氟烷七氟醚对酶诱导缺氧大鼠脂过氧化反应的影响（氟烷性肝炎的…

雄性ＳＤ大鼠饮用含苯巴比妥（１ｍｇ／ｍｌ）的饮水一周后，随机分为６组，每组６例：ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％Ｏ２／８６％Ｎ２；ＮＨ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ氟烷；ＮＳ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ七氟醚；ＨＳ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ七氟醚。吸入时间１ｈ，２４ｈ后测定血浆及肝匀浆中ＭＤＡ、ＳＯＤ、游离巯基     

氟烷,安氟醚,七氟醚肝毒性与TXB2,6—keto—PGF1α含量变化（氟…

雄性ＳＤ大鼠饮用含苯巴比妥钠（１ｍｇ／ｍｌ）的饮水１周后，随机分为四组，每组８例，分别吸入：Ｃ，１４％Ｏ２／８６％Ｎ２；Ｅ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ安氟醚；Ｓ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ七氟醚；Ｈ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ氟烷１ｈ。２４ｈ后发现Ｈ组血浆ＡＬＴ活性显著高于其它各组，并有明显的小叶中心性肝细胞坏死及汇管区炎细胞浸润，血窦重度充血。Ｅ组可见部分肝小叶内有     

氟烷七氟醚对酶诱导缺氧大鼠血浆氨基酸谱的影响（氟烷性肝炎…

雄性ＳＤ大鼠饮用含苯巴比妥（１ｍｇ／ｍｌ）的饮水一周后，随机分为６组，每组６例：ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％Ｏ２／８６％Ｎ２；ＮＳ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ七氟醚；ＨＳ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ七氟醚；ＮＨ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／８６％２／１．２ＭＡＣ氟烷。吸入时间１ｈ、２４ｈ后用高效液相色谱法测定血浆中１１种游离氨基酸的     

氟烷七氟醚对酶诱导缺氧大鼠血浆氨基酸谱的影响（氟烷性肝炎的研究Ⅱ）

雄性ＳＤ大鼠饮用含苯巴比妥（１ｍｇ／ｍｌ）的饮水一周后，随机分为６组，每组６例：ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％Ｏ２／８６％Ｎ２；ＮＳ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ七氟醚；ＨＳ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ七氟醚；ＮＨ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ氟烷。吸入时间１ｈ、２４ｈ后用高效液相色谱法测定血浆中１１种游离氨基酸的含量。结果ＮＨ与ＨＨ组酪、精、丝、甘、丙、苏、谷氨酰胺含量升高，而支链氨基酸无明显变化。提示氟烷性肝炎的氨基酸谱的变化类似于急性暴发性肝衰竭。     

氟烷七氟醚对酶诱导缺氧大鼠脂过氧化反应的影响（氟烷性肝炎的研究Ⅰ）

雄性ＳＤ大鼠饮用含苯巴比妥（１ｍｇ／ｍｌ）的饮水一周后，随机分为６组，每组６例：ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％０；１８６％Ｎｅ；ＮＨ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ氟烷；ＮＳ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ七氟醚；ＨＳ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ七氟醚。吸入时间１ｈ，２４ｈ后测定血浆及肝匀浆中ＭＤＡ、ＳＯＤ、游离琉基的含量。结果ＨＨ、ＮＨ组肝匀浆及血浆中ＭＤＡ、ＳＯＤ的含量均高于其它各组（Ｐ＜０．０１，Ｐ＜０．０５），余各组间均无显著差异（Ｐ＞０．０５）。ＮＨ、ＨＨ组血浆及肝匀浆中游离琉基的含量显著低于其它各组（Ｐ＜０．０１）。提示氟烷所致的肝脂过氧化反应增强的作用可能与其肝毒性有关，而七氟醚无促进肝脏脂过氧化反应增强的作用。     

大鼠氟烷性肝炎血、肝中微量元素的测定及其临床意义─—与七氟醚麻醉比较（氟烷性肝炎的研究Ⅳ）

雄性ＳＤ大鼠饮用含苯巴比妥钠（１ｍｇ／ｍｌ）的饮水１周后，随机分为四组，每组８例：ＮＣ，２１％Ｏ＿２／７９％Ｎ＿２；ＨＣ，１４％Ｏ＿２／８６％Ｎ＿２；ＨＳ，１４％Ｏ＿２／８６％Ｎ＿２／１．２ＭＡＣ七氟醚；ＨＨ，１４％Ｏ＿２／８６％Ｎ＿２／１．２ＭＡＣ氟烷。吸入时间为１ｈ。２４ｈ后用原子吸收分光光度法测定血浆及肝匀浆中锌、铜、铁、钙的含量。结果ＨＨ组肝匀浆中铜、锌的含量显著低于对照组（Ｐ＜０．０１），钙离子显著高于对照组（Ｐ＜０．０１），ＨＨ组血浆中铁、铜、锌含量均显著高于对照组（Ｐ＜０．０５）。提示氟烷肝损害过程中铜、铁、锌由损伤肝组织向血浆中释放，这种释放程度与肝损害程度相平行。而且体内微量元素平衡的改变又会加重氟烷性肝损害的发生与发展。     

氟烷、七氟醚大鼠肝毒性的病理学研究

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠饮用含苯巴比妥（１ｍｇ／ｍｌ）的饮水一周后，随机分为６组，每组８例。ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％Ｏ２／８６％Ｎ２；ＮＨ，２１％Ｏ２／７９／Ｎ２／１．２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／８６％Ｎ２／１． ２ＭＡＣ氟烷；ＮＳ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ七氟醚；ＨＳ，１４％Ｏ２。／８６％Ｎ２／１．２ＭＡＣ七氟醚。吸人时间为川、时，２４小时后处死动物。应用体视学方法及电子计算机图象分析，对肝脏病理进行定量研究。缺氧情况下吸入氟烷几乎所有的大鼠均发生广泛的肝脏小叶中心性肝细胞变性坏死，并伴血谷丙转氨酶的升高。而同作情况下吸入七氟醚及对照组均无明显的肝毒性发生。缺氧可导致肝线粒体肿胀。结果提示吸入麻醉药七氟醚就肝毒性而言明显优于氟烷。     

氟烷,七氟醚大鼠肝素性的病理学研究

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠饮用含苯巴比妥（１ｍｌ／ｍｌ）的饮水一周后，随机分为６组，每组８例。ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％Ｏ２／８６％Ｎ２；ＮＨ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ氟烷；ＮＳ，２１％Ｏ２／７９％Ｎ２／１．２ＭＡＣ七氟烷；ＨＳ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ七氟醚。吸入时间为１小时，２４小时后处死动物。应     

氟烷,七氟醚对酶诱导,缺氧大鼠肝细胞钙平衡的影响：钙离子…

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ（ＳＤ）大鼠饮用含苯巴妥（１ｍｇ／ｍｌ）的水一周后，随机分为６组，分别吸入下列气体１小时：ＮＣ，２１％Ｏ２／７９％Ｎ；ＨＣ，１４％Ｏ２／８６％Ｎ；ＮＳ，２１％Ｏ２／Ｎ２／１。２ＭＡＣ七氟醚；ＨＳ，１４％Ｏ２／Ｎ２／１。２ＭＡＣ七氟醚；ＮＨ，２１％Ｏ２／Ｎ２／１。２ＭＡＣ氟烷；ＨＨ，１４％Ｏ２／Ｎ２／１。２ＭＡＣ氟烷。２４小时后用草酸钾－焦锑酸钾沉淀法对肝脏钙离子进行     

大鼠氟烷性肝炎血,肝中微量元素的测定及其临床意义──与七…

雄性ＳＤ大鼠饮用含苯巴比妥钠（１ｍｇ／ｍｌ）的饮水１周后，随机分为四组，每组８例：ＮＣ，２１％Ｏ２／７９％Ｎ２；ＨＣ，１４％Ｏ２／８６％Ｎ２；ＨＳ，１４％Ｏ２／８６％Ｎ２／１．２ＭＡＣ氟烷。吸入时间为１ｈ。２４ｈ后用原子吸收分光光度法测定血浆及肝匀浆中锌，铜，铁，钙的含量。结果ＨＨ组肝匀浆中铜，锌的含量显著低于对照组（Ｐ＜０．０１），钙离子显著高于对照组（Ｐ＜０．０１），ＨＨ组血浆中铁，铜，锌含量     

Comparison of haemodynamic changes induced by sevoflurane and halothane in paediatric patients

The purpose of this study is to investigate the haemodynamic effects of 1 MAC and 2 MAC of sevoflurane in children in comparison with halothane. Thirty-eight children (aged from one to six years, average age; 3.6± 0.2 yr) were randomly assigned to four groups, depending on the dose and agent (1 and 2 MAC of sevoflurance: SI and S2; 1 and 2 MAC of halothane: H1 and H2, respectively). After collecting control data during 0.2 MAC of either anaesthetic, end-expired anaesthetics were kept at 1 MAC or 2 MAC for 15 min. Mean blood pressure (mBP) and stroke volume index (SV1), measured by impedance cardiometry, decreased in all groups without differences between groups. Heart rate (HR) increased in groups S1, S2 and H2 but not in group H1. The HR in S2 was higher than that in H2. The cardiac index (CI), a product of SVI and HR, tended to decrease but not significantly in all groups. These results suggested that the haemodynamic depressant effects of sevoflurane in children were similar to those of equipotent halothane concentration except for HR.     

吸入不同浓度氧化亚氮对全麻患者双腔喉罩囊内压的影响

目的 评价吸入不同浓度氧化亚氮对全麻患者双腔喉罩囊内压的影响.方法 择期全麻患者48例,ASAⅠ或Ⅱ级,年龄25～64岁,随机分为4组(n=12):C组、N1组、N2组及N3组.根据患者身高和体重选择合适型号的双腔喉罩.依次静脉注射异丙酚、瑞芬太尼、利多卡因及维库溴铵行麻醉诱导,喉罩置入成功后,套囊内注入空气,调节囊内压使其达加cm H2O(基础值),连接麻醉机行机械通气,C组、N1组、N2组及N3组分别吸入100%O2、65%O2+35%N2O、50%O2+50%N2O及35%O2+65%N2O,于吸入15、30、45、60、75、90 min时(T1-6)测定喉罩囊内压.结果 与C组比较,N1-3组T1-6时囊内压升高;与N1组比较,N2,3组T1-6时囊内压升高;与N2组比较,N3组,T1-6时囊内压升高(P<0.05).与T0时比较,C组T2-6时囊内压降低,N1组T2-6时囊内压升高,N2,3组T1-6时囊内压升高(P<0.05).N1-3组囊内压与吸入时间呈正相关(相关系数分别为0.968、0.987、0.973,P<0.05).结论 吸入N2O可使喉罩囊内压升高,呈浓度及时间依赖性.     

Microcirculatory response to halothane and isoflurane anesthesia.

Microcirculatory hemodynamics are often used to monitor tissue and organ survival. This study investigated the effect of halothane and isoflurane anesthesia on peripheral microcirculation using the cremaster muscle during intravital microscopy. Twenty-three Sprague-Dawley rats were studied in four groups. Two groups served as controls and did not undergo flap isolation but did receive halothane (N = 6) or isoflurane (N = 5). After induction with a single dose of intraperitoneal pentobarbital (40 mg per kilogram), rats were ventilated with either 2 minimum alveolar concentration (MAC) halothane or 2 MAC isoflurane. Esophageal temperature, electrocardiography, central venous pressure, mean arterial pressure, and blood gases were measured over 4 hours. In groups receiving surgery with either halothane (N = 6) or isoflurane (N = 6), the cremaster muscle was isolated on the neurovascular pedicle. Microcirculatory responses to both halothane and isoflurane anesthesia were evaluated by measuring red blood cell (RBC) velocity, vascular diameters in arterioles (A1, A2-1, A2-2, and A3) and the main venule (V1), functional capillary perfusion, and leukocytic endothelial interactions in postcapillary venules (rolling, adherent, and transmigrating leukocytes). Hemodynamic variables were compared among all four groups, and microcirculatory variables were compared between the two surgical groups. During isoflurane anesthesia in animals with flaps, significantly higher (p < 0.05) RBC velocities were recorded in arterioles A1 (24.4%), A2-2 (28.2%), and A3 (17.4%). Capillary perfusion was significantly higher in animals with flaps and halothane anesthesia (17.8%; p < 0.05). The number of rolling leukocytes (39.4%) was significantly higher during isoflurane anesthesia in animals with flaps (p < 0.05). Better flow hemodynamics in the peripheral microcirculation were seen during halothane anesthesia, and were confirmed by greater functional capillary perfusion and fewer activated leukocytes. In the isoflurane group, RBC velocity alone cannot serve as an indicator of microcirculatory function.     

Additive contribution of nitrous oxide to halothane MAC in infants and children

Fifty-one infants and small children (14.7 +/- 7.2 mo) were studied to determine the MAC of halothane in O2 (n = 11) and in the presence of three different nitrous oxide (N2O) concentrations (25% [n = 13], 50% [n = 13], and 75% [n = 14]). In the three N2O groups, after randomly assigning patients to an N2O group, anesthesia was induced with halothane and N2O using a pediatric circle system. After endotracheal intubation, halothane and N2O end-expired concentrations were adjusted to predetermined concentrations. The initial halothane concentrations in each group were based on the assumption that each percent N2O reduced halothane concentrations by 0.01 vol % (assumed halothane MAC = 1.0 vol %). Based on the response of the preceding subject in each group, halothane concentrations were increased or decreased depending on whether the response was to move or not to move, respectively, in response to the surgical incision. The mean duration of constant end-tidal concentrations before skin incision was 10 min. End-tidal gases were sampled and measured from a separate distal sampling port of an endotracheal tube during controlled ventilation (Perkin-Elmer Mass Spectrometer). The MAC value for halothane in O2 was 0.94 +/- 0.08 vol % (mean +/- SD). The MAC values of halothane in the presence of 25%, 50%, and 75% N2O were 0.78 +/- 0.12 vol %, 0.44 +/- 0.10 vol %, and 0.29 +/- 0.06 vol %, respectively. All concentrations of N2O significantly reduced the MAC of halothane. A regression analysis through all four data points yielded a linear relationship (r2 = 0.87) with a predicted MAC for N2O of 105 vol %. Unlike halothane and isoflurane, the predicted MAC of N2O in infants and children is similar to that reported by others in adults. Similar to the results of clinical studies in adults, the contribution of N2O to halothane MAC in children is additive.     

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)     

The effect of nitrous oxide on cortical cerebral blood flow during anesthesia with halothane and isoflurane, with and without morphine, in the rabbit

The effect of nitrous oxide on cortical cerebral blood flow (CBF) was examined during a varying background anesthetic state in the New Zealand White rabbit. Seventy percent nitrous oxide resulted in significant and similar increases in CBF during anesthesia with both 0.5 MAC of halothane (44 +/- 14 to 63 +/- 17 ml.100 g-1.min-1) (mean +/- SD) and anesthesia with isoflurane (34 +/- 9 to 41 +/- 11 ml.100 g-1.min-1). During anesthesia with 1.0 MAC halothane or isoflurane, N2O also increased CBF, but the increments (halothane, 73 +/- 34 to 111 +/- 54 ml.100 g-1 min-1; isoflurane 34 +/- 13 to 69 +/- 34 ml.100 g-1.min-1) were significantly greater than those observed at 0.5 MAC. When 0.5 MAC halothane or isoflurane was supplemented with morphine (10 mg/kg followed by an infusion of 2 mg.kg-1.min-1), the CBF effect of N2O was not significantly different from that observed with 0.5 MAC alone. It was concluded that, in the rabbit, the effects of N2O on cortical CBF vary with the background anesthetic state and that the increase in CBF caused by N2O becomes greater as the end-tidal concentration of halothane or isoflurane increases from 0.5 to 1.0 MAC. Morphine, when added to 0.5 MAC of halothane or isoflurane, does not alter the effect of 70% N2O on cortical CBF.     

Neurologic outcome in rats following incomplete cerebral ischemia during halothane, isoflurane, or N2O

Using rats in which incomplete cerebral ischemia was induced, the authors evaluated the effects of halothane (H) and isoflurane (I) on neurologic outcome compared to nitrous oxide (N2O) controls. Incomplete cerebral ischemia was produced by right carotid artery occlusion combined with hemorrhagic hypotension. Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke). Two levels of cerebral ischemia were tested. At moderate ischemia with hypotension of 30 mmHg, an FIO2 of 0.3, and ischemic periods of 30 or 45 min, N2O produced a deficit of 4.7-5.0 and a mortality rate of 90-100%. In contrast, halothane (1 MAC) and isoflurane (1 MAC) resulted in similar deficit scores (H = 1.1-1.8, I = 1.4-1.6) and mortality rates (H = 17-30%, I = 17-20%). Cerebral blood flow (CBF) measured with radioactive microspheres showed a 60-65% decrease in the ischemic hemisphere at this level of hypotension. With severe ischemia with hypotension = 25 mmHg, FIO2 = 0.2, and a 30-min period of ischemia, deficit scores increased to 3.0 and 3.9 with 1 MAC halothane and 1 MAC isoflurane, respectively. Mortality rates also increased to 40% with halothane and 70% with isoflurane. Increasing the concentration of halothane or isoflurane to 2 MAC did not significantly improve outcome. Brain histology demonstrated extensive neuronal damage in striatal, hippocampal, and neocortical regions of N2O control treated rats, and less damage with little difference between H- and I-treated rats at each level of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

氟烷肝毒性相关基因的鉴定

目的 鉴定氟烷肝毒性相关基因.方法 拟行肝血管瘤切除术的女性病人8例,随机分成2组(n=4):氧化亚氮复合麻醉组(C组)和氟烷复合麻醉组(H组).两组均于T8,9间隙行硬膜外穿刺,头向置管3.5 cm.C组麻醉诱导:吸入70%N2O,静脉注射琥珀酰胆碱2mg/kg后气管插管;麻醉维持:吸入70%N2O,硬膜外间断注射0.25%地卡因5 ml.H组麻醉诱导:吸入氟烷1.5 MAC及70%N2O后气管插管;麻醉维持:硬膜外间断注射0.125%地卡因5 ml,吸入氟烷1.5 MAC及70%N2O.两组术中静脉输注琥珀酰胆碱20～40μg·kg-1·min-1.切除血管瘤后,取血管瘤旁正常肝组织,抽提mRNA,并逆转录成cDNA,同时分别以Cy5-dUTP(H组)及Cy3-dUTP(C组)标记;将荧光标记的cDNA与基因芯片混合并杂交,然后扫描芯片,分析Cy5和Cy3荧光信号强度和比值,从组间及组内差异表达的基因中筛选氟烷肝毒性相关基因.结果 与C组比较,H组8 192条基因中差异表达的基因31条,主要包括肝脏代谢类基因、信号转导相关基因及应激相关基因等,其中13条高表达,18条低表达;与线粒体呼吸有关的甘油醛-3-磷酸脱氢酶基因及NADH脱氢酶基因低表达,Na+ -K+ -ATP酶基因低表达,而热休克蛋白70基因和血红素加氧酶-1基因高表达.结论 氟烷肝毒性相关基因包括肝脏代谢类基因、信号转导相关基因及应激相关基因.