吸入麻醉药预处理对兔缺血再灌注心肌Bcl-2、Bax及p53基因表达的影响

目的探讨吸入异氟醚、七氟醚及地氟醚预处理对兔在体心脏局部缺血再灌注过程中心肌细胞Bcl-2、Bax及p53基因表达的影响。方法 40只新西兰白兔随机分成5组(n=8):假手术对照组(P组)、缺血再灌注对照组(IR组)、异氟醚预处理组(Ⅰ组)、七氟醚预处理组(S组)、地氟醚预处理组(D组)。除P组外,每组接受左冠脉前降支3 h阻断和3 h再灌注。吸入药预处理组在缺血前分别吸入1MAC的异氟醚、七氟醚或地氟醚,30 min后洗脱15 min。取心肌缺血区边缘组织用流式细胞仪测凋亡指数(AI)和Bcl-2、Bax及p53基因的蛋白表达量。结果 AI:P组为(0.93±0.27)％,IR组为(14±4)％,I、s、D组较IR组显著减少,分别为(6.7±1.8)％、(6.7±1.6)％、(7.4±2.0)％(P<0.01)。Bcl-2、p53、Bax基因的蛋白表达:Bcl-2基因的蛋白表达量I、S、D组高于IR组,Bax基因和p53基因的蛋白表达量I、S、D组低于IR组。结论 异氟醚、七氟醚及地氟醚预处理抑制缺血再灌注所致心肌细胞凋亡与上调BcI-2基因的蛋白表达、下调p53和Bax基因的蛋白表达有关。     

环孢素对系膜细胞血管紧张素Ⅱ1型受体表达的影响

目的 :探讨免疫抑制剂环孢素对肾脏系膜细胞表达血管紧张素Ⅱ受体的影响 ,并初步探讨其临床意义。方法 :体外培养大鼠系膜细胞株 ,用RT -PCR方法测定不同浓度环孢素 (0 ,2 5 0 ,5 0 0 ,10 0 0ng/ml)作用 2 4h对细胞表达血管紧张素 1型受体 (AT1)mRNA的影响 ;用免疫组织化学方法测定不同浓度环孢素作用 2 4hAT1蛋白的表达 ;用流式细胞术检测环孢素 (10 0 0ng/ml)作用 2 4h细胞表达AT1的阳性率。 结果 :环孢素可以促进系膜细胞AT1受体mRNA的表达 ,呈明显剂量依赖效应。免疫组织化学结果提示环孢素刺激 2 4h细胞表达AT1明显增强 ,流式细胞术分析显示 ,环孢素作用后 ,环孢素组细胞AT1阳性率 (43.4± 4 .0 5 ) % ,较对照组 (2 5 .1± 3.4 2 ) %明显增加 ,差异显著 (P <0 .0 5 )。结论 :环孢素可以上调系膜细胞血管紧张素 1型受体的表达 ,这可能是体内环孢素激活RAS系统并使其参与肾小球病变的重要原因之一。     

异氟醚预处理对心脏瓣膜置换术病人血清一氧化氮与肌钙蛋白Ⅰ的影响

目的探讨异氟醚预处理对心肌缺血-再灌注损伤的保护效应及机制。方法择期行心脏瓣膜置换术的风湿性心脏瓣膜病病人32例,随机分为异氟醚组和对照组,每组16例。异氟醚组以1.5%~2%异氟醚吸入复合芬太尼维持麻醉,心肺转流(CPB)开始前洗脱10min,CPB后以芬太尼维持麻醉;对照组以芬太尼维持麻醉。分别于麻醉前(T0)、CPB前(T1)、CPB30min(T2)、术后8h(T3)、24h(T4)抽取中心静脉血测定一氧化氮(NO)、NO合酶(NOS)与心肌肌钙蛋白I(cTnI)浓度。结果两组病人T0时NO、NOS与cTnI浓度差异无显著意义;异氟醚组T1、T2时NO、NOS浓度明显高于对照组(P<0·05),T3、T4时cTnI浓度明显低于对照组(P<0·05)。结论异氟醚具有心肌预适应作用,其机制可能与增加NO释放有关。     

肾脏局部血管紧张素受体表达与IgA肾病病理损伤的相关性

目的 观察应用ARB类药物对肾脏局部血管紧张素受体表达的影响,探讨血管紧张素受体表达与IgAN肾病(immunoglobulin A nephrology,IgAN)肾脏病理损伤的关系.方法 选取2013年1月至2014年12月在中日友好医院肾内科行肾穿刺活检,且病理诊断为IgAN的患者172例,采用Lee分级方法进行病理分级,应用免疫组化方法检测AT1、AT2和MAS受体在肾活检组织中的表达,观察应用ARB类药物对上述三种血管紧张素受体的影响,分析三种受体表达水平与Lee分级的相关性.结果 Lee分级Ⅲ级IgAN患者中,应用ARB大于30 d者肾脏血管的AT1受体表达较未应用者显著减少,肾小球的AT2受体表达量较未应用者显著增多.IgAN患者肾脏血管、肾小管间质上AT1受体的表达水平与Lee分级存在显著正相关.Ⅴ级IgAN患者肾小球上AT2受体的表达量较Ⅰ~Ⅳ级患者显著增多.结论 应用ARB类药物治疗可影响IgAN患者肾脏局部AT1、AT2受体表达,肾脏局部AT1、AT2受体表达与IgAN肾脏病理损伤程度存在一定相关性.     

血管紧张素Ⅱ受体A1166C基因多态性对体外循环中血压的影响

目的 研究血管紧张素Ⅱ1型受体(AT1R)基因多态性对体外循环(CPB)术中转流平稳期病人动脉血压的影响。方法 详细记录82例病人CPB转流平稳期的平均动脉压(MAP)，放免法测定所有病人CPB前和CPB中血浆血管紧张素Ⅱ的浓度，用PCR-RFLP方法检测其ATIR基因型，根据突变与否分为突变组与正常组。结果 突变组7例，正常组75例。突变组病人观察期内MAP的平均值(MMAP)、最小值(Mini)和扩血管药的用量与正常组相比差异有显著性，其与血浆中血管紧张素Ⅱ的浓度无关。结论 AT1R基因多态性对CPB转流平稳期血压状态有明显影响，可能是CPB中某些情况下循环高灌注和CPB预后不良的原因之一。     

血管紧张素II受体在人扩张皮肤中的表达及意义

目的:观察血管紧张素II(AngiotensinII,AngII)1型(AngIItype1,AT1)受体和2型(AngIItype2,AT2)受体蛋白和基因以及血管紧张素原(Angiotensinogen,AGT)基因在人扩张后皮肤和正常皮肤组织中表达的变化。方法:采用常规病理学技术和免疫组织化学方法检测扩张与未扩张皮肤组织的病理特征以及AT1和AT2受体表达的变化,提取扩张与未扩张皮肤组织的总RNA后,用逆转录-多聚酶链式反应法(RT-PCR法)对AGT及AT1和AT2受体在扩张与未扩张皮肤组织中基因的表达变化进行观察。结果:在正常皮肤和扩张后皮肤组织中AT1和AT2受体蛋白和mRNA均有表达。在扩张后皮肤中AT1受体蛋白和mRNA表达显著增加,与正常皮肤组织中的mRNA表达量相比增加约3倍(P<0.05vs正常皮肤);而AT2受体蛋白和mRNA表达仅有轻度增加,且差异并不显著(P>0.05vs正常皮肤)。和AT1受体基因表达的变化趋势类似,AGTmRNA也在扩张后皮肤中表达显著增强,约是正常皮肤的4倍(P<0.05vs正常皮肤)。结论:在皮肤扩张过程中血管紧张素系统被激活,AngII受体AT1表达增加,AngII可能通过AT1受体参与扩张后皮肤组织的病理改变。     

地氟烷预处理对幼鼠心肌细胞血管紧张素受体Ⅰ型表达的影响

目的 观察地氟烷预处理对缺氧,复氧心肌细胞血管紧张素受体Ⅰ型(AT1受体)表达的影响。方法无菌取新生2—3 d的SD幼鼠心室,采用胰蛋白酶消化成散在的单个细胞。加入DMEM培养液培养至第7天。随机分为四组,组1:细胞不经任何处理;组2:缺氧2 h,复氧1 h;组3:1.5 MAC地氟烷预处理20 min,清洗10 min,其余处理同组2;组4:地氟烷预处理前5 min,培养液中加入AT1受体阻断剂洛沙坦(Losartan),终浓度为10-6mol/L。比色法测培养液中肌酸激酶(CK)、乳酸脱氢酶(LDH)活性;Rt-PCR测各组细胞AT1受体的基因表达(mRNA)。结果 组2CK、LDH活性及AT1受体mRNA的相对含量均高于组1(P<0.01);组3 CK、LDH活性及AT1受体mRNA均降低(与组2和组1比较,P<0.01);组4与组3比较CK、LDH活性及AT1受体mRNA的相对含量上升(P<0.05或0.01),但仍低于组2(P<0.01)。结论 地氟烷预处理可部分逆转缺氧/复氧所致的心肌细胞损伤,其保护效应的发生机制部分由AT1受体介导。     

血管紧张素Ⅱ受体1表达水平与肝纤维化分期的相关性研究

目的：探讨肝组织中血管紧张素Ⅱ受体1（AT1）的表达与纤维化分期的相关性。方法：应用免疫荧光法检测35例肝组织中AT1的表达,并在荧光显微镜下分别对各检测样本随机选择10个视野（×200）,进行AT1表达的阳性细胞计数。结果：镜下观察每个视野F0～F3期肝纤维化组织中AT1荧光表达阳性细胞的数量分别为F0期：0;F1期：36.31±8.56;F2期：48.62±10.70;F3期：90.66±13.50。F3期与F0、F1、F2期比较差异具有统计学意义（P〈0.01）,F2期与F0、F1期比较差异亦有统计学意义（P〈0.05）。结论：在肝纤维化形成的过程中,AT1受体的表达水平与肝纤维化分期有明显的相关性。     

良性前列腺增生合并高血压患者前列腺中血管紧张素Ⅱ及其受体AT1分布及表达的研究

目的研究高血压对良性前列腺增生（BPH）前列腺组织中血管紧张素Ⅱ（AngⅡ）及其受体AT1的分布及表达的影响。方法用免疫组织化学方法检测41例单纯BPH和41例BPH合并高血压前列腺组织中AngⅡ和AT1受体的分布及表达。结果前列腺组织中，AngⅡ主要分布于腺上皮细胞，AT1受体主要分布于前列腺间质和血管内皮细胞。高血压组AngⅡ表达高于单纯BPH组（P〈0．01），而AT1受体表达则显著低于单纯BPH组（P〈0．01）。结论肾素一血管紧张素系统可能参与BPH的发生发展，深入研究其作用将有助于理解BPH的发病机制及高血压与BPH的相关性。     

血管紧张素Ⅱ受体在皮肤血管瘤不同时期的表达

目的：观察血管紧张素Ⅱ 1型受体（AT1）和2型受体（AT2）在毛细血管瘤组织中的表达，探讨血管紧张素Ⅱ与毛细血管瘤发生、发展及自然消退可能的关系.方法：采用免疫组织化学的方法检测AT1和AT2受体在29例毛细血管瘤和9例正常皮肤组织中的表达和分布规律.结果：在增生期毛细血管瘤组织中扩张的微血管内皮细胞仅见AT1受体表达，未见AT2受体表达.在消退期毛细血管瘤组织中扩张的微血管内皮细胞可同时检测到AT1和AT2受体阳性染色信号.结论：血管紧张素Ⅱ可能通过AT1和AT2受体参与血管瘤的发生、发展及自然消退。     

小儿先天性心脏病术中影响安氟醚摄取的因素

目的 了解小儿先天性心脏病（先心病）术中影响安氟醚摄取的因素。方法 将５岁以下先心病病儿６０例随机分为Ａ组：室间隔缺损（ＶＳＤ）及房间隔缺损（ＡＳＤ）病儿体外循环（ＣＰＢ）前、后匀吸入安氟醚（１５例）;Ｂ组：ＶＳＤ及ＡＳＤ病儿单纯ＣＰＢ后吸入安氟醚（１５例）。Ｃ组：法鲁氏四联症（Ｆ４）病儿ＣＰＢ前、后均吸入安氟醚（１５例）。Ｄ组：Ｆ４病儿单纯ＣＰＢ后吸入安氟醚（１５例）。将安氟醚的吸入浓度（Ｆ１）     

Cardiovascular effects of, and catecholamine response to, high dose fentanyl or NLA in patients for valve replacement]

We measured the cardiovascular effect of, and catecholamine and other hormonal responses to, anesthetic doses of fentanyl and original NLA in 25 patients for open heart surgery. The patients were randomly divided into three groups (group N, F30, F75). During induction, in group N; droperidol 0.25 mg.kg-1 and fentanyl 5 micrograms.kg-1, in group F30; fentanyl 30 micrograms.kg-1, and in group F75; fentanyl 75 micrograms.kg-1 were administered intravenously. Additional fentanyl was administered at a rate of 100 to 200 micrograms.h-1. Droperidol 0.25 mg.kg-1 was administered in group N when cardiopulmonary bypass (CPB) was disconnected. Plasma samples were assayed for norepinephrine, epinephrine, ACTH and cortisol before and after induction, during sternotomy, 60 minutes after institution of CPB, after weaning from CPB, and before as well as after extubation. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) and rate pressure product (RPP) were calculated simultaneously at the blood samplings. In all groups, no remarkable change in cardiovascular dynamics was observed. CPB was associated with marked increases in catecholamines, but high dose fentanyl in dose of 75 micrograms.kg-1 was able to suppress epinephrine level more than in group N. In high dose fentanyl group (F30, F75) ACTH was within normal ranges, even during CPB. The results suggest that high dose fentanyl is a complete anesthetic in patients for cardiac surgery. But a large dose of fentanyl causes small decreases in heart rate and arterial blood pressure. Our data indicate that group F30 is an attractive anesthetic technique for patients with valvular disease.     

Desflurane Confers Neurologic Protection for Deep Hypothermic Circulatory Arrest in Newborn Pigs

Background: Cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA), as used for infant heart surgery, carry a risk of ischemic neurologic injury. Volatile anesthetics have neuroprotective properties against both global and focal ischemia at normothermia. The authors examined the hemodynamic and neuroprotective effects of desflurane in a piglet CPB-DHCA model.

Methods: Twenty piglets aged 5-10 days received a desflurane- (6-9% expired) or fentanyl-based anesthetic before and during CPB (before and after DHCA). DHCA lasted 90 min at 19[degrees]C brain. Cardiovascular variables (heart rate, arterial pressure, blood gases, glucose, brain temperature) were monitored. On postoperative day 2, neurologic and histologic outcomes were determined.

Results: Cardiovascular variables before, during, and after CPB were physiologically similar between groups. The desflurane group had better neurologic performance (P = 0.023) and greater postoperative weight gain (P = 0.04) than the fentanyl group. In neocortex, the desflurane group had less tissue damage (P = 0.0015) and fewer dead neurons (P = 0.0015) than the fentanyl group. Hippocampal tissue damage was less in the desflurane group (P = 0.05), but overall, neuronal cell counts in the CA1 sector of the right hippocampus were similar to those in the fentanyl group.     

地氟醚预处理对缺血/再灌注心肌的保护作用

目的　探讨地氟醚预处理抗心肌缺血／再灌注损伤作用及其可能机制。方法 ２０例心脏瓣膜置换术病人随机分为地氟醚观察组与芬太尼对照组,观察血浆过氧化脂质（ＬＰＯ）水平、红细胞超氧化物歧化酶（ＳＯＤ）活性、心脏指数（ＣＩ）、每搏指数（ＳＩ）、肌酸激酶同工酶（ＣＫ－ＭＢ）、心肌细胞形态变化及开放主动脉后心脏复跳情况。结果观察组再灌注后血浆ＬＰＯ与ＣＫ－ＭＢ浓度显著低于对照组,红细胞ＳＯＤ活性相对大于对照组,电镜下心肌细胞损害明显轻于对照组,ＣＩ、ＳＩ、心脏自动复跳率高于对照组。结论　地氟醚通过诱导预适应具有心肌保护作用。     

Desflurane confers neurologic protection for deep hypothermic circulatory arrest in newborn pigs

BACKGROUND: Cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA), as used for infant heart surgery, carry a risk of ischemic neurologic injury. Volatile anesthetics have neuroprotective properties against both global and focal ischemia at normothermia. The authors examined the hemodynamic and neuroprotective effects of desflurane in a piglet CPB-DHCA model. METHODS: Twenty piglets aged 5-10 days received a desflurane- (6-9% expired) or fentanyl-based anesthetic before and during CPB (before and after DHCA). DHCA lasted 90 min at 19 degrees C brain. Cardiovascular variables (heart rate, arterial pressure, blood gases, glucose, brain temperature) were monitored. On postoperative day 2, neurologic and histologic outcomes were determined. RESULTS: Cardiovascular variables before, during, and after CPB were physiologically similar between groups. The desflurane group had better neurologic performance (P = 0.023) and greater postoperative weight gain (P = 0.04) than the fentanyl group. In neocortex, the desflurane group had less tissue damage (P = 0.0015) and fewer dead neurons (P = 0.0015) than the fentanyl group. Hippocampal tissue damage was less in the desflurane group (P = 0.05), but overall, neuronal cell counts in the CA1 sector of the right hippocampus were similar to those in the fentanyl group. CONCLUSIONS: Desflurane-based anesthesia yields hemodynamics during CPB with DHCA that are similar to those with fentanyl-based anesthesia. However, desflurane-based anesthesia improves neurologic and histologic outcomes of CPB-DHCA in comparison with outcomes with fentanyl-based anesthesia.     

Effects of propofol,desflurane, and sevoflurane on recovery of myocardial function after coronary surgery in elderly high-risk patients

BACKGROUND: The present study investigated the effects of propofol, desflurane, and sevoflurane on recovery of myocardial function in high-risk coronary surgery patients. High-risk patients were defined as those older than 70 yr with three-vessel disease and an ejection fraction less than 50% with impaired length-dependent regulation of myocardial function. METHODS: Coronary surgery patients (n = 45) were randomly assigned to receive either target-controlled infusion of propofol or inhalational anesthesia with desflurane or sevoflurane. Cardiac function was assessed perioperatively and during 24 h postoperatively using a Swan-Ganz catheter. Perioperatively, a high-fidelity pressure catheter was positioned in the left and right atrium and ventricle. Response to increased cardiac load, obtained by leg elevation, was assessed before and after cardiopulmonary bypass (CPB). Effects on contraction were evaluated by analysis of changes in dP/dt(max). Effects on relaxation were assessed by analysis of the load-dependence of myocardial relaxation. Postoperative levels of cardiac troponin I were followed for 36 h. RESULTS: After CPB, cardiac index and dP/dt(max) were significantly lower in patients under propofol anesthesia. Post-CPB, leg elevation resulted in a significantly greater decrease in dP/dt(max) in the propofol group, whereas the responses in the desflurane and sevoflurane groups were comparable with the responses before CPB. After CPB, load dependence of left ventricular pressure drop was significantly higher in the propofol group than in the desflurane and sevoflurane group. Troponin I levels were significantly higher in the propofol group. CONCLUSIONS: Sevoflurane and desflurane but not propofol preserved left ventricular function after CPB in high-risk coronary surgery patients with less evidence of myocardial damage postoperatively.     

Effects of Propofol, Desflurane, and Sevoflurane on Recovery of Myocardial Function after Coronary Surgery in Elderly High-risk Patients

Background: The present study investigated the effects of propofol, desflurane, and sevoflurane on recovery of myocardial function in high-risk coronary surgery patients. High-risk patients were defined as those older than 70 yr with three-vessel disease and an ejection fraction less than 50% with impaired length-dependent regulation of myocardial function.

Methods: Coronary surgery patients (n = 45) were randomly assigned to receive either target-controlled infusion of propofol or inhalational anesthesia with desflurane or sevoflurane. Cardiac function was assessed perioperatively and during 24 h postoperatively using a Swan-Ganz catheter. Perioperatively, a high-fidelity pressure catheter was positioned in the left and right atrium and ventricle. Response to increased cardiac load, obtained by leg elevation, was assessed before and after cardiopulmonary bypass (CPB). Effects on contraction were evaluated by analysis of changes in dP/dtmax. Effects on relaxation were assessed by analysis of the load-dependence of myocardial relaxation. Postoperative levels of cardiac troponin I were followed for 36 h.

Results: After CPB, cardiac index and dP/dtmax were significantly lower in patients under propofol anesthesia. Post-CPB, leg elevation resulted in a significantly greater decrease in dP/dtmax in the propofol group, whereas the responses in the desflurane and sevoflurane groups were comparable with the responses before CPB. After CPB, load dependence of left ventricular pressure drop was significantly higher in the propofol group than in the desflurane and sevoflurane group. Troponin I levels were significantly higher in the propofol group.     

Desflurane pharmacokinetics during cardiopulmonary bypass

OBJECTIVE: To describe the washin and washout of desflurane when first administered during cardiopulmonary bypass (CPB) for cardiac surgery. DESIGN: A single-arm prospective study. SETTING: University-affiliated hospital operating room. PARTICIPANTS: Ten adult patients presenting for cardiac surgery. INTERVENTIONS: Consenting patients presenting for cardiac surgery received anesthesia with midazolam and fentanyl. Patients were cooled to 32 degrees C on CPB, then desflurane 6% was administered and blood samples drawn repeatedly from the arterial and venous bypass cannulae as well as from the membrane oxygenator inlet and exhaust from 2 to 32 minutes of desflurane administration. Just before rewarming, final (maximum) washin samples were taken. On rewarming, desflurane was discontinued, and blood and gas samples were taken 2 to 24 minutes thereafter. MEASUREMENTS AND MAIN RESULTS: CPB time was 116 +/- 10 minutes, and ischemic time was 81 +/- 6 minutes. Mean pump flow was 4.49 +/- 0.03 L/min, and mean arterial pressure was 70.1 +/- 1 mmHg during the study period. Arterial washin of desflurane was initially rapid; arterial concentrations reached 50% of administered concentrations within 4 minutes, but then slowed, reaching 68% of inspired concentrations at 32 minutes (desflurane concentration 4.0% +/- 0.3%). Arterial washout of desflurane was more rapid; arterial concentrations fell to 18% of the maximum concentration reached within 4 minutes, and only 8% of the maximum arterial concentration was present in blood 20 minutes later. CONCLUSION: Desflurane showed rapid initial washin and washout on CPB when administration was started at 32 degrees C and stopped at time of rewarming.     

芬太尼对地氟醚麻醉诱导和气管插管MAC的影响

目的和方法观察地氟醚和芬太尼+地氟醚麻醉诱导的特点及测定两者半数气管插管最低肺泡浓度(MACEI     

不同速度输注异丙酚对低温体外循环期间患者麻醉深度的影响

目的 探讨不同速度输注异丙酚静脉麻醉下低温体外循环期间大脑状态指数(cerebral state index,CSI)及爆发抑制比(burst supression ratio,BS%)的变化.方法 择期行低温体外循环下心脏瓣膜置换手术患者44例,年龄(18～60)岁.随机分为两组,每组22例.麻醉诱导采用静脉注射异丙酚1mg/ks～1.5 mg/kg,芬太尼10μg/kg,维库溴铵0.1 mg/kg.麻醉维持采用持续静脉输注异丙酚4 mg·kg-1·h-1(P4组)或6 rag·kg-1·h-1(P6组),芬太尼5gμ·kg-·1h-1.记录体外循环(cardio pulmonany bypass,CPB)前5 min(T0)、CPB后2 min(T1)、CP8开始后30 min(T2)、CPB开始后60 min(T3)、停CPB后15 min(T4)时的CSI、BS%、鼻咽温度、平均动脉压(MAP)、心率(HR).结果 CPB期间两组的CSI均下降,与体外循环前比较差异有统计学意义(P<0.05或0.01),P6组CPB 30 min、60 min的CSI与P4组比较为差异有统计学意义(P<0.01).P6组在CPB 30 rain、60 min时出现爆发抑制比,与CPB前比较为差异有统计学意义(P<0.01),与P4组比较为差异有统计学意义(P<0.01).结论 低温CPB期间持续输注异丙酚6 mg·kg-1·h-1时,CSI处于较低水平,BS%明显增多,应适当减少异丙酚的输注速度,以维持合适的麻醉深度.