ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

During rapid opioid detoxification, increased sympathetic activity and a greater median frequency (MF) of activity on electroencephalography (EEG) have been reported. The purpose of this study was to evaluate a new index for detoxification that combines sympathetic activity and MF data. After informed consent was obtained, eight patients were sedated with propofol. The MF of EEG activity derived from frontal electrodes was determined. Heart rate variability was evaluated in 256-second segments by power spectral analysis, and sympathetic activity was determined by the low frequency component. The Hoffman Index for narcotic detoxification was weighted 70% to sympathetic activity and 30% to MF to normalize the difference in scales and to provide adequate weight to the sympathetic component. Opioid detoxification was produced by infusion of 25 mg naloxone for 30 minutes, followed by a 24-hour infusion of 1 mg per hour. The MF showed a rapid increase during high-dose infusion of naloxone, but the peak response occurred 1 to 2 hours later. Sympathetic activation and the Hoffman Index increased more slowly after the start of naloxone infusion, but peak increases in all components occurred at approximately the same time. The peak increases in Hoffman Index (110% of baseline), MF (260%), and sympathetic activity (304%) during administration of naloxone were significant and correlated with respect to time (r = 0.89–0.94). The Hoffman Index showed an early increase related to MF and a well-defined peak response indicative of sympathetic and MF activity. The behavior of the Hoffman Index in relation to the MF and sympathetic activity more clearly indicated the onset of opioid detoxification and the maximum response to opioid reversal than did MF or sympathetic activity alone.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Patients receiving chronic anticonvulsant therapy have been reported to show resistance to certain nondepolarizing neuromuscular blockers. In this study, the effects of chronic phenytoin therapy on the onset, duration, and recovery of rocuronium action was assessed. Thirty-six patients scheduled for various neurosurgical procedures were studied: 18 receiving chronic phenytoin therapy (Group I) and 18 controls (Group II). Rocuronium 0.6 mg/kg (2 × DE95) was administered after induction of general anesthesia with 4–6 mg/kg thiopental sodium and 3–5 &mgr;g/kg intravenous (IV) fentanyl. Maintenance anesthesia consisted of N2O in O2, 0.5% end-tidal isoflurane, and a fentanyl infusion. Neuromuscular block was monitored with acceleromyography of the adductor pollicis-brevis muscle by using a TOF-GUARD Biometer monitor (Biometer International A/S, Odense, Denmark). According to the amplitude of the first response of train-of-four, neither the lag time nor the onset time differed between the two groups. However, the recovery index was significantly shorter in patients chronically treated with phenytoin (mean recovery index: control group, 8.3 ± 1.7 minutes; phenytoin group, 6.7 ± 2.3 minutes;P< .05). In addition, the times of recovery to 10%, 25%, 75%, and 90% of the baseline response were also significantly shorter in the phenytoin group than in the control group. We conclude that the duration of action of rocuronium and the recovery index were affected by chronic phenytoin therapy.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Analysis of patient data from a new neuroscience intensive care unit (NSICU) permitted evaluation of whether such a specialty ICU favorably altered clinical outcomes in critically ill neuroscience patients, and whether such a care model produced an efficient use of resources. A retrospective review was performed to compare (1) the clinical outcomes, as defined by percent mortality and disposition at discharge, between patients with a primary diagnosis of intracerebral hemorrhage treated in 1995 in medical or surgical ICUs and those treated in the same medical facility in an NSICU in 1997; and (2) the efficiency of care, as defined by length of ICU stay, total cost of care, and specific resource use, between patients treated in the NSICU and national benchmark standards for general ICUs during the 1997 fiscal year (FY). In the latter, extracted patient population data on neurosurgery patients requiring ICU treatment during FY 1997 were used with the following adjacent-disease related group (A-DRG)-coded diseases: craniotomy with and without coma or intracerebral hemorrhage, and skull fracture with and without coma lasting longer than 1 hour. Outcome measures of percent mortality and disposition at discharge in patients with intracerebral hemorrhage were significantly improved (P< .05), compared with those in a similar cohort treated 2 years earlier in a general ICU setting. Also, patients treated in the NSICU had shorter hospital stays (P< .01) and lower total costs of care (P< .01) than a national benchmark. The data suggest that a neuroscience specialty ICU arena staffed by specialty-trained intensivists and nurses is beneficial.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

A systematic search (Medline, Cochrane library, Embase, bibliographies, to 5.2000, no language restriction) was performed for published reports of randomized comparisons of propofol and methohexital for anesthesia during electroconvulsive therapy. We analyzed 15 trials with data on 706 patients. The duration of motor seizure was shorter with propofol (range, 18–39 seconds) than with methohexital (range, 26–48 seconds, weighted mean difference 8.4 seconds [95% CI, 6.6–10.0]). With both propofol and methohexital, there was little evidence of an association between dose and duration of motor seizure (for propofol: r2= 0.25,P= .08; for methohexital: r2= 0.11,P= .27). Two small trials investigated clinical outcome; results were inconclusive. Data on adverse effects were sparse. Duration of seizure was not proven to be a useful measure of treatment success in the study of electroconvulsive therapy with propofol or methohexital. The impact of the technique of anesthesia on the underlying disease needs to be established.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Expression of the calcium-independent nitric oxide synthase (NOS2) contributes to damage in neurologic disease and trauma. The effects of local anesthetics on NOS2 expression have not been examined. The authors tested the effects of four local anesthetics on the expression of NOS2 in immunostimulated rat C6 glioma cells. Incubation with local anesthetics alone did not induce nitrite accumulation; however, the nitrite production induced by stimulation with bacterial endotoxin lipopolysaccharide (LPS) and interferon-&ggr; (IFN-&ggr;) was increased in a dose-dependent manner by bupivacaine (maximal 3-fold at 360 &mgr;M), tetracaine (maximal 7-fold at 360 &mgr;M), and lidocaine at higher doses (5-fold increase at 3.3 mM). Significant increases in nitrite production were observed in concentrations of bupivacaine or tetracaine as low as 120 &mgr;M, which correspond to 30 &mgr;g/mL (.003% weight/volume). In contrast, ropivacaine had little effect on nitrite production (160% of control values) and only at the highest concentration (3.3 mM, corresponding to 890 &mgr;g/mL or 0.089% w/v) tested. Increased nitrite production was not caused by cytotoxic effects of the drugs used, as assessed by release of intracellular lactate dehydrogenase. Increased nitrite production was accompanied by increased NOS2 catalytic activity, steady state mRNA levels, and promoter activation. These results demonstrate that submillimolar doses of two commonly used local anesthetics can increase glial NOS2 expression.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

The excessive release of glutamate during cerebral ischemia may play an important role in subsequent neuronal injury. Both lamotrigine and hypothermia have independently been shown to attenuate the release of glutamate. In this study, the authors sought to determine whether these effects were additive. Thirty-five New Zealand White rabbits were randomized to one of six groups: a normothermic control group; a lamotrigine-treated group; two hypothermic groups at 33°C or 34.5°C; or two groups treated with both hypothermia at 33°C or 34.5°C plus lamotrigine. Animals were anesthetized before implanting microdialysis probes in the hippocampus. Esophageal temperature was maintained at 38°C in the control and lamotrigine groups, while the temperatures of animals in the hypothermia and hypothermia-plus-lamotrigine groups were cooled to 33°C or 34.5°C. Two 10 minute periods of global cerebral ischemia were produced by inflating a neck tourniquet. Levels of glutamate in the microdialysate were then determined using high-performance liquid chromatography. Extracellular glutamate concentrations increased only slightly from baseline during the first ischemic period. Glutamate levels during the second ischemic episode in the hypothermia-plus-lamotrigine group (34.5°C) were significantly lower than those in the hypothermia group alone (34.5°C), lamotrigine, or control groups (P< .01). The fact that mild hypothermia (34.5°C) plus lamotrigine (20 mg/kg) together were more effective in inhibiting extracellular glutamate accumulation than hypothermia (34.5°C) or lamotrigine (20 mg/kg) alone, suggests the potential for increased neuroprotection by the addition of lamotrigine to mild hypothermia.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Twenty-four adult male Wistar rats, weighing 220 to 290 g, were anesthetized with 30 mg/kg intraperitoneal sodium thiopental, then underwent a tracheostomy. After diffuse impact–acceleration brain injury (BI) was induced, each rat was paralyzed and mechanically ventilated with 30% O2in nitrous oxide (N2O). The rats were assigned randomly to two groups, each of which received one of the two volatile anesthetic agents, sevoflurane or isoflurane. The anesthetics were administered at 0.5, 0.75, 1.0, and 1.25 minimal alveolar concentration (MAC) for 30 minutes each, respectively, and anesthesia was maintained at 0.75 MAC during the last hour of the study period. Intracranial pressure (ICP), mean arterial pressure (MAP), rectal and intrahemispheric temperatures, and end-tidal volatile anesthetic concentrations were monitored continuously throughout the 3 hours, with measurements recorded every 15 minutes. At baseline, there were no significant differences between the two groups regarding the monitored physiologic values. In the sevoflurane group, MAP fell significantly after 45 minutes, and a similar change was observed in the isoflurane group after 30 minutes (P< .05,P< .01, andP< .001, respectively). Intracranial pressure increased significantly at 45 minutes in the sevoflurane group (P< .01) and remained elevated from 60 minutes until the end of the study period (P< .01,P< .001). Although ICP increased in the isoflurane group, the change was not significant. Cerebral perfusion pressure (CPP) decreased in parallel with MAP, with the reduction in the sevoflurane group being more pronounced than that in the isoflurane group. The results demonstrated that, under the conditions of diffuse BI, animals that were anesthetized with sevoflurane had higher ICP and lower CPP levels than those anesthetized with isoflurane.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Hypertonic-hyperoncotic saline solutions (HHS) have been used for small-volume resuscitation and to treat intracranial hypertension and cerebral edema in neurocritical care. Little is known on the response of brain cells to direct exposure in HHS, which may occur in blood-brain barrier disruption. We studied the effects of HHS on healthy and glutamate-injured brain cellsin vitro. To model a hypertonic-hyperoncotic environment, rat hippocampal neurons and cerebral astrocytes were exposed to hypertonic saline and hydroxyethyl starch (HES) added to medium for 15 minutes (final osmolarity: 350 mOsm/L in the neuronal, 373 mOsm/L in the glial medium; 2.5 mg/mL HES in both media). To simulate excitotoxicity, cells were exposed to 100 &mgr;M glutamate for 8 minutes before exposure to HHS. Cell viability was analyzed by morphology and vital dye staining; intracellular water space (WS) and glucose use were measured by scintillation spectrometry using 3-O-methyl[14C]-d-glucose and [3H]2-deoxy-d-glucose ([3H]2-DG). After 24 hours, exposure to HHS added to medium caused a 30% reduction in viability of healthy neurons (P< .05), but did not exacerbate the glutamate-induced 50% decrease in neuronal survival. One hundred percent astrocyte viability remained unchanged. The WS of astrocytes and surviving neurons was negligibly altered. Exposure to HHS added to medium caused a 35% reduction in [3H]2-DG in healthy and glutamate-injured neurons (P< .05), but did not affect [3H]2-DG in astrocytes. Our data show that HHS may potentially injure hippocampal neurons. Preserved WS values imply that live cells maintained volume regulation capabilities, indicating a lack of dehydration 24 hours after exposure to HHS. Impaired glucose use predisposes neurons to disturbed metabolism, which may influence neuronal outcome after brain injury.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID

摘要:

Although it is known that development of lipid peroxidation after ischemia occurs predominantly in vulnerable regions, temporal profiles of antioxidants after ischemia have not been regionally elucidated. After reperfusion periods of 0, 3, 24, and 72 hours following 20 minutes of four-vessel occlusion (n = 6 in each group), the concentration of total glutathione (GSH) and the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) were assayed in the hippocampus, parietal cortex, striatum, thalamus, and brain stem.The levels of all antioxidants were unchanged in all regions without reperfusion; however, the concentration of total GSH significantly decreased in the hippocampus at 3 hours after the onset of reperfusion, and showed a maximum decrease in the hippocampus (68% of the sham-control level), parietal cortex (78% of the sham-control level), and striatum (76% of the sham-control level) after 24 hours of reperfusion. After 72 hours of reperfusion, these regions and the thalamus showed restoration and an increase in the total GSH concentration, respectively. The activities of SOD, GSH-Px, and catalase were stable during the reperfusion period, but the hippocampus showed significant increases in these enzyme activities and the parietal cortex and striatum showed significant increases in SOD activities at 72 hours after the onset of reperfusion. These results indicate that endogenous antioxidants take 72 hours for restoration in vulnerable regions after 20 minutes of four-vessel occlusion in rats.

ISSN:0898-4921    

出版商:OVID    

年代:2001

数据来源: OVID