硬膜外阻滞和N2O—O2—安氟醚吸入麻醉对围术期老年男性R—A—A系统…

２０例择期行前列腺摘除或膀胱肿瘤部分切除病人，随机分为两组，每组１０例，分别行硬膜外麻醉和氧化亚氮－氧气－氨氟醚吸入麻醉，测定麻醉和手术过程中血浆素活性，血管紧张素Ⅱ和醛固酮浓度的变化，并进行比较。     

不同麻醉法对血浆肾素,血管紧张素II,醛固酮,皮质醇水平的…

观察全麻复合硬膜外阻滞和全麻两种麻醉时血浆肾素、血管紧张素Ⅱ、醛固酮、皮质醇变化。２５例择期上腹部手术患者，随机分两组：Ａ组为全麻复合硬膜外阻滞１２例，Ｂ组为全麻１３例。分别于麻醉前、麻醉插管后２分钟、进腹探查时、术中２小时、拔管后即刻抽取中心静脉血测肾素、血管紧张素Ⅱ、醛固酮、皮质醇的浓度。结果示Ａ组麻醉前后无明显变化（Ｐ〉０．０５）；Ｂ组术中肾素活性和皮质醇显著增高（Ｐ〈０．０１）。此外，手术     

不同麻醉法对血浆肾素、血管紧张素Ⅱ、醛固酮、皮质醇水平的影响

观察全麻复合硬膜外阻滞和全麻两种麻醉时血浆肾素、血管紧张素Ⅱ、醛固酮、皮质醇变化。２５例择期上腹部手术患者，随机分两组：Ａ组为全麻复合硬膜外阻滞１２例，Ｂ组为全麻１３例。分别于麻醉前、麻醉插管后２分钟、进腹探查时、术中２小时、拔管后即刻抽取中心静脉血测肾素、血管紧张素Ⅱ、醛固酮、皮质醇的浓度。结果示Ａ组麻醉前后无明显变化（Ｐ＞０．０５）；Ｂ组术中肾素活性和皮质醇显著增高（Ｐ＜０．０１）。此外，手术期间Ａ组比Ｂ组心率慢，血压低（Ｐ＜０．０１）。表明全麻复合硬膜外阻滞是一种应激反应较轻的麻醉方法。     

不同麻醉方式下腹腔镜胆囊切除病人血浆肾素与血管紧张素浓度的变化

观察硬膜外阻滞与全麻下腹腔镜胆囊切除术（ＬＣ）时病人围手术期血浆肾素活性（ＰＲＡ）与血管紧张素Ⅱ（ＡⅡ）的浓度变化，并与开腹胆囊切除术（ＯＣ）比较，结果发现两种麻醉下行ＬＣ时ＰＲＡ与血浆ＡⅡ浓度均明显高于ＯＣ组，而以硬膜外阻滞者增高更为显著。提示不同麻醉方式下行ＬＣ时对人体应激系统和生理代谢的影响不尽相同。     

不同麻醉方式下腹腔镜胆囊切除病人血浆肾素与血管紧张素…

观察硬膜外阻滞与全麻下腹腔镜胆囊切除术（ＬＣ）时病人围手术期血浆肾素活性（ＰＲＡ）与血管紧张素Ⅱ（ＡⅡ）的浓度变化，并与开腹胆囊切除（ＯＣ）比较，结果发现两种麻醉下行ＬＣ时ＰＲＡ与血浆ＡⅡ浓度均明显高于ＯＣ组，而以硬膜外阻滞者增高更为显著，提示不同麻醉方式下行ＬＣ时对人体应激系统和生理代谢的影响不尽相同。     

硬膜外麻醉下子宫肌瘤切除术患者血浆ANP和RAAS′的调控

研究了１５例子宫肌瘤切除患者应用０．７５％布比卡因硬膜外麻醉血浆心钠素（ＡＮＰ）和肾素活性（ＰＲＡ），血管紧张素Ⅱ（ＡⅡ）－醛固酮（ＡＬ）系统（ＲＡＡＳ）的变化及相互调控。结果表明，血浆ＡＮＰ水平在麻醉１０ｍｉｎ后各时点明显低于麻醉前（Ｐ〈０．０５），ＰＲＡ在麻醉１０ｍｉｎ后亦明显低于麻醉前（Ｐ〈０．０１），而ＡⅡ和ＡＬ无显著改变（Ｐ〉０．０５）。提示０．７５％布比卡因硬膜外麻醉行子宫切除术ＡＮＰ     

硬膜外阻滞对产程中肾素活性、血管紧张素Ⅱ、醛固酮和皮质醇水平的影响

目的：评价硬膜外阻滞对产程中肾素活性（ＰＲＡ）、血管紧张素Ⅱ（ＡⅡ）、醛固酮（ＡＬＤ）和皮质醇（ＣＯＲ）应激水平的影响。方法：麻醉组１２例初产妇接受硬膜外阻滞,另选１２例条件相似、未接受麻醉的初产妇与麻醉组产妇配对作对照组。用放免法测定两组产妇宫口开大３ｃｍ、宫口开全及胎儿娩出时血浆ＰＲＡ、ＡⅡ、ＡＬＤ和ＣＯＲ浓度。结果：麻醉组产妇ＰＲＡ、ＡⅡ和ＣＯＲ水平在宫口开全时明显降低（Ｐ〈０．０５）,而对照组四种激素水平在各时点均无明显变化（Ｐ〉０．０５）。结论：硬膜外阻滞可以抑制产妇产程中的应激激素分泌。     

硬膜外麻醉下子宫肌瘤切除术患者血浆ANP和RAAS的调控

研究了１５例子宫肌瘤切除术患者应用０．７５％布比卡因硬膜外麻醉血浆心钠素（ＡＮＰ）和肾素活性（ＰＲＡ）、血管紧张素Ⅱ（ＡⅡ）－醛固酮（ＡＬ）系统（ＲＡＡＳ）的变化及相互调控。结果表明，血浆ＡＮＰ水平在麻醉１０ｍｉｎ后各时点明显低于麻醉前（Ｐ＜０．０５），ＰＲＡ在麻醉１０ｍｉｎ后亦明显低于麻醉前（Ｐ＜０．０１），而ＡⅡ和ＡＬ无显著改变（Ｐ＞０．０５）。提示０．７５％布比卡因硬膜外麻醉行子宫切除术ＡＮＰ和ＲＡＡＳ的变化，在维持和调节有效循环血量及外周血管阻力中发挥着重要的作用。     

硬膜外阻滞配合全身麻醉行胃癌根治术对肾素—血管紧张素—醛…

硬膜外阻滞配合全身麻醉（ＥＡ＋ＧＯＥ）与单纯全身麻醉（ＧＯＥ）行胃癌根治术，两种麻醉方法对ＲＡＡＳ无明显影响（Ｐ〉０．０５），提示两种麻醉方法对内稳态无明显影响，均为本手术较理想的麻醉方法，ＥＡ＋ＧＯＥ法还具有抑制气管内插管对心血管的应激反应，减少吸入麻醉药用量，术后清醒快，苏醒期无痛，以及便于术后硬膜外止痛等优点。     

全麻复合硬膜外阻滞对血液动力学的影响

目的 观察浅全麻复合硬膜外阻滞对血液动力学的影响。方法 随机将２１例择期行腹腔镜胆囊切除手术病人分为全身麻醉组（ＧＡ组,１１例）和浅全麻复合硬膜外阻滞组（ＧＡ＋ＥＡ组,１０例）,采用Ｓｗａｎ－Ｇａｎｚ导管技术,分别监测ＧＡ组吸入０．６ＭＡＣ、１．０ＭＡＣ安氟醚与ＧＡ＋ＥＡ组吸入０．６ＭＡＣ安氟醚基础上硬膜外注入２％利多卡因７ｍｌ前后血液动力学的变化。结果 两组吸入０．６ＭＡＣ安氟醚,ＭＡＰ均显著下     

Comparative study of etomidate-alfentanil anesthesia with N2O/O2 or with air/O2

Systolic, diastolic blood pressures, heart rate, glycaemia, blood gases and clinical status were studied preinduction, 10' after anesthesia induction and intubation, 3', 30', 60' and 90' after surgical incision, when awake on the operating table and 60' after awakening in 20 hysterectomy patients. Etomidate (0.3 mg/kg + continuous infusion), alfentanil (75 micrograms/kg + increments of 15 micrograms/kg) anesthesia was used with a N2O/O2 mixture (10 pt) or with air/O2 (10 pt), both at a FIO2 = 0.33. This technique gave a smooth induction and recovery. Cardiovascular changes were moderate. The additional dose of alfentanil was 5.25 +/- 0.65 mg in the N2O/O2 group and 6.45 +/- 0.85 mg in the air/O2 group. The incidence of vomiting was 15%. Statistical analysis of both groups indicated no major difference between the two types of anesthesia, for the cardiovascular, acid base data and glycaemia. This technique is a simple and effective way of anesthetising patients, but from a clinical point of view the etomidate/alfentanil anesthesia combined with N2O/O2 gives better results than when combined with air/O2.     

Sufentanil-N2O2/O2 or halothane-N2O/O2 anesthesia in surgery of infants and children with congenital heart defects. Hemodynamics and plasma catecholamines

Sufentanil-nitrous oxide/oxygen anesthesia was compared to halothane-nitrous oxide/oxygen anesthesia in 44 infants and children undergoing cardiac surgery. Patients were randomly assigned to one of the two techniques studied, with 22 patients in each group. The mean weight was 8.3 (4.4-15.8) kg in the sufentanil (S) group and 11.7 (5.2-18) kg in the halothane (H) group. All patients were premedicated with IM atropine 0.01 mg/kg, morphine 0.2 mg/kg, and flunitrazepam 0.04 mg/kg. In the S group 1 micrograms/kg S was given intravenously for induction, followed by a cumulative dose of 4 micrograms/kg S until the beginning of surgery. In the H group anesthesia was induced with H 0.5-1.0 vol.% and for deepening of anesthesia increasing H concentrations of 0.5-1.0-1.5 vol.% were applied. Following intubation all patients were ventilated with nitrous oxide/oxygen (1:1). There were no significant differences between the two groups in systolic, diastolic and mean arterial blood pressures or in heart-rate response to induction and intubation. Peripheral arterial oxygen saturation increased significantly in cyanotic patients in both groups following induction. There were dose-dependent decreases in heart rate and small but significant decreases in mean and diastolic arterial pressure in the S group during deepening of anesthesia. There was a significantly greater decrease in systolic, diastolic and mean blood pressures during the same period in the H group whereas the reduction in heart rate was minimal. In addition, in 5 of 22 patients receiving H there were episodes of nodal rhythms with dramatic decreases in systemic arterial pressure and peripheral arterial oxygen saturation in cyanotic patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebrospinal fluid pressure during O2 encephalography and N2O inhalation.

Cerebrospinal fluid (CSF) pressure was studied in 8 patients and 5 dogs during pneumoencephalography (PEG) or ventriculography in which either O2 or N2O was used as the contrast gas prior to and during N2O inhalation. In 7 patients, the use of O2 as the contrast gas increased CSF pressure 8.7 torr (range 4 to 12 torr) following N2O inhalation. In 1 patient, when N2O was used as the contrast gas, CSF pressure did not change after N2O inhalation. These findings were confirmed in anesthetized animals ventilated at a constant PaCO2. The authors conclude that if N2O inhalation is required during PEG, maximum patient safety can be achieved if the contrast gas is also N2O.     

Comparison of induction, maintenance, and recovery characteristics of sevoflurane-N2O and propofol-sevoflurane-N2O with propofol-isoflurane-N2O anesthesia.

Induction of, maintenance of, and recovery from sevoflurane anesthesia were compared with propofol and isoflurane anesthesia when administered with nitrous oxide to patients undergoing gynecologic surgery. Seventy-five healthy (ASA I or II), consenting patients were randomly assigned to receive either (I) propofol for induction of anesthesia and isoflurane-nitrous oxide for maintenance (control), (II) propofol for induction and sevoflurane-nitrous oxide for maintenance, or (III) sevoflurane-nitrous oxide for induction and maintenance of anesthesia. Inhaled induction of anesthesia with sevoflurane-nitrous oxide was rapid (109 +/- 25 s to loss of consciousness) and without any untoward hemodynamic changes or episodes of coughing and laryngospasm. Mean arterial blood pressure after induction of anesthesia with propofol (71 +/- 11, 73 +/- 12 mm Hg for groups I and II, respectively) was lower than when sevoflurane (80 +/- 14 mm Hg) was used. The emergence time after discontinuation of isoflurane-nitrous oxide (6.7 +/- 2.2 min) was significantly longer than after propofol-sevoflurane-nitrous oxide or sevoflurane-nitrous oxide alone (4.1 +/- 2.2 and 4.0 +/- 2.0 min for groups II and III, respectively). However, later recovery events did not differ between groups. Serum fluoride levels increased after administration of sevoflurane but not isoflurane. The levels of fluoride ions correlated with the degree of exposure to sevoflurane in MAC-hours. In conclusion, induction of anesthesia with either propofol or sevoflurane-nitrous oxide was rapid and without significant side effects. Emergence and early recovery after maintenance of anesthesia with sevoflurane-nitrous oxide was significantly faster than that after an isoflurane-nitrous oxide combination.     

A comparison of cerebral ischemic flow thresholds during halothane/N2O and isoflurane/N2O anesthesia in rats.

Isoflurane/N2O anesthesia has been reported to reduce the cerebral blood flow (CBF) threshold at which electroencephalographic changes occur in humans during carotid occlusion (when compared to halothane/N2O). To further evaluate this observation, normocapnic, normothermic rats were anesthetized with 0.75 MAC isoflurane or halothane in combination with 60% N2O. The electrocorticogram (ECoG) and the cortical DC potential were recorded using glass microelectrodes. Both carotid arteries were occluded, and mean arterial pressure (MAP) was reduced over 3-5 min (by phlebotomy) to predetermined values between 30 and 75 mmHg. This MAP was maintained for 10 min, and CBF was then measured in cortical gray matter using [3H]-nicotine. Flows were then correlated with ECoG changes and with the presence or absence of cortical depolarization (which reflects the loss of transmembrane ion homeostasis). In other rats, the cortical cerebral metabolic rate for glucose (CMRglu) was determined autoradiographically using [14C]-deoxyglucose. Finally, the time to depolarization was determined in rats killed with KCl and in rats subjected to hypotension (MAP = 30-35 mmHg) followed by abrupt bilateral carotid occlusion. The distributions of CBF values in the anesthetic groups were essentially identical. The incidence of either major ECoG changes or isoelectricity did not differ between anesthetics. The CBF associated with major ECoG changes (excluding isoelectricity) were 35 +/- 12 and 39 +/- 18 ml.100 g-1.min-1 in the halothane/N2O and isoflurane/N2O groups respectively (mean +/- SD, difference not significant [NS]). Isoelectricity was seen at 7 +/- 4 ml.100 g-1.min-1 (median = 6.5) with halothane/N2O and 17 +/- 19 ml.100 g-1.min-1 (median = 11) with isoflurane/N2O (again, NS). The incidence of sustained depolarization did not differ between anesthetics (9 of 25 for halothane/N2O, 8 of 24 with isoflurane/N2O). CBF associated with sustained depolarization was 13 +/- 12 ml.100 g-1.min-1 (median = 10) with halothane/N2O, compared with 9 +/- 6 ml.100 g-1.min-1 (median = 9) for isoflurane/N2O (NS). In rats subjected to cardiac arrest, the time to depolarization was longer with isoflurane/N2O (102 +/- 19 s vs. 77 +/- 7 s). In rats subjected to carotid occlusion at a MAP = 30-35 mmHg, the time to depolarization was again longer with isoflurane/N2O (210 +/- 78 s vs. 122 +/- 44 s). Cortical CMRglu was lower with isoflurane/N2O (25 +/- 5 mumol.100 g-1.min-1) than with halothane (43 +/- 13 mumol.100 g-1.min-1, P = 0.03). The results indicate that isoflurane/N2O anesthesia delays the onset of ischemic cell depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)