持续静脉输注不同时间的依托咪酯对肾上腺皮质功能的影响

目的 观察持续静脉输注不同时间的依托咪酯对肾上腺皮质功能的影响.方法 选择择期手术患者60例,随机均分为六组,依托咪酯组(8～10 μg·kg-1·min-1)分别持续输注依托咪酯乳剂1 h(E1组),2 h(E2组),4 h(E4组);丙泊酚组(4～6 mg·kg-1 ·h-1),分别持续输注丙泊酚1h(P1组),2 h(P2组),4 h(P4组).于麻醉前5 min(T0),给药后1 h(T1),2 h(T2),4 h(T3),6h(T4),24 h(T5)6个时点测定血中的皮质醇(Cor)、醛固酮(ALD)浓度和促肾上腺皮质激素(ACTH)含量.结果 与T0时比较,T1、T2时E1组、T1～T3时E2和E4组Cor降低(P＜0.05);T1、T2时E1组、T2、T3时E2组、T1～T4时E4组、T1时P2和P4组ALD浓度降低(P＜0.05);T2时E2组、T2和T3时E4组ACTH含量升高(P＜0.05).六组各时点所有数值均在正常范围内,T5时80％的ALD浓度和所有Cor浓度、ACTH含量恢复至术前水平,未发生相关性肾上腺皮质功能不全的症状.结论 依托咪酯对肾上腺皮质功能的抑制是短暂的,可安全地用于4h内无肾上腺皮质功能不全患者的全麻维持.     

国产依托咪酯乳剂用于全身麻醉诱导的多中心研究

目的观察和比较依托咪酯乳剂与丙泊酚应用于健康成人全麻诱导时血流动力学的改变和不良反应的情况。方法选择来自五个研究中心的健康成年患者共489例,随机分为丙泊酚(P)组(n=246)和依托咪酯(E)组(n=243),两组患者全麻诱导均用咪唑安定0.03mg/kg、芬太尼2μg/kg、维库溴铵0.1mg/kg,在此基础上P组用丙泊酚2.0mg/kg,E组用依托咪酯乳剂0.3~0.4mg/kg完成诱导。记录患者在基础状态(T0)、插管前1min(T1)、插管即刻(T2)及插管后1min(T3)、2、3、4、5min(T4)、10min(T5)、15min(T6)的SBP、DBP、MAP、SpO2和HR。术后回访观察肌颤、注射痛、恶心、呕吐和浅表性静脉炎等不良反应的发生情况。结果与T0比较,两组患者在T1、T2时SBP、DBP、MAP有明显的波动(P<0.05或P<0.01),但E组变化幅度显著低于P组(P<0.05)。E组患者注射痛的发生率显著低于P组(P<0.01)。结论依托咪酯乳剂可安全地用于健康成人的麻醉诱导;与丙泊酚相比,依托咪酯乳剂对血流动力学的影响轻且不良反应少。     

右美托咪定对心脏瓣膜置换术患者的心肌保护作用

目的观察右美托咪定对心脏瓣置换术患者的心肌保护作用。方法风湿性心脏病行二尖瓣置换术患者30例,均择期全麻CPB下手术,年龄18~65岁,ASAⅡ或Ⅲ级。采用随机数字表法均分为右美托咪定组(D组)和生理盐水组(C组)。麻醉诱导后D组开始静注右美托咪定0.5μg/kg,然后静脉持续泵入0.5μg·kg-1·h-1至手术结束;C组静注等量生理盐水。记录用药前(T0)、用药后即刻(T1)、切皮后(T2)、劈胸骨后(T3)、CPB前(T4)、停CPB后10min(T5)、手术结束(T6)的MAP和HR。于T0、T5、T6、术后6h(T7)、24h(T8)抽取中心静脉血ELISA法检测心型脂肪酸结合蛋白(H-FABP)、肌酸激酶(CK-MB)、肌钙蛋白I(cTnI)浓度。结果与T0时比较,T2、T3时两组MAP明显升高,T1、T2和T4时D组HR明显减慢,而T5、T6时两组HR明显增快(P0.05)。与C组比较,T3时D组MAP明显降低、T4时MAP明显升高(P0.05),T1~T3时HR明显减慢(P0.05)。与T0时比较,T5~T8时两组血清H-FABP、CK-MB和cTnI浓度明显升高(P0.05)。与C组比较,T5~T8时D组血清H-FABP浓度,T7、T8时CK-MB和cTnI浓度明显降低(P0.05)。结论麻醉诱导后给予0.5μg/kg负荷量右美托咪定,随后持续静脉输注0.5μg·kg-1·h-1,可维持体外循环前血压稳定,减轻CPB至术后24h心肌损伤。     

右美托咪定对体外循环下心脏瓣膜置换术患者脑损伤的影响

目的 评价右美托咪定对体外循环(CPBB)下心脏瓣膜置换术患者脑损伤的影响 方法 择期CPB下心脏瓣膜置换术患者40例,性别不限,年龄43～64岁,ASA分级Ⅱ或Ⅲ级,采用随机数字表法,将患者随机分为两组(n=20):对照组(C组)和右美托咪定组(D组).麻醉诱导前D组静脉注射右美托咪定0.6 μg/kg(15 min内),随后以0.2 μg·kg-1·h-1速率输注至术毕,C组给予等容量生理盐水.分别于CPB开始前(T1)、升主动脉开放(T2)、CPB结束(T3)及术后6 h(T4)时抽取桡动脉和颈静脉球部血样行血气分析,计算动脉-颈内静脉血氧含量差(Da-jvO2)、脑氧摄取率(CERO2),于T1-4及术后 24 h(T5)时测定预内静脉球部血浆S-100β蛋白和神经元特异性烯醇化酶(NSE)的浓度.结果 与C组比较,D组T2,3时SjvO2升高,Da-jvO2和CERO2降低,T2-4时血浆S-100β蛋白和NSE浓度降低(P＜0.05) 结论 右美托咪定可降低CPB下心脏瓣膜置换术患者脑氧代谢率,减轻脑损伤.     

右美托咪定对心脏瓣膜置换术患者肠黏膜损伤的影响

目的研究右美托咪定对心肺转流(CPB)下心脏瓣膜置换术患者肠黏膜损伤的影响及机制。方法择期行心瓣膜置换术的风湿性心脏病患者40例,男17例,女23例,年龄32~64岁,体重40~75kg,ASAⅡ或Ⅲ级,随机均分为右美托咪定组(D组)和对照组(C组)。麻醉诱导前D组静注右美托咪定负荷量1μg/kg持续10min,随后以0.3μg·kg-1·h-1速率持续输注至术毕;C组输注等容量生理盐水。两组麻醉诱导及维持方法相同。测定CPB开始前(T0)、主动脉阻断30min(T1)、停CPB即刻(T2)、术毕(T3)、术后6h(T4)、24h(T5)时血浆丙二醛(MDA)浓度、总抗氧化能力(T-AOC)和肠型脂肪酸结合蛋白(I-FABP)浓度。结果与T0时比较,两组T1~T5时血浆MDA浓度、I-FABP明显升高(P0.05),T1~T4时D组血浆T-AOC明显降低(P0.05)。T1~T5时D组血浆MDA、I-FABP明显低于C组(P0.05),T1~T4时D组血浆T-AOC明显高于C组(P0.05)。结论右美托咪定可以减轻CPB下心脏瓣膜置换术患者肠黏膜损伤,其机制与抑制氧化应激反应有关。     

雷米芬太尼后处理对心肺转流诱导犬心肌损伤和炎症因子的影响

目的 探讨雷米芬太尼后处理对心肺转流(CPB)诱导犬心肌损伤和炎症因子的影响.方法 健康成年雄性犬12只,随机均分为雷米芬太尼组(R组)和对照组(C组).两组动物经麻醉和开胸后,建立CPB心肌缺血-再灌注模型,阻断升主动脉60 min.R组于主动脉阻断55 min时自主动脉根部随温血灌注液持续输注雷米芬太尼5 min,速度为4μg·kg-1·min-1,灌注液输注速率2 ml·kg-1·min-1持续5 min.C组于相同时点行温血再灌注,灌注液输注速率同R组.分别于CPB前5 min(T0)、阻断升主动脉后30 min(T1)、开放升主动脉后5 min(T2)、停CPB 30 min(T3)和停CPB 2 h(T4)采集股动脉血,检测心肌肌钙蛋白I(cTnI)的浓度和血浆肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)、IL-8.记录主动脉开放后心脏自动复跳情况,电镜下观察心肌组织超微结构改变.结果 与T0时比较,两组cTnI、TNF-α在CPB后各时点均明显升高(P＜0.05或P＜0.01),升主动脉开放后各时点IL-6、IL-8均明显升高(P＜0.01).R组升主动脉开放后各时点cTnI、TNF-α、IL-6、IL-8均明显低于C组(P＜0.01).R组心肌组织结构损伤程度轻于C组.结论 雷米芬太尼后处理可抑制犬CPB诱导促炎细胞因子的释放,减轻心肌再灌注损伤.     

依托咪酯和异丙酚复合麻醉对腹部手术患者脑氧代谢影响的比较

目的 比较依托咪酯和异丙酚复合麻醉对腹部手术患者脑氧代谢的影响.方法 择期全麻下拟行腹部手术患者36例,ASA Ⅰ或Ⅱ级,随机分为异丙酚复合麻醉组(P组)和依托咪酯复合麻醉组(E组),每组18例.两组均静脉注射咪达唑仑0.08 mg/kg、芬太尼3μg/kg、维库溴铵0.1 mg/kg,P组静脉注射异丙酚1.5 mg/kg、E组静脉注射依托咪酯0.3 mg/kg行麻醉诱导,P组静脉输注异丙酚4～6mg·kg-1·h-1、E组静脉输注依托咪酯0.4～0.7 mg·kg-1·h-1,术中均间断注射维库溴铵和芬太尼维持麻醉.分别于麻醉前(T1)、气管插管后即刻(T2)、手术开始30 min(T3)及术毕即刻(T4)时监测HR、MAP和SpO2,抽取桡动脉血和颈内静脉球部血样行血气分析,测定乳酸浓度,计算动脉血氧含量(CaO2)、颈内静脉氧含量(cjvO2)、脑氧摄取率(CERO2).结果 两组HR、MAP和SpO2均在正常范围内.与T1时相比,两组SaO2、SjvO2、PaO2、PjvO2升高,T2-4时Da-jvO2和CERO2降低(P<0.01);两组问比较各时点SaO2、SjrO2、PaO2、PjvO2、CaO2、CjvO2、Da-jvO2、CERO2及乳酸水平差异均无统计学意义(P>0.05).结论 依托眯酯和异丙酚复合麻醉均可降低腹部手术患者的脑氧代谢率,且无明显差别.     

电针对依托咪酯复合麻醉患者肾上腺皮质功能的影响

目的 探讨电针对依托咪酯复合麻醉患者肾上腺皮质功能的影响.方法 择期腹部手术患者80例,性别不限,年龄30 ～ 64岁,ASA分级Ⅰ级或Ⅱ级,采用随机数字表法,将其分为4组(n=20):丙泊酚对照组(P组)、依托咪酯组(E组)、依托咪酯+电针组(EEA组)和依托咪酯+假电针组(ES组).E组、EEA组和ES组采用咪达唑仑-依托咪酯-舒芬太尼-阿曲库铵行麻醉诱导,采用依托咪酯-瑞芬太尼维持麻醉;P组采用咪达唑仑-丙泊酚-舒芬太尼-阿曲库铵行麻醉诱导,采用丙白酚-瑞芬太尼维持麻醉.EEA组于麻醉诱导前至术毕行电针刺激[疏密波(2/50 Hz),波宽300 μs,刺激电流由0开始,以0.1 mA的梯度逐渐增大,逐渐达到患者能耐受的最大水平].于麻醉诱导前(T0)、手术开始后2 h(T1)、术毕(T2)、术后2 h(T3)时抽取静脉血样,采用ELISA法测定血清皮质醇、促肾上腺皮质激素(ACTH)、肾上腺素、去甲肾上腺素的浓度.结果 与P组比较,E组、EEA组和ES组T1-T3时血清皮质醇浓度降低,T3时血清ACTH浓度升高,EEA组T1、T2时血清肾上腺素浓度、T1-T3时血清去甲肾上腺素浓度降低(P＜0.05);与E组比较,EEA组T1-T3时血清皮质醇浓度升高,T3时血清ACTH浓度降低,T1、T2时血清肾上腺素浓度、T1-T3时血清去甲肾上腺素浓度降低(P＜0.05),ES组上述指标差异无统计学意义(P＞0.05).结论 电针可减轻依托咪酯复合麻醉对患者肾上腺皮质功能的抑制作用.     

丙泊酚靶控输注用于重症心脏瓣膜病患者全麻诱导

目的探讨丙泊酚滴定法靶控输注用于重症心脏瓣膜病患者全麻诱导的安全性和有效性。方法重症心脏瓣膜病患者47例,随机分成丙泊酚组(P组,n=24)和依托咪酯组(E组,n=23)。P组以丙泊酚靶控输注,初始血浆靶浓度1.0μg/ml,采用改良警觉/镇静(MOAA/S)评分行镇静评分,每2分钟递增靶浓度0.2μg/ml,至患者MOAA/S评分≤1分时给予芬太尼5μg/kg、维库溴铵0.1mg/kg。E组使用依托咪酯0.25～0.30mg/kg和同剂量的芬太尼、维库溴铵并行气管插管。记录入室(T1)、MOAA/S评分≤1分(T2)、诱导期收缩压最低点(T3)、插管前(T4)、插管完毕(T5)、插管后5min(T6)时的SBP、DBP、HR、CVP;记录血管活性药物的使用情况。结果与T1时比较,P组T2～T6时SBP、DBP明显下降,HR明显减慢(P0.05或P0.01),E组T2～T4、T6时的SBP,T2～T6时的DBP明显下降,T2～T4时HR明显减慢(P0.05或P0.01),T3、T4时两组CVP明显降低(P0.05或P0.01)。与E组比较,P组T5时的SBP,T5、T6时的DBP明显降低,T5、T6时HR明显减慢(P0.05或P0.01)。P组患者在T2时的血浆靶浓度平均值为1.61μg/ml。结论丙泊酚滴定法靶控输注用于重症心脏瓣膜病患者全麻诱导的安全性与依托咪酯相似,并且能更好地抑制气管插管后的应激反应。     

国产依托咪酯在全麻诱导和维持中的应用

目的 探讨依托咪酯在全麻诱导和维持中的应用.方法 选择ASA Ⅰ或Ⅱ级,年龄20～70岁,需要全身麻醉行腹部手术、开胸手术或开颅手术的患者95例.随机分为依托咪酯组(E组,n=45)和丙泊酚组(P组,n=50).麻醉诱导:提前5 min静脉注射咪唑安定0.075 mg/kg,预注维库溴铵总量(0.1 mg/kg)的1/4,静脉注射芬太尼3μg/kg、依托咪酯0.4 mg/kg(E组)或丙泊酚2 mg/kg(P组)、再注射维库溴铵总量的3/4.麻醉维持:雷米芬太尼0.05～0.1μg·kg-1·min-1,依托咪酯0.6～1.2 mg·kg-1·h-1(E组)或丙泊酚4～10 mg/kg(P组),维库溴铵酌情追加.记录入室、插管前、插管即刻、插管后1、3、5、10 min及切皮时的SBP、DBP、HR、SpO2,诱导期BP和HR的最高和最低值、麻醉时间、手术时间、患者清醒时间、拔管时间.麻醉前、插管后和术后24 h分别经桡动脉抽血2 ml,采用放免法测定血浆皮质醇浓度.观察有无肌颤、注射痛、恶心、呕吐、血栓性静脉炎等不良反应.结果 (1)两组患者的麻醉时间、手术时间、手术完毕后的清醒时间以及拔管时间等比较差异均无统计学意义;(2)与入室时比较,插管前两组SBP、DBP均明显降低(P<0.05或P<0.01),尤其P组降低更为明显;插管后3、5、10 min P组SBP、DBP明显降低(P<0.05或P<0.01);插管后1、3 min E组HR明显增快(P<0.05或P<0.01),而P组在插管后1 min HR也明显增快(P<0.05),插管后3、5、10 min时减慢(P<0.05);(3)诱导期间两组患者最高SBP、HR和最低SBP、HR的比较差异均无统计学意义;(4)与麻醉前比较,两组患者在插管后血浆皮质醇浓度升高(P(0.05或P(0.01),而P组升高更为显著;(5)两组均有注射痛发生,但E组(11%)发生率较P组(44%)低(P<0.01),两组均未出现肌颤、恶心呕吐、静脉炎等其他不良反应.结论 使用临床剂量的依托咪酯作为麻醉诱导和术中维持的静脉全麻药是安全可行的,诱导前预注射小剂量咪唑安定和肌肉松弛药可有效预防肌颤的发生.     

Anesthesia and cardiac electrophysiology (Part I)

Cardiac arrhythmias are a common complication of surgery and anesthesia. They are more likely to occur in patients with heart disease and the presence of a transitory imbalance can supply the underlying substrate for reentry, triggered activity, or abnormal automaticity. The physiologic impact of a given arrhythmia depends on its duration, on ventricular response, and on the underlying cardiac disease. Optimal management of arrhythmias in the anesthetized patient will depend on knowledge of the trigger mechanisms, the effects of anesthetic drugs on cardiac electrophysiology, and situations that favor arrhythmias. The anesthesiologist must cope with a plethora of problems related to the patient's clinical state and the trauma of surgical manipulation. Experience with electrocardiography and the application of various devices (pacemakers, cardioverters, implantable defibrillators) and knowledge of the pharmacodynamics and pharmacokinetics of new intravenous drugs will be essential for patient management. The purpose of the present review is to provide the anesthesiologist with an overview of current views on the diagnosis and management of arrhythmias during anesthesia.     

Smooth muscle and cardiac glycosides (author's transl)

Actions of cardiac glycosides (C.G.) on smooth muscles are reviewed. 1. C.G. inhibit the Na-K ATPase of smooth muscle membrane, though the degree and mode of the inhibition vary among the types of smooth muscles. 2. The uptake of C.G. by smooth muscles has been reported to be influenced by K+, Na, ATP, and temperature. The difference between the uptake and its effect can be observed. 3. Intracellular K concentration decreased and intracellular Na concentration increased by the treatment with C.G. 4. They depolarized the membrane; the action being affected by extracellular ion concentration. An increase in spike discharges is observed. 5. C.G. potentiate or inhibit the concentrations of smooth muscles, depending on the types of smooth muscles and the causes of the contraction. C.G. can also cause transient contraction of smooth muscle. 6. C.G. influence the Ca content and Ca movements of smooth muscles. 7. C.G. cause the release of noradrenaline, acetylcholine, or prostaglandins. These substances can affect the contractile responses of smooth muscles.     

Non–heart-beating donors (then) and donation after cardiac death (now)

In the 1960s and 1970s, before the acceptance of brain death, donated organs were obtained from non–heart-beating donors. Today, this type of donor is referred to as a donor after cardiac death (DCD). After the acceptance of brain death criteria, most of the organs for transplantation were obtained from heart-beating donors. However, because of the shortage of brain-dead heart-beating donors in the 1980s, Maastricht surgeons started using organs obtained from DCD. Subsequently, they defined 4 different categories of non–heart-beating donors. In the United States, DCD donation has only recently gained widespread use. In this article, we present a historical overview of DCD donation; examine current practices for organ preservation and outcomes for kidney, kidney-pancreas, liver, and lung transplantation performed using organs obtained from DCD donors; and reported to the Organ Procurement and Transplantation Network/United Network for Organ Sharing database.     

Inhaled epoprostenol (prostacyclin) and pulmonary hypertension before cardiac surgery

OBJECTIVE: Pulmonary hypertension is commonly found in patients undergoing valvular surgery and can be worsened by cardiopulmonary bypass. Inhaled epoprostenol (prostacyclin) has been used for the treatment of pulmonary hypertension, but its effects compared with those of placebo on hemodynamics, oxygenation, echocardiographic examination, and platelet function have not been studied during cardiac surgery. METHODS: Twenty patients with pulmonary hypertension undergoing cardiac surgery were randomized in a double-blind study to receive inhaled epoprostenol (60 microg) or placebo. The inhalation occurred after induction of anesthesia and before surgical incision. The effects on left and right systolic and diastolic cardiac functions evaluated by means of pulmonary artery catheterization and transesophageal echocardiography, as well as oxygenation and platelet aggregation, were studied. RESULTS: Inhalation of epoprostenol significantly reduced indexed right ventricular stroke work from 10.7 +/- 4.57 g. m. m(-2) to 7.8 +/- 3.94 g. m. m(-2) (P =.003) and systolic pulmonary artery pressure from 48.4 +/- 18 mm Hg to 38.9 +/- 11.9 mm Hg (P =.002). The effect was correlated with the severity of pulmonary hypertension (r = 0.76, P =.01) and was no longer apparent after 25 minutes. There was no significant effect on systemic arterial pressures, left ventricular function, arterial oxygenation, platelet aggregation, and surgical blood loss. CONCLUSION: Inhaled epoprostenol reduces pulmonary pressure and improves right ventricular stroke work in patients with pulmonary hypertension undergoing cardiac surgery. A dose of 60 microg is hemodynamically safe, and its effect is completely reversed after 25 minutes. We did not observe any evidence of platelet dysfunction or an increase in surgical bleeding after administration of inhaled epoprostenol.     

Acadesine (AICA-riboside) improves postischemic cardiac recovery.

To test if acadesine (5-aminoimidazole-4-carboxamide riboside), a purine precursor, has cardioprotective effects, 16 dogs were placed on total cardiopulmonary bypass and subjected to global myocardial ischemia. Hemodynamic recovery was compared between a control (n = 8) group receiving standard cardioplegia and an acadesine (n = 8) group pretreated with intravenous acadesine (2.5 mg.kg-1.min-1 for 5 minutes, then 0.5 mg.kg-1.min-1) before ischemia, during ischemia, and until 10 minutes after removal of the aortic cross-clamp. Additionally, in the acadesine group the cardioplegia also contained 20 mumol/L acadesine. While the dogs were on cardiopulmonary bypass, global warm myocardial ischemia was induced by aortic cross-clamping for 5 minutes under normothermic conditions to simulate an angioplasty accident. Five minutes after aortic cross-clamping, hypothermic cardioplegia (30 mL/kg) was administered. The left anterior descending coronary artery was occluded before the first infusion of cardioplegia to simulate poor cardioplegia delivery that can occur during an emergency coronary artery bypass procedure after an angioplasty accident. The left anterior descending artery occlusion was released, and additional cardioplegia (15 mL/kg) infusions were made every 30 minutes thereafter during 120 minutes of cardioplegic ischemia. Thirty minutes after reperfusion, all animals in both groups were weaned from bypass and recovery data were obtained to compare with baseline preischemic values. There were no significant differences in heart rate, left atrial pressure, or systemic vascular resistance between groups after weaning from bypass. Peak developed pressure recovered to 79% +/- 19% (mean +/- standard deviation) of baseline in the acadesine group compared with 56% +/- 22% in the control group (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)