艾司洛尔对缺氧复氧诱导的心肌细胞AMPK/GSK-3β通路及凋亡的影响

目的 探讨艾司洛尔对缺氧复氧诱导的心肌细胞凋亡的影响,并初步研究其作用机制.方法 体外培养大鼠心肌细胞(H9c2),并建立缺氧/复氧(I/R)损伤模型,随机分为对照组、H/R组和艾司洛尔低、中、高剂量(0.2、5.0、25.0μmol/L)组;噻唑蓝(MTT)法检测各组H9c2细胞存活率变化情况;膜联蛋白V-异硫氰酸荧...     

艾司洛尔对气管插管应激反应的影响

目的：探讨艾司洛尔对气管插管应激反应的影响。方法：选择全麻下非心脏手术患者60例,随机分为生理盐水组（C组）和艾司洛尔组（E组）各30例。观察两组患者全麻诱导前,予以艾司洛尔或生理盐水前的基础值,及插管前,插管时,插管后1min,3min,5min的无创血压、心率及心输出量的变化。结果：在气管插管后,C组患者的平均动脉压、心率、心输出量上升的幅度均明显大于E组（P〈0．05）。结论：艾司洛尔可以抑制气管插管应激反应。     

盐酸艾司洛尔注射液中杂质的分离、合成与结构鉴定

目的:研究盐酸艾司洛尔注射液中杂质的结构和产生的原因。方法:采用制备高效液相色谱方法制备分离盐酸艾司洛尔注射液的杂质并采用IR、MS1、H-NMR、13C-NMR等方法进行结构鉴定;合成制备了此杂质并进行结构确证。结果:该杂质为4-{[2-羟基-3-[(1-甲基乙基)氨基]]丙氧基}苯丙酸盐酸盐,为盐酸艾司洛尔注射液在储藏过程的降解产物。结论:本研究可为盐酸艾司洛尔注射液质量评价提供依据。     

艾司洛尔和乌拉地尔对拔管期心血管反应及脑电图双频谱指数、心率变异性的影响

观察全麻患者拔管前静注艾司洛尔或乌拉地尔对心血管反应及脑电图双频谱指数、心率变异性的影响。60例手术患者分成3组，Ⅰ组为对照组，Ⅱ组为艾司洛尔组，Ⅲ组为乌拉地尔组。观察拔管前、拔管后1、3、5、7、9、10min3组收缩压（SP）、舒张压（DP）、心率（HR）、双频谱指数（BIS）、心率变异性（HRV）变化。Ⅰ组SP、DP、HR拔管后1、3min显著升高（P＜0.05)；Ⅱ组HR拔管后5、7、9、10min均显著下降（P＜0.01)，SP、DP均无显著性差异。Ⅲ组HR拔管后1、3、5min显著升高（P＜0.01)，SP、DP拔管后1min显著下降（P＜0.05)。艾司洛尔、乌拉地尔均可减轻拔管引起的心血管反应，但不能阻止拔管时交感神经活性增强。乌拉地尔用于单纯血压升高的患者拔管有利，而艾司洛尔对于心率增加的患者大为有利。     

牛磺酸、艾司洛尔单用及合用对麻醉大鼠缺血性心律失常的作用

本实验用麻醉大鼠冠状动脉左前降支结扎方法,研究了牛磺酸、艾司洛尔两药单用及合用的抗缺血性心律失常作用。结果表明,牛磺酸70mg·kg~(-1),140mg·kg~(-1)可使心律失常发生时间推迟,减少重性早博(PVCs)次数,缩短室性心动过速(VT)、心室纤颤(VF)累计持续时间并降低其发生率,恢复窦律时间提前。艾司洛尔25mg·kg~(-1)推迟心律失常发生时间,缩短VT累计持续时间,降低VF发生率.牛磺酸70mg·kg~(-1)与艾司洛尔25mg·kg~(-1)合用,其抗心律失常效果较单用增强。血流动力学实验结果表明.两药合用较艾司洛尔单用对心缩力的抑制减弱。离体大鼠心脏用牛磺酸40mmol·L~(-1)灌流后,抑制苯肾上腺素对心脏的正性肌力和正性频率作用。     

高效毛细管电泳法研究美托洛尔、艾司洛尔和维拉帕米的对映体的手性分离

目的：用高效毛细管电泳法分离美托洛尔、艾司洛尔和维拉帕米的对映体的手性分离。方法：在６５ｍｍｏｌ·Ｌ－１磷酸盐缓冲溶液中加入５．５ｍｍｏｌ·Ｌ－１羧甲基βＣＤ（ＣＭβＣＤ）手性选择剂,ｐＨ＝４．５,紫外λ２１２ｎｍ检测。结果：美托洛尔、艾司洛尔和维拉帕米的对映体得到基线手性分离。结论：此方法分析速度快,手性分离效果好,可用于上述药物对映体的临床研究。     

The electrocardiographic and hemodynamic effect of metohexital and propofol with and without esmolol

BACKGROUND: Metohexital and propofol are short-acting induction agents, which have a tendency to prolong the QTc interval of the ECG. We studied whether this increase could be prevented by combining a beta-blocking agent, esmolol, with these drugs. Simultaneously, we studied the hemodynamic effects of these combinations. METHODS: In a randomized, double-blind study, 80 ASA I-II young adults were premedicated with oxycodone and atropin and allocated to one of four groups: propofol (P), propofol + esmolol (P + E), metohexital (E) or metohexital + esmolol (M + E). The doses were 2 mg/kg propofol/metohexital and 1 mg/kg esmolol. Alfentanil 15 microg/kg was used in all groups. The hemodynamic parameters were measured non-invasively and the electrocardiographic parameters using the signal processing method. RESULT: The highest QTc values, which often exceeded the normal upper limit of 440 ms, were recorded at the baseline or immediately after the administration of the induction drugs. The intervals were significantly shorter if esmolol was co-administered with either propofol or metohexital. The heart rate increased in the group M and decreased in the group P + E but remained unchanged in the groups P and M + E. Systolic and diastolic arterial pressures decreased during the study in all groups, most prominently in group P + E. CONCLUSIONS: During the anesthesia induction, the QTc interval was significantly shorter when esmolol was co-administered with either propofol or metohexital. The hemodynamic responses were properly controlled with the combination of metohexital and esmolol as well as with propofol alone, but the combination of propofol and esmolol tended to cause hemodynamic depression.     

The use of esmolol in whole-body hyperthermia: Cardiovascular effects

Whole-body hyperthermia (WBH) is a well-described investigational adjunct to systemic chemotherapy for the treatment of advanced malignancies. The hemodynamic consequences of this physiologic state may include tachycardia, which can produce acute myocardial ischemia in patients with coronary artery disease. Ischemic heart disease is currently considered a contraindication to WBH. We chose to investigate the consequences of using a new β₁-adrenergic antagonist, esmolol, to attempt to control the tachycardia associated with WBH. After institutional approval and patient consent, nine consecutive patients with normal cardiac function presenting for WBH with carboplatin infusion were studied. Along with standard monitors, radial arterial and oximetric thermodilution pulmonary artery catheters were placed. Patients were sedated and heated in a radiant warmer (Enthermics). Spontaneous ventilation was maintained and hemodynamic data were gathered at 37°C, and at 41.8°C (before, during and after esmolol infusion). Heart rate and cardiac output increased (by 46% (p = 0.001) and 35% (p=0.04) respectively) while mean arterial pressure and systemic vascular resistance fell (by 18% (p = 0.02) and 44% (p = 0.006) respectively) during hyperthermia. Heart rate was significantly reduced during esmolol administration (mean dose 180 μg/kg/min) in the absence of changes in cardiac index and calculated oxygen delivery. Ventricular filling pressures and stroke work were unchanged. No heart failure, pulmonary edema, or other adverse event was observed. Hemodynamic changes seen during esmolol administration were completely reversed 15 min after the infusion was stopped. We conclude that the administration of moderate doses of esmolol is safe for this population of patients undergoing WBH, and that this technique raises the question of whether patients with ischemic heart disease could safely undergo WBH.     

Direct effects of esmolol and landiolol on cardiac function, coronary vasoactivity, and ventricular electrophysiology in guinea-pig hearts

The ultra-short acting, selective β(1)-adrenergic antagonists landiolol and esmolol are widely used perioperatively; however, little is known about their acute direct actions on the heart. The current study utilized the Langendorff perfused heart system to measure changes in cardiac function and hemodynamics in response to each drug. Furthermore, electrophysiological analysis was performed on isolated ventricular myocytes. Direct application of esmolol significantly decreased systolic left ventricular pressure and heart rate at concentrations > 10 μM, while it dose-dependently increased coronary perfusion pressure. Esmolol also shortened the action potential duration (APD) in a concentration-dependent manner, an action maintained even when the delayed rectifier K(+) current or ATP sensitive K(+) current was blocked. Moreover, esmolol inhibited both the inward rectifier K(+) current (I(K1)) and the L-type Ca(2+) current (I(CaL)) and increased the outward current dose-dependently. In contrast, landiolol had minimal cardiac effects. In the Kyoto Model computer simulation, inhibition of either I(K1) or I(CaL) alone failed to shorten the APD; however, an additional increase in the time-independent outward current caused shortening of the APD, equal to that induced by esmolol. In conclusion, esmolol directly inhibits cardiac performance significantly more so than landiolol, an effect revealed to be at least in part mediated by esmolol-induced APD shortening.     

预注艾司洛尔对丙泊酚注射痛的缓解作用

目的：评估预先注射艾司洛尔对丙？白酚注射痛的缓解作用。方法：选取需行宫、腔镜探查术者90例,随机分为3组：试验（艾司洛尔）组、阳性对照（利多卡因）组、阴性对照（生理盐水）组。各组受试者先静脉注人试验药物,30s后静脉注人丙泊酚。观察询问各组受试者注射丙泊酚期间的疼痛情况,并记录用药前后的血压和心率变化。结果：艾司洛尔组和利多卡因组受试者疼痛程度及注射痛发生率较生理盐水组明显降低（P〈0．05）,试验组预注艾司洛尔后心率比注射艾司洛尔前及注射丙泊酚后明显降低（P〈0．05）,其余数据无显著变化（P〉0．05）。结论：与利多卡因相似,预先注射艾司洛尔也能安全有效地缓解丙泊酚注射痛。