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。     

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     

氟烷、安氟醚、七氟醚肝毒性与TXB_2、6－keto－PGF（1α）含量变化（氟烷性肝炎的研究Ⅲ）

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％Ｏ＿２／８６％Ｎ＿２；Ｅ，１４％Ｏ＿２／８６％Ｎ＿２／１．２ＭＡＣ安氟醚；Ｓ，１４％Ｏ＿２／８６％Ｎ＿２／１．２ＭＡＣ七氟醚；Ｈ，１４％Ｏ＿２／８６％Ｎ＿２／１．２ＭＡＣ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小叶中心性坏死及空泡变性。Ｈ组肝匀浆及血浆中ＴＸＢ＿２含量显著高于其它各组。６－ｋｅｔｏ－ＰＧＦ１ａ各组间均无显著差异。提示氟烷性肝炎与ＴＸＡ＿２／ＰＧＩ＿２平衡失调有一定的关系。     

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     

高渗氯化钠羟乙基淀粉40注射液高容量血液稀释对大鼠肝脏缺血再灌注损伤的影响

目的 探讨高渗氯化钠羟乙基淀粉40注射液高容量血液稀释对大鼠肝脏缺血再灌注损伤的影响.方法 雄性Wistar大鼠30只,体重300～350 g,随机分为3组(n=10):假手术组(S组)、缺血再灌注组(IR组)和高容量血液稀释组(HH组).S组仅开腹,不阻断血管;IR组阻断肝门静脉和左肝动脉30 min,再灌注2 h;HH组30 min内经尾静脉输注高渗氯化钠羟乙基淀粉40注射液10 ml/kg进行高容量血液稀释,输注完毕后15 min,行肝脏缺血再灌注.再灌注2 h时,下腔静脉取血样,测定血清谷丙转氨酶(ALT)和谷草转氨酶(AST)的活性;取左肝叶组织,光镜下观察病理学结果,采用比色法测定丙二醛(MDA)含量,采用黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性.结果 与S组比较,IR组和HH组血清ALT和AST的活性、肝组织MDA含量升高,肝组织SOD活性降低(P<0.01),肝组织病理学损伤明显;与IR组比较,HH组血清ALT和AST的活性、肝组织MDA含量降低,肝组织SOD活性升高(P<0.01),肝组织病理学损伤减轻.结论 高渗氯化钠羟乙基淀粉40注射液高容量血液稀释可减轻大鼠肝脏缺血再灌注损伤,可能与氧自由基生成减少有关.     

Differential effects of halothane and isoflurane on lumbar dorsal horn neuronal windup and excitability

Background. Windup of spinal nociceptive neurones may underlietemporal summation of pain, influencing the minimum alveolarconcentration (MAC) of anaesthetics required to prevent movementto supramaximal stimuli. We hypothesized that halothane andisoflurane would differentially affect windup of dorsal hornneurones. Methods. We recorded 18 nociceptive dorsal horn neurones exhibitingwindup to 1 Hz electrical hindpaw stimuli in rats. Effects of0.8 and 1.2 MAC isoflurane and halothane were recorded in thesame neurones (counterbalanced, crossover design). Windup wascalculated as the total number of C-fibre (100–400 mslatency) plus afterdischarge (400–1000 ms latency) spikes/20stimuli (area under curve, AUC) or absolute windup (C-fibreplus afterdischarge–20xinitial response). Results. Increasing isoflurane from 0.8 to1.2 MAC did not affectAUC, but increased absolute windup from 429 (62) to 618 (84)impulses/20 stimuli (P<0.05) and depressed the initial C-fibreresponse from 14 (3) to 8 (2) impulses (P<0.05). Increasinghalothane from 0.8 to1.2 MAC depressed AUC from 690 (79) to537 (65) impulses/20 stimuli (P<0.05) and the initial responsefrom 18 (2) to 13 (2) impulses (P<0.05), but absolute windupwas not affected. Absolute windup was 117% greater during 1.2MAC isoflurane compared with 1.2 MAC halothane. Conclusions. Windup was significantly greater under isofluranethan halothane anaesthesia at 1.2 MAC, whereas the initial C-fibreresponse was suppressed more by isoflurane. These findings suggestthat these two anaesthetics have mechanistically distinct effectson neuronal windup and excitability.     

Hemodynamic and organ blood flow responses to halothane and sevoflurane anesthesia during spontaneous ventilation.

This study compared systemic hemodynamic and organ blood flow responses to equipotent concentrations of halothane and sevoflurane during spontaneous ventilation in the rat. The MAC values for halothane and sevoflurane were determined. Cardiac output and organ blood flows were measured using radiolabeled microspheres. Measurements were obtained in awake rats (control values) and at 1.0 MAC halothane or sevoflurane. The MAC values (mean +/- SEM) for halothane and sevoflurane were 1.10% +/- 0.05% and 2.40% +/- 0.05%, respectively. The PaCO2 increased to a similar extent in both groups compared with control values. During halothane anesthesia, heart rate decreased by 12% (P < 0.01), cardiac index by 26% (P < 0.01), and mean arterial blood pressure by 18% (P < 0.01) compared with control values. Stroke volume index and systemic vascular resistance did not change. During sevoflurane anesthesia, hemodynamic variables remained unchanged compared with control values. Coronary blood flow decreased by 21% (P < 0.01) and renal blood flow by 18% (P < 0.01) at 1.0 MAC halothane, whereas both remained unchanged at 1.0 MAC sevoflurane. Cerebral blood flow increased to a greater extent with halothane (63%; P < 0.01) than with sevoflurane (35%; P < 0.05). During halothane anesthesia, hepatic arterial blood flow increased by 48% (P < 0.01), whereas portal tributary blood flow decreased by 28% (P < 0.01). During sevoflurane anesthesia, hepatic arterial blood flow increased by 70% (P < 0.01) without a concomitant reduction in portal tributary blood flow. Total liver blood flow decreased only with halothane (16%; P < 0.05).(ABSTRACT TRUNCATED AT 250 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.     

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.     

EFFECTS OF TWO DIFFERING HALOTHANE CONCENTRATIONS ON THE METABOLIC AND ENDOCRINE RESPONSES TO SURGERY

The effects of two differing concentrations of halothane, 2.1MAC or 1.2 MAC, on the metabolic and endocrine responses toabdominal hysterectomy were investigated. The changes in bloodglucose and lactate values, and plasma glycerol, cortisol, insulinand catecholamine concentrations were similar in both groups.We conclude that high concentrations of halothane do not suppressthe responses to pelvic surgery, and that accurate quantificationof the dose of halothane, within the concentration range of1.2 to 2.1 MAC, is not essential in studies of metabolic changesassociated with surgery.     

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)     

Nitrous oxide does not hinder the repair of halothane-induced hepatic injury in the rat

Nitrous oxide administration may limit DNA synthesis by inactivating methionine synthetase, and may thus hamper the repair of an injured organ such as the liver. To test this possibility, we pretreated rats with phenobarbital and exposed them to 0.3 MAC halothane in 9% oxygen for 46 min, followed immediately and again 24 hr later by 70% nitrous oxide (0.25 MAC) at an FIO2 of 0.30 for 2 hr. The results from this group were compared with an anesthetic control group in which 0.35% isoflurane (0.25 MAC) was substituted for the nitrous oxide. Additional groups were given a third exposure to nitrous oxide or isoflurane 48 hr after the halothane exposure. All rats were killed 24 hr after their last anesthetic exposure. A second (nonanesthetic) control group of phenobarbital-pretreated rats received 0.3 MAC halothane in 9% oxygen for 46 min and no anesthetic thereafter. They were killed 24, 48, or 72 hr later. Histologic changes in the livers of rats did not differ among the groups given nitrous oxide, isoflurane, or no additional anesthetic after exposure to halothane alone. Thus neither nitrous oxide nor isoflurane appears to hinder the repair of hepatic injury produced by halothane in the hypoxic rat model.