异氟醚预处理延迟相对兔缺血再灌注心肌Bcl-2蛋白表达及IL-10水平的影响

目的:探讨异氟醚预处理延迟相对缺血再灌注心肌的保护作用及其机制。方法:30只健康新西兰雄性大白兔随机分成3组:假手术组(C组)、缺血再灌注组(I/R组)、2.0%异氟醚预处理延迟相组(S组),每组10只。C组仅开胸160min,I/R组行左冠脉阻断40min,再灌注120min,S组吸入2.0%异氟醚2小时,24小时后处理同I/R组。各组分别于左冠脉阻断前20min(T1)、左冠脉阻断20min(T2)、左冠脉阻断40min(T3)、再灌注1小时h(T4)、再灌注2小时(T5)5个时点抽血测血清IL-10水平。再灌注结束后免疫印迹法测心肌Bcl-2表达水平,用伊文思蓝和TTC染色测心肌梗死面积。结果:与I/R组比,S组IL-10水平增高(P<0.05),Bcl-2表达增高(P<0.05),心肌梗死面积减少(P<0.05)。结论:异氟醚预处理延迟相通过上调心肌Bcl-2表达和IL-10生成来减轻缺血再灌注损伤发挥保护作用。     

Stress hormone changes in general anesthesia of long duration: isoflurane-nitrous oxide vs sevoflurane-nitrous oxide anesthesia

STUDY OBJECTIVE: There are few comparative studies of stress hormone changes during general anesthesia with long duration between isoflurane-nitrous oxide and sevoflurane-nitrous oxide anesthesia. We investigated perioperative changes of stress hormone in these two anesthetic methods with duration of more than 10 hours. DESIGN: Prospective study. SETTING: Operating room and high care unit of a university hospital. PATIENTS: Twenty patients with ASA physical status I or II for surgery for laryngeal or pharyngeal cancer with expected duration of more than 10 hours. INTERVENTIONS: Anesthesia was induced with midazolam, thiopental, and vecuronium and was maintained with sevoflurane (sevoflurane group) or isoflurane (isoflurane group) with nitrous oxide 4 L/min in oxygen 2 L/min. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of epinephrine, norepinephrine, cortisol, adrenocorticotropic hormone, and anti-diuretic hormone (ADH); serum concentrations of glucagon and insulin; and blood glucose concentration were measured before inhalation of anesthetics, after 5 and 10 hours, and at 1, 6, and 12 hours after the end of inhalation. Epinephrine and norepinephrine concentrations increased continuously during and after surgery in the isoflurane group whereas it increased only after surgery in the sevoflurane group. Both concentrations were higher in the isoflurane group during anesthesia. Cortisol increased continuously whereas adrenocorticotropic hormone increased only during surgery. Anti-diuretic hormone increased with its peak during surgery and the isoflurane group had significantly higher values than the sevoflurane group. Glucose increased both during and after surgery, insulin increased only after surgery, and glucagon decreased during surgery in both groups. CONCLUSIONS: In inhalation anesthesia with the duration of more than 10 hours, isoflurane-nitrous oxide and sevoflurane-nitrous oxide had the same effects on stress hormone changes except for epinephrine, norepinephrine, and ADH. Epinephrine, norepinephrine, and ADH concentrations were higher in isoflurane-nitrous oxide anesthesia.     

Diminished effect of inhibition of nitric oxide synthase on regional cerebral vascular resistance in conscious and in isoflurane anesthetized rats during hemorrhage

Effects of a nitric oxide (NO) synthase inhibitor on regional cerebral vascular resistance (rCVR) and regional cerebral blood flow (rCBF) were studied during a severe hemorrhage in conscious and in isoflurane anesthetized groups of rats. Half of each group was infused with N^G-nitro-l-arginine-methyl ester (l-NAME), a NO synthase inhibitor, at a rate of 2 mg·kg⁻¹·min⁻¹ for 30 min. Half of the lNAME infused and half of the normal saline infused rats were bled to reduce the mean arterial blood pressure (MAP) to 44–49 mmHg. rCBF was measured using [¹⁴C]iodoantipyrine. rCVR was calculated as the ratio of MAP to rCBF. In the conscious non-hemorrhagic rats, l-NAME markedly increased rCVR in all the brain regions that we studied. In the conscious rats without l-NAME treatment, hemorrhage decreased rCVR in most of the brain regions. With l-NAME treatment in this group, hemorrhage increased rCVR only in the rostral part of the brain. Isoflurane decreased rCVR in most of the brain regions except the cortical area. l-NAME markedly increased rCVR in all the brain regions that we studied in the isoflurane anesthetized rats. In the isoflurane anesthetized rats, hemorrhage did not reduce rCVR in any of the brain regions. In the isoflurane anesthetized hemorrhagic rats, l-NAME did not significantly affect rCVR in any of the brain regions that we studied. We found that l-NAME increased rCVR to a greater extent in the non-hemorrhagic rats than in the hemorrhagic rats in both the conscious and in the isoflurane anesthetized rats. The effect of l-NAME appeared to be similar both under conscious and under isoflurane anesthetized conditions.     

Interactions of nicardipine to inhalation anesthetics sevoflurane and isoflurane

The hemodynamic effects and pharmacokinetics of nicardipine under general anesthesia were compared between two different volatile anesthetics, sevoflurane and isoflurane. Sixteen adult neurosurgery patients were divided into sevoflurane and isoflurane groups. Anesthesia was maintained with either sevoflurane or isoflurane (0.5–1.5%) and nitrous oxide in oxygen. When the blood pressure was stabilized [0.5 minimum alveolar concentration (MAC) in both anesthetics] during surgery, nicardipine 1 mg, i.v. was administered. Plasma catecholamines and nicardipine concentration were measured, and the pharmacokinetics of nicardipine were calculate. The decrease in blood pressure and the increase in heart rate 30 min after nicardipine administration were significant in the isoflurane group but not in the sevoflurane group. Although plasma catecholamine levels increased after nicardipine administration in the isoflurane group, no significant changes were observed in the sevoflurane group. The sevoflurane group had a significantly longer elimination half-life, a larger area under the plasma concentration curve, and smaller clearance of nicardipine compared to the isoflurane group. In summary, the effects of nicardipine on blood pressure and heart rate were significantly longer under isoflurane anesthesia than under sevoflurane anesthesia. However, the etabolism and excretion of nicardipine were significantly delayed under sevoflurane anesthesia.     

芬太尼—异氟醚静吸复合麻醉在心内直视手术中的应用

本文介绍了芬太尼—异氟醚静吸复合麻醉用于心内直视手术的经验,芬太尼20～30μg/kg,分次静注,同时吸入异氟醚.潘侃朗宁维持肌肉松弛.与大剂量芬太尼(50～100μg/kg)麻醉相比.两种方法的麻醉效果均满意,镇痛好,心血管变化轻     

Differential effects of isoflurane,halothane, and ketamine on the regional methionine-enkephalinlike immunoreactivity in the mouse brain

The widely used measurement index for anesthetic potency, minimum alveolar concentration (MAC), is hypothesized to be the sum of the effects on multiple neural systems whose contribution to anesthesia differs depending on the agents used. The present study, which compared the effects of halothane, isoflurane, and ketamine, at equipotent level of anesthesia, on the methionine-enkephalinergic neurons in 9 brain regions, showed a significant difference in the methionine-enkephalin-like immunoreactivity (Met-ENK-like IR) among the anesthetics in each region. The order of the Met-ENK-like IR was: halothane > ketamine > isoflurane in the caudatus putamen; halothane > isoflurane ≊ketamine in the nucleus accumbens and the ventral pallidum; halothane ≊isoflurane > ketamine in the globus pallidus, the nucleus dorsomedialis hypothalami, and the nucleus ventromedialis hypothalami; and halothane > isoflurane > ketamine in the arcuate nucleus, the periaqueductal gray, and the nucleus reticularis parvocellularis. These findings indicate that these three anesthetics affect the methionine-enkephalinergic neurons in the motor and pain controlling pathways in different fashions.     

氧流量对异氟烷的消耗与摄取的影响

目的：探讨不同氧流量对异氟烷的消耗量和体内摄取的影响。方法：２４例异氟烷全身麻醉的病人，按新鲜氧流量不同随机分为３组。氧流量分别为２．０、１．０和０．３Ｌ·ｍｉｎ－１。以微量泵向呼吸环路吸入远端输入异氟烷，调节输入速度使肺泡异氟烷浓度维持在最低肺泡有效浓度的１１倍。监测异氟烷吸入及呼出体积分数，以吸呼体积分数差作为摄取指标，观察异氟烷的消耗量及体内摄取量的变化。结果：异氟烷的消耗量随氧流量的增大而明显增加；体内摄取量各组间差异无显著性。结论：在维持相同最低肺泡有效浓度时，异氟烷的消耗量随着新鲜氧流量的增加而增加；体内对异氟烷的摄取量与新鲜氧流量的大小无关     

Effects of thiopental, halothane and isoflurane on the calcium-dependent and -independent release of GABA from striatal synaptosomes in the rat

The effects of the anesthetic agents thiopental, halothane and isoflurane on the release of GABA induced by depolarization and/or reversal of the GABA carrier were investigated in a synaptosomal preparation obtained from the rat striatum. Veratridine (1 μM) and KCl (9 mM) elicited a significant Ca²⁺-dependent release of [³H]GABA. The KCl-evoked release was not significantly modified in the presence of nipecotic acid (10⁻⁵ M), a selective blocker of the neuronal GABA carrier. The [³H]GABA release was significantly decreased by ω-conotoxin (10⁻⁷ M, a blocker of the N voltage-dependent Ca²⁺ channels, but was affected by neither nifedipine (10⁻⁴ M) nor ω-Aga-IVA (10⁻⁷ M) which block the L and Ca²⁺ channels, respectively. Thiopental application (10⁻⁵ to 10⁻³ M) was followed by a dose-related, significant, decrease in both the veratridine and KCl-induced releases, whether nipecotic acid was present or not. In contrast, halothane and isoflurane (1–3%) failed to alter [³H]GABA release. Altogether, these results suggest that reduction of the depolarization-evoked GABA release might contribute to thiopental anesthesia, but this seems unlikely for volatile anesthetics.     

Postsynaptic depression induced by isoflurane and Althesin in neocortical neurons

Summary The effects of two general anaesthetics, isoflurane — a volatile agent, and Althesin — a steroid preparation, were studied on the membrane electrical properties and spike activities of 64 neurons in in vitro slice preparations of neocortex excised from anterior cingulate and sensorimotor areas of guineapig brain. Spontaneous activity was depressed, and the thresholds for spikes evoked by intracellular injections of current pulses were increased in most neurons during applications of isoflurane in clinical concentrations (0.5–2.5 minimum alveolar concentration or MAC) and Althesin (15–100 M). The MAC values are equivalent to 1–4% isoflurane in the gaseous phase. Applications in the higher ranges (1.5–2.5 MAC and 300–1500 M) usually induced a small hyperpolarization (range, 3–8 mV) and an increase (10–30%) in input conductance. The repetitive spike firing evoked by current-pulse injections was inhibited and not uncommonly, abolished completely by an anaesthetic application. A striking feature in the actions of both agents on all neurons was the dose-dependent, reversible depression in amplitude and duration of the postspike afterhyperpolarizations (AHPs). These effects could not be attributed to anaesthetic induced changes in resting potentials, input conductances, or to the reduced number of evoked spikes. Bicuculline (50 M) was applied concomitantly in 8 neurons with the anaesthetics to block Cl-conductances mediated by GABA-receptors that otherwise may contaminate the AHPs. In the presence of bicuculline, both anaesthetics produced a greater reduction in the amplitude and duration of the AHPs which are generated through Ca²⁺-mediated K⁺-conductance. The changes in input conductance induced by Althesin were partially blocked by bicuculline indicating that endogenous actions of GABA contributed to the effects of Althesin. These investigations have shown that isoflurane and Althesin attenuate the excitabilities of neocortical neurons by postsynaptically depressing the medium-duration AHPs and thereby decreasing their abilities to fire spikes repetitively. It is concluded that these effects produced by anaesthetic administration would result in a disruption in the organized pattern of neocortical arousal.     

Comparison of the placental transfer of halothane,enflurane, sevoflurane,and isoflurane during cesarean section

The concentrations of placental transfer of halothane (H), enflurane (E), sevoflurane (S), and isoflurane (I) were measured in 46 patients during cesarean section. The mean inhalation times of H (0.5%), E (1%), S (0.8%), and I (0.6%) were 13 min 27 s, 13 min 49s, 13 min 20s, and 8 min 8s, respectively. The mean concentrations in the maternal artery (MA) were 5.2mg·dl⁻¹ in H, 12.3 mg·dl⁻¹ in E, 5.2mg·dl⁻¹ in S, and 2.4mg·dl⁻¹ in I. The concentration ratio between the MA and the fetal umbilical vein (UV) was 0.44 for H, 0.49 for E, and 0.38 for S, and these ratios were not significantly different for these anesthetics. Although the concentration ratio for I (0.27) was significantly lower than those of the other three anesthetics, the UV:MA ratio was calculated to be 0.4 for an inhalation time 13 min. Our result, therefore, suggests that if the inhalation times were equal, the ratios of placental transfer would not differ among these four inhalational anesthetics. The Apgar scores in these four groups were not different from that in the group given only 66% nitrous oxide in oxygen as anesthetic (N₂O group). The cardiovascular changes induced by skin incision were bigger in the N₂O group than in the other groups. The use of a low concentration of H, E, S, or I is, therefore, suggested to be a useful and acceptable anesthetic method for cesarean section.