉中应用七氟烷具有参考意义。     

七氟烷与氯胺酮在小儿短小手术麻醉中的应用比较

七氟烷是一种吸入麻醉剂,气味略带香甜,对呼吸道无刺激性,吸人感觉舒适,小儿易于接受,目前在我国各大医院已得到较广泛的应用。本文对七氟烷吸入麻醉与经典的氯胺酮静脉麻醉用于小儿短小手术的麻醉起效时间、麻醉效果、副作用、苏醒质量和安全性进行比较。     

Desfluran的吸入麻醉

Ｄｅｓｆｌｕｒａｎ是１９９５年被批准的吸入性卤化麻醉剂，在药学上明显优于迄今已上市的麻醉气体氟烷、恩氟烷和异氟烷。它在血中溶解度低，因而在各个手术期较易控制麻醉深度，在麻醉结束时病人觉醒较快。这种性质类似第二个新型吸入麻醉剂七氟烷，使Ｄｅｓｆｌｕｒａｎ可供门诊麻醉和用低速新鲜气流麻醉时使用。它的另一个优点是体内代谢率极低，从而使可能产生毒性降解物的危险减少到最低限度。其缺点是麻醉强度相当低，沸点低     

氧合器吸入七氟烷对体外循环高血压临床观察

目的观察一种灌注医师可自主操作的，经氧合器吸入七氟烷用于治疗体外循环期间高血凰的临床效果。方法选择60例体外循环期间高血压的患者，通过氧合器吸入七氟烷，观察其降压效果，评价其临床使用价值。结果60例患者中，53例单凭通过氧合器吸入七氟烷达到满意降压效果，另外7例需加用其他药物才能达到要求的降压效果。结论经氧合器吸入七氟烷用于治疗体外循环期间高血压，降压迅速，效果确切，可控性强，并可维持一定时间，很少导致低血压。     

七氟烷在小儿麻醉中的应用体会

七氟烷是一种新型的吸入全身麻醉剂,它具有血气分配系数低,对循环呼吸影响比较小,无呼吸道刺激,麻醉诱导快速且易于接受,麻醉维持具有良好的可控性,现在已较广泛应用于小儿手术麻醉中,高浓度诱导用于成人,但已经证实患儿可耐受高浓度吸入及浓度的快速改变,并能降低患儿术中发生心搏骤停风险等特点,本研究就七氟醚在小儿麻醉中的应用情况进行分析。     

七氟烷强化停跳液对心肌的保护作用

近年来,吸入麻醉药可模拟缺血预处理发挥心肌保护作用,减轻再灌注期间心肌功能抑制。七氟烷为一种较新的吸入麻醉药,1995年经美国FDA批准在美国上市。由于麻醉快通道的发展,对吸入麻醉药在脏器保护方面的认识［1］,促进了七氟烷在体外循环中的应用。有报道七氟烷在体外循环（ car-diopulmonary bypass ,CPB）中的心肌保护作用,但多集中于缺血预处理［2］。本研究观察七氟烷对心肌的保护作用,报告如下。     

七氟烷吸入麻醉对老年腹腔镜手术患者血流动力学和术后认知功能的影响

近年来研究发现吸入麻醉药应用后会对患者,特别是老年患者产生术后认知功能障碍,从而影响患者的康复[1].七氟烷是一种血气分配系数低、麻醉诱导迅速、苏醒快、对血流动力学影响较小的吸入麻醉药,近年来在临床上应用日趋广泛[2].本研究观察七氟烷和异氟烷吸入麻醉对老年患者血流动力学和术后认知功能的影响,现报告如下.     

七氟烷用于小儿诱导麻醉30例临床分析

吸入诱导法常用于小儿麻醉，本研究对60例小儿采用七氟烷或异氟烷，在面罩加压深吸气方法下，施行快速吸入诱导麻醉，观察比较两种药物的诱导平稳程度以及对呼吸道的刺激性，供临床参考。     

七氟烷复合瑞芬太尼在小儿麻醉中的临床应用

目的观察七氟烷用于小儿患者手术时的诱导和苏醒特征,以及复合瑞芬太尼在麻醉中的可行性和效果。方法 60例患儿(ASA1-2级),5%七氟烷吸入诱导,2%～3%七氟烷吸入和瑞芬太尼泵入维持,观察诱导反应、切皮反应、血压、心率、心电图、血氧饱和度、和呼吸情况及苏醒情况。结果诱导平稳,切皮反应轻,生命征稳定,呼吸平稳,苏醒快。结论七氟烷吸入诱导是小儿全麻一种有效且耐受性好的方法。七氟烷复合瑞芬太尼在小儿手术中的安全性高、麻醉深度容易掌控,是一种理想的麻醉方法。     

Ca(2+)-activated K+ current induced by external ATP in PC12 cells

1. The effect of external ATP on the membrane current was investigated in PC12 cells by whole-cell voltage-clamp techniques. 2. Lower concentrations of ATP (1 or 10 mumol/L) induced only an inward current at 1 mmol/L EGTA in the K+ pipette solution, while higher concentrations of ATP (100 mumol/L and 1 mmol/L) induced an outward current following the inward current. 3. Lowering the EGTA concentration in the pipette solution induced a larger outward current following ATP application. The membrane potential at which the outward current crossed with the control before ATP application was more negative at lower concentrations of EGTA in the pipette. 4. The development of the outward current was blocked by a Ca(2+)-free external solution, 5 mmol/L tetraethylammonium and a Cs+ pipette solution instead of K+, indicating that the outward current was a Ca(2+)-activated K+ current. 5. Charybdotoxin (0.1 mumol/L) and iberiotoxin (0.1 mumol/L), but not apamin (0.2 mumol/L) blocked the development of the outward current, indicating the ATP-induced outward current is a BK-type Ca(2+)-activated K+ channel current and not the SK type. 6. UTP had no effect on the membrane current, indicating that the ATP-induced current change was not mediated by P2u but by P2x purinoceptor. 7. In conclusion, stimulation of P2x purinoceptors by ATP induces a Ca(2+)-permeable inward current that results in increases in intracellular Ca2+ concentrations and activation of a BK-type Ca(2+)-activated K+ current in PC12 cells.     

Ginseng saponins induce store-operated calcium entry in Xenopus oocytes

1 We investigated the effect of the active ingredients of Panax ginseng, ginsenosides, on store-operated Ca2+ entry (SOCE) using a two-electrode voltage clamp technique in Xenopus oocytes in which SOCE is monitored through Ca(2+)-activated Cl- currents. 2 Under hyperpolarizing voltage clamp conditions, treatment with ginsenosides produced a biphasic Ca(2+)-activated Cl- current consisting of a rapid transient inward current and a slowly developing secondary sustained inward current. The transient inward current was inactivated rapidly, whereas the sustained inward current persisted for nearly 10 min. The effect of ginsenosides on the biphasic current was dose-dependent and reversible. The EC50 was 42.8+/-11.6 and 46.6+/-7.1 microg ml(-1) for the transient and sustained inward current, respectively. 3 In the absence of extracellular Ca2+ ginsenosides induced only a transient inward current but in the presence of extracellular Ca2+ ginsenosides induced the biphasic current. Magnitudes of the sustained currents were dependent on extracellular Ca2+ concentration. Sustained inward current induced by ginsenosides, but not transient inward current, and ginsenoside-induced store-operated Ca2+ (SOC) currents (ISOC) were blocked by La3+, a Ca2+ channel blocker, suggesting that the sustained inward current and ISOC was derived from an influx of extracellular Ca2+. 4 Treatment with 2-APB and heparin, which are IP3 receptor antagonists, inhibited the ginsenoside-induced biphasic current. Treatment with the PLC inhibitor, U73122, also inhibited the ginsenoside-induced biphasic current. Intraoocyte injection of ATP-gammaS, but not adenylyl AMP-PCP, induced a persistent activation of ginsenoside-induced sustained current but did not affect the transient current. 5 In rat hippocampal neurons, ginsenosides inhibited both carbachol-stimulated intracellular Ca2+ release and intracellular Ca2+ depletion-activated SOCE. 6 These results indicate that ginsenoside might act as a differential regulator of intracellular Ca2+ levels in neurons and Xenopus oocytes.     

Glibenclamide specifically blocks ATP-sensitive K+ channel current in atrial myocytes of guinea pig heart

Effects of glibenclamide on the control membrane ionic currents, acetylcholine or adenosine-induced K+ current, and nicorandil-induced K+ current were examined in single atrial myocytes of guinea pig heart. The nystatin-whole cell clamp technique was used. Nicorandil evoked the time-independent K+ current which is probably the current through the ATP-sensitive K+ channel. Glibenclamide inhibited this current in a concentration-dependent fashion, although it had no effect on the other currents. We concluded that glibenclamide specifically inhibits the ATP-sensitive K+ channel current in cardiac myocytes.     

Characterization of a palytoxin-induced non-selective cation channel in mouse megakaryocytes

We used the whole-cell clamp and fura-2 techniques to study the membrane current and intracellular Ca2+ concentration ([Ca2+]i) changes of mouse megakaryocytes in response to palytoxin (PTX), a highly potent marine toxin. At a holding potential of -60 mV, PTX induced a sustained inward current in a dose-dependent manner. The reversal potentials measured in the presence of various extracellular major cations indicated that the PTX-induced channel had a non-selective permeability to alkali metal ions. Although elimination of intracellular Ca2+ had no effect on the PTX-induced current, removal of external Ca2+ inhibited the current activation. During the sustained phase of the PTX-induced current, treatment with ADP activated an additional current. Pretreatment with ouabain, an inhibitor of Na+-K+-ATPase, suppressed the PTX-induced current. During the stable phase of the PTX-induced current, challenge with NiCl2 (5 mM) or 2,4-dichlorobenzamil (DCB, 25 microM), a non-selective cation channel blocker, partially reversed the current. Simultaneous measurement of the membrane current and [Ca2+]i showed that PTX induced the current response without increasing the [Ca2+]i. Taken together, these results indicate that PTX induces a non-selective cation channel in mouse megakaryocytes. This channel is distinct from the ADP-operated channel and is sensitive to ouabain, NiCl2 and DCB.     

Tricarbonyldichlororuthenium (II) dimer (CORM2) activates non-selective cation current in human endothelial cells independently of carbon monoxide releasing

Tricarbonyldichlororuthenium (II) dimer (CORM2) has been developed as carbon monoxide (CO) donor. We found that CORM2 activated a type of specific current which was distinct from the big-conductance Ca(2+)-activated K(+) current activated by CO in human umbilical vein endothelial cells (HUVECs). So the aim of the present study was to characterize the CORM2-induced current and to access the relation with CO releasing. CORM2 (100 microM) activated a kind of bi-directional current in HUVECs when the ramp protocol (holding potential 0 mV, from -120 mV to +120 mV) was applied. The current was not blocked by apamin, TRAM-34 and iberiotoxin, the small, intermediate and big-conductance Ca(2+) -activated K(+) channel blockers, and it was not sensitive to the pipette solution chelated with EGTA. CORM2 still activated the current when the chloride in the pipette solution was substituted by equal mol gluconic acid. Substitution of the sodium in the bath with choline significantly reduced the current activated by CORM2. The current was regarded as the non-selective cation current. The current showed slightly inward rectifier property and was not sensitive to Gd(3+) (100 microM), La(3+) (10 microM) or 2-aminoethoxydiphenyl borate (100 microM). CO (10 microM), CORM3 (100, 200 microM) and RuCl(3) (100 microM) were used as controls and showed no effect of the current activation. In conclusion, CORM2 activated the non-selective cation current in HUVECs independently of its CO releasing.     

Membrane current responses to externally-applied ATP in the longitudinal muscle of the chicken rectum.

1. Membrane current responses to ATP in enzymically-dispersed single smooth muscle cells from the chicken rectum were investigated by the whole-cell voltage clamp technique. 2. In cells dialysed with a KCl-rich solution under voltage clamp at a holding potential of -40 mV, ATP (10 microM) produced an inward current followed by an outward current. When the holding potential was changed to 0 mV and -80 mV, the biphasic current response to ATP was converted to an outward current alone and an inward current alone, respectively. 3. External application of tetraethylammonium (TEA, 5 mM), intracellular dialysis with a CsCl-rich solution, or inclusion of EGTA (10 mM) in the pipette abolished the outward current response to ATP. 4. Neither depletion of Ca2+ store with caffeine (10 mM) nor block of voltage-gated Ca2+ channels with nifedipine (10 microM) affected the biphasic current response to ATP. After removal of the extracellular Ca2+ the outward current response to ATP was abolished. 5. alpha,beta-methylene ATP (100 microM) elicited a current similar to the ATP-induced current. In the presence of alpha,beta-methylene ATP (100 microM), application of ATP (100 microM) was without effect. 6. In CsCl-filled cells, ATP analogues elicited an inward current and the order of potency was ATP not equal to alpha, beta-methylene ATP > ADP >> AMP. 7. Inclusion of GTP gamma S (0.2 mM) or GDP beta S (2 mM) in the pipette did not affect the ATP-induced inward current in CsCl-filled cells.(ABSTRACT TRUNCATED AT 250 WORDS)     

Properties of palytoxin-induced whole cell current in single rat ventricular myocytes

Summary We examined the properties of the current induced by palytoxin in single ventricular cells of rats. The current was measured by a whole cell voltage clamp method. When the cell was held at –75 mV, palytoxin induced a sustained inward current in a concentration-dependent manner (2–100 pmol/1). The time-course of the inward current paralleled that of the depolarization. At a holding potential of + 50 mV, it caused an outward current. Palytoxin-induced current reversed at 0mV and its current-voltage relation was almost linear at either negative or positive voltage. Substitution of external NaCl with choline-Cl suppressed the palytoxin-induced inward current but not the outward current, by shifting the reversal potential to levels more negative than – 50 mV A cardiac glycoside, cymarin (10 and 100 mol/l) partially inhibited the palytoxin-induced current without changing the reversal potential, only when applied before palytoxin. Palytoxin decreased the nicardipine-sensitive Ca ²⁺ current. These data suggest that palytoxin-induced inward current is carried by extracellular Na⁺ and the outward current is carried mainly by intracellular K⁺, and that the inward current is responsible for the toxin's depolarizing action. The antagonism by cysmarin indicates that the site of action of palytoxin is in the vicinity of the binding site of cardiac glycosides. Send offprint requests to K. Ito at the above address     

Inhibition by sodium nitroprusside of a calcium store depletion-activated non-selective cation current in smooth muscle cells of the mouse anococcygeus.

1. The effects of sodium nitroprusside (SNP) on the non-selective cation current activated in response to intracellular calcium store depletion were studied using the whole-cell patch-clamp technique in single smooth muscle cells isolated from the mouse anococcygeus. Voltage-dependent calcium currents were blocked with extracellular nifedipine, and caesium and tetraethylammonium chloride were used to block voltage-dependent potassium currents. Calcium stores were depleted with caffeine (10 mM), carbachol (50 microM) or cyclopiazonic acid (CPA 10 microM; an inhibitor of the sarcoplasmic reticulum [SR] calcium-ATPase). 2. At a holding potential of -40 mV, both CPA and caffeine activated inward currents which consisted of two clearly distinguishable components; an initial transient current followed by a smaller sustained current. In the case of CPA, the amplitudes of the transient and sustained components were 19.7 +/- 2.1 pA and 3.5 +/- 0.3 pA respectively, whilst the equivalent values for caffeine were 188 +/- 21 and 4.8 +/- 0.3 pA. As described previously, the transient current results from activation of a calcium-dependent chloride conductance whilst the sustained current is a non-selective cation current, activated following intracellular calcium store depletion. 3. The muscarinic receptor agonist, carbachol, also activated a transient followed by a sustained current with amplitudes of 238 +/- 55 and 4.7 +/- 0.5 pA respectively. Superimposed on the sustained current were regular, oscillations of calcium-activated chloride current. 4. Both the transient and the sustained currents activated by CPA were absent in cells pretreated with SNP (10 microM). Application of SNP to a cell following activation of the sustained current by CPA inhibited the current by 88.6 +/- 3.8%. SNP (10 microM) did not inhibit the transient current activated by caffeine but abolished the sustained current. 5. SNP (10 microM) had no effect on the initial transient current activated by carbachol (50 microM). However, it did inhibit the oscillations in the inward current. In recordings from cells bathed in extracellular solution containing the chloride channel blocker, anthracene-9-carboxylic acid (A-9-C; 1 mM), carbachol activated only a sustained current. This current was inhibited by 88.1 +/- 6.5% by a concomitant application of SNP (10 microM) and was absent in cells pretreated with the nitrovasodilator. 6. The effects of SNP on the currents activated by caffeine (10 mM) were mimicked by 8-bromo-cyclic GMP (200 microM); thus the nucleotide had no effect on the transient current activated by caffeine but abolished the sustained current. The effects of SNP, but not those of 8-bromo-cyclic GMP, were inhibited by the nitric oxide-sensitive guanylyl cyclase inhibitor, 1H-[1, 2, 4]oxadiazolo[4, 3-a]quinoxaline-1-one (ODQ; 1 microM). ODQ alone produced a significant increase in the size of the sustained current activated by caffeine (7.8 +/- 0.7 pA). 7. These findings suggest that SNP activates guanylyl cyclase to inhibit the non-selective cation current activated as a result of intracellular calcium store depletion in mouse anococcygeus cells. Since the non-selective cation current appears to underlie the calcium entry process responsible for maintaining the sustained contractions to agonists in this tissue, this action of SNP may represent an important mechanism by which nitrates relax non-vascular smooth muscle.     

干扰电联合药物离子导入治疗退行性膝关节炎

目的观察应用干扰电加直流电药物离子导入治疗退行性膝关节炎的疗效并进行分析。方法185例退行性膝关节炎患者随机分为治疗组92例,对照组93例。治疗组采用干扰电加直流电药物离子导入疗法;对照组采用调制中频电加直流电药物离子导入疗法,两组均行2个疗程治疗。结果治疗组各项症状如疼痛、肿胀、屈曲程度、行走能力及上下楼能力等综合评分均优于照组（P〈0．01）。讨论干扰电疗法治疗以疼痛为主要表现的关节炎、软组织病安全、有效。     

Regulation by GTP and its stable thiol derivatives of calcium current components in rat nodose ganglion neurons

The calcium current components of acutely dissociated nodose ganglion neurons were characterized using the whole-cell variation of the patch-clamp technique. Many neurotransmitters regulate neuronal calcium currents via GTP binding (G) proteins and in some cases affect calcium current components selectively. To determine whether G proteins regulated these current components in the absence of ligand binding, recording pipettes contained 0.1 mM GTP, guanosine 5'-O-(thiodiphosphate) (GDP-beta-S), or guanosine 5'-O-(thiotriphosphate) (GTP-gamma-S). Nodose ganglion neurons had three calcium current components, similar to T, N, and L current components found in other sensory neurons. Isolated T currents did not diminish in magnitude during a 20-min recording, but there was a progressive loss of currents containing the N and L current components. The reduction of current magnitude was primarily dependent on the extent of intracellular dialysis and not on the holding potential (Vh) or stimulus frequency. When GDP-beta-S was substituted for GTP in the pipette solution, there was no change in the T current or in the rate of run-down of N and L current components. Substitution of GTP-gamma-S for GTP in the pipette solution resulted in a moderate (approximately 40%) loss of isolated T current. This effect was most evident on T currents evoked at relatively positive clamp potentials (Vc, -30 to -15 mV) and occurred relatively late (approximately 10 min) in the recording. In the presence of GTP-gamma-S, currents evoked from Vh = -80 mV, containing the N and L current components, were reduced 40-60%, with a lesser effect on those currents evoked from Vh = -40 mV, containing primarily the L current component. The average time to peak current (Ip) was increased 3-4-fold in the presence of GTP-gamma-S, and the Vc at which the maximal peak current was evoked was shifted +10 to 20 mV. These effects were evident within 2-5 min after initiation of the whole-cell recording. Pretreatment of neurons with pertussis toxin attenuated or blocked the effects of GTP-gamma-S. We conclude that nodose ganglion neurons have T-, N-, and L-type calcium current components, which had different stability during whole-cell recording. Activation of G proteins with GTP-gamma-S reduced N greater than T much greater than L currents, effects reduced in the presence of pertussis toxin. Thus, the calcium current components of nodose ganglion neurons were regulated by cytosolic constituents and by Gi- or Go- type G proteins.