摘要:

To overcome anesthetic-induced depression of myogenic motor-evoked potentials (MEPs), several techniques of stimulation using paired pulses or trains of pulses are used. This study investigated the effect of sevoflurane on myogenic MEPs induced by single and paired transcranial electrical stimulation of the motor cortex. Nine patients undergoing elective spinal surgery were anesthetized with fentanyl-N2O-ketamine. Partial neuromuscular blockade (single-twitch height 15% of baseline) was maintained with vecuronium. Single and paired (interstimulus interval 2 milliseconds) electrical stimuli were delivered to the scalp, and compound muscle action potentials were recorded from the left and right tibialis anterior muscles. In all patients, baseline MEPs were recorded from both the left and right anterior tibialis muscles (in a total of 18 legs). During the administration of 0.25 MAC and 0.5 MAC sevoflurane, MEPs induced by stimulation with a single pulse could be recorded in 12 of 18 and 4 of 18 legs, respectively, and MEP amplitude was significantly reduced to 48% and 4% of the control value, respectively. During the administration of 0.75 MAC sevoflurane, MEPs following single-pulse stimulation could not be recorded in any legs. The success rate of MEP recording during the administration of sevoflurane was greater after paired stimulation than after single stimulation, and percentage MEP amplitude (percentage of the control value after single stimulation but before sevoflurane) after paired stimulation was significantly higher than after single stimulation before and during the administration of 0.25 MAC and 0.5 MAC sevoflurane. The success rate of MEP recording and MEP amplitude after paired stimulation decreased in a dose-dependent manner during the administration of sevoflurane. These results suggest that although facilitation by the second stimulus was considerable, paired stimuli are still not sufficient to overcome the depressant effects of sevoflurane in clinically used concentrations.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Thiopental intravenous injections before temporary clipping and mild hypothermia have protective effects in the setting of cerebral ischemia, and are used clinically in some centers. However, it is not known whether mild hypothermia affects thiopental-induced electroencephalogram (EEG) burst suppression. In this study, the authors compared the onset and duration of EEG suppression by thiopental in normothermic (n = 10) and mildly hypothermic (n = 10) patients undergoing cerebral aneurysm surgery. Spectral analysis was used to compare the prethiopentonal continuous EEG patterns in normothermic and mild hypothermie patients. The patients' body temperatures were controlled by a circulating water mattress and intravenous fluids (normothermia = 36.4 ± 0.1°C, mild hypothermia = 33.3 ± 0.1°C). Immediately before temporary clipping, thiopental sodium (5 mg/kg) was administered intravenously. Onset time (the amount of time from thiopental injection to the first complete EEG suppression), duration of suppression (the amount of time from the first complete EEG suppression to recovery on continuous EEG from burst suppression), and maximum duration of isoelectric EEG (the longest time interval between two bursts during burst suppression) were measured. Onset time was shortened (25.8 ± 1.4 versus 43.5 ± 5.6.seconds), and duration of suppression (531.0 ± 56.6 versus 165.0 ± 16.9 seconds) and the maximum duration of isoelectric EEG (47.7 ± 5.8 versus 22.8 ± 2.0 seconds) were prolonged in the patients with mild hypothermia. In two normothermic patients, the standard dose of thiopental did not produce burst suppression, but only a mild decrease in spectral edge frequency. The authors concluded that the effects of mild hypothermia on thiopental-induced EEG suppression are not simply additive, but synergistic.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Hyperventilation may reverse increases in cerebral blood flow velocity caused by inhalation of nitrous oxide (N2O). This study sought to determine whether inhalation of 50% nitrous oxide after the induction of hyperventilation increases cerebral blood flow velocity as measured by transcranial Doppler ultrasonography. Seven volunteers breathed air/O2through a modified Circle system at normocapnia followed by air/O2with hyperventilation, and then N2O/O2with hyperventilation. Expired gas concentrations were measured in the expiratory limb of the circuit distal to a one-way valve. Hyperventilation reduced end-tidal carbon dioxide from 38 ± 1mmHg to 26 ± 1mmHg. Hypocapnia was maintained during inhalation of N2O (EtCO2=28 ± 1mmHg). Mean cerebral blood flow velocity decreased 34% with hyperventilation (38 ± 4 cm/second versus 59 ± 9 cm/second,p< 0.05) and returned to baseline with the addition of nitrous oxide (58 ± 7 cm/second), despite persistent hypocapnia. The addition of nitrous oxide to the inspired gas mixture after induction of hypocapnia reversed reductions in cerebral blood flow velocity associated with hyperventilation. Potential benefits of induced hypocapnia in patients with intracranial pathology may be offset by the administration of N2O.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

A number of studies have shown that polymerized bovine hemoglobin (HBOC-201) does not cause clinically significant side effects. This has been demonstrated in spite of the fact that a primary increase in oxygen extraction ratio has been associated with an increase in systemic vascular resistance (SVR) and a decrease in cardiac index (CI). The current study investigated the effects of HBOC-201 on cerebral circulation. Middle cerebral artery mean flow velocity (Vm) was measured using Transcranial Doppler Sonography. After institutional review board approval and informed consent were obtained, 12 patients (mean age 59 ± 10 years), scheduled for hepatic resection, were enrolled. Anesthesia during the induction period consisted of etomidate (0.3 mg/kg), fentanyl (3 mcg/kg), and vecuronium (0.1 mg/kg). Anesthesia during the maintenance period consisted of isoflurane (0.6–0.8 vol%)/O2/N2O (FiO2= 0.3), fentanyl, and vecuronium. End-tidal carbon dioxide partial pressure (PetCO2), arterial carbon dioxide partial pressure (PaCO2), mean arterial blood pressure (MAP), CI, SVR, mean flow velocity, and pulsatility index were measured in each patient. Hemodilution was performed in all patients, followed by randomized assignment to two groups: Group 1 (n = 6) received 0.4 g/kg HBOC-201, Group 2 (n = 6) received a corresponding volume of hydroxyethyl starch (mw 70,000). Measurements were taken at six points (PMs): before hemodilution (PM 1); following hemodilution (PM2); and at 3, 10, 20, and 30 minutes (PM 3–6) after infusion of HBOC-201 or starch. Systemic vascular resistance rose in Group 1 as compared with Group 2, with significant differences at PM 3–6. The greatest difference was at PM 6 (Group 2 = 1071 dyne·s·Cm−5; Group 1 = 2154 dyne·s·cm−5). Cardiac indices were significantly lower in Group 1 (1.7–1.8 1/minute-m−2) than in Group 2 (2.4–2.71/minute-m−2) after PM 3. After hemodilution, mean flow velocity showed an insignificant increase in both groups, ranging from 39 to 46 cm/second. Although SVR increased significantly following HBOC-201-infusion, the results of this study did not reveal changes in cerebral blood flow that establish significant group-to-group differences.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

A previous study indicated that diaspirin-crosslinked hemoglobin (DCLHb) decreases cerebral ischemia after subarachnoid hemorrhage. However, the study was limited in that DCLHb was given to animals with an intact vasculature. As extravasated hemoglobin has been implicated in the pathogenesis of cerebral vasospasm, DCLHb in the subarachnoid space might in theory have a detrimental effect on cerebral perfusion after subarachnoid hemorrhage. In the current study, autologous blood was administered into the cistema magna of isoflurane-anesthetized rats. After 30 minutes, the animals received one of the following in the cistema magna (n = 8 for each group): The control group received mock cerebral spinal fluid, the “blood” group received autologous blood, the “DCLHb” group received DCLHb, and the “Alb” group received human serum albumin. After 20 minutes, areas of reduced cerebral blood flow (CBF, 0–20 and 21–40 ml/100 g/min) were assessed in five coronal brain sections with14C-iodoantipyrine. The data were evaluated by analysis of variance. The areas of 0–20 ml/100 g/min CBF were greater in all five brain sections in the Blood group than in the other three groups; were greater in four brain sections in the DCLHb group than in the Control group; and were greater in three brain sections in the Alb group than in the Control group (p< 0.05). The areas of 21–40 ml/100 g/min CBF were greater in three sections in the Blood group than in the other three groups; and were greater in two brain sections in the DCLHb group than in the Alb group (p< 0.05). These data support a hypothesis that subarachnoid blood induces cerebral hypoperfusion, and that although molecular hemoglobin decreases CBF, the potential adverse effects are less than those produced by blood.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

This study sought to test the hypothesis that intravenous basic fibroblast growth factor (bFGF) inhibits the development of brain injury during transient focal ischemia. Halothane-anesthetized cats (n = 39) underwent left middle cerebral artery occlusion for 60 minutes. After the onset of reperfusion, wounds were closed and the cats were allowed to emerge from anesthesia. Experimental cats were treated with intravenous bFGF at a dose of either 2 or 5 μg/kg per hour, beginning 45 minutes after initiation of ischemia and continuing until 24 hours of reperfusion, when neurologic function and infarction volume were evaluated. The cats in the control group received diluent. Three of thirteen cats treated with bFGF 2 μg/kg/hour and six of sixteen cats treated with bFGF 5 μg/kg/hour died during the 24 hour reperfusion period. There was no difference in injury volume or neurologie evaluation score in the control group (n = 10; hemisphere injury, 1301 ± 306 mm3, mean±SE; score 53 ± 3), and cats treated with either 2 μg/kg/hour (n = 10; hemisphere injury, 1170 ± 292 mm3; score 50 ± 3) or 5 μg/kg/hour bFGF (n = 10; hemisphere injury, 1343 ± 374 mm3; score 50 ± 2). The data collected do not support the hypothesis that intravenous bFGF is neuroprotective in a cat model of transient focal ischemia.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

This article describes the effect of isoflurane on amino acid release and tissue content induced by energy deprivation in slices of rat hippocampus. Energy deprivation (95% N2/ 5% CO2and glucose free medium) (ED) induced an increase in the release of all amino acids measured, with the exception of glutamine. The tissue content of all amino acids except γ-aminobutyric acid (GABA) and arginine was concomitantly reduced. Isoflurane (1.5% and 3.0%) reduced glutamate release during ED by 27% and 28% (p < 0.05 as compared with release without isoflurane), respectively, whereas the tissue content was slightly increased. Similarly, GABA release was reduced by 25% and 25% (p < 0.05 as compared with release without isoflurane) accompanied by an insignificant enhancement in tissue content as compared with ED without isoflurane. Isoflurane reduced the release of taurine and most of the other amino acids. The total amount of all amino acids (both released and retained) was not significantly altered by the anesthetic. These observations demonstrate that isoflurane can modify the changes in amino acid handling induced by energy deprivation.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Sodium nitroprusside (SNP) is commonly used for controlled systemic hypotension during aneurysm surgery after acute subarachnoid hemorrhage (SAH). Few experimental studies have assessed cerebrovascular responsiveness to SNP acutely after a representative SAH (i.e., following arterial rupture within the subarachnoid space). Instead, most studies have focused on delayed reactivity after slow injections of unpressurized blood throughout several days. In the authors' study, SAH was created by endovas-cular rupture in spontaneously breathing rats under urethane anesthesia without craniotomy. After 3 hours, proximal middle cerebral arteries (MCAs) were harvested and mounted as ring preparations in vitro. After preconstriction with 30 mM prostaglandin F2a, concentration-response curves were generated to express SNP's sequential relaxation of preconstricted tone. The effective concentration of SNP for 50% relaxation was significantly lower after SAH (p < 0.001) as compared with non-operated and shamoperated controls. There was also a significantly greater maximum percentage relaxation from preconstricted tone (p < 0.001) with SNP. The results of this study suggest that SNP is a potent and efficacious dilator of MCAs in the hours immediately after acute SAH.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

In order to understand why exogenous epinephrine decreases the convulsive dose of lidocaine, the authors investigated cerebral circulation and plasma lidocaine concentrations in Wistar rats under general anesthesia. In the first experiment, baseline evaluations of each rat's electroencephalogram (EEG), mean arterial pressure (MAP), regional cerebral blood flow (r-CBF), cerebrospinal fluid (CSF) pressure, and cerebral perfusion pressure (CPP) were made. The rats were then assigned to one of three groups: Group L (n = 6) received intravenous lidocaine (5 mg/kg/min); Group LE (n = 6) received intra-venous lidocaine (5 mg/kg/min) and epinephrine (2.5 μg/kg/min); and Group E (n = 5) received intravenous epinephrine (2.5 μ/kg/min). Cumulative doses of lidocaine at the onset of EEG spike activity in Groups L and LE were compared. Blood-brain barrier (BBB) permeability was evaluated by observing extravasation of Evans blue (EB) dye. In the second experiment, additional rats were allocated to two treatment groups: Group L' (n = 6) received intravenous lidocaine (5 mg/kg/min); Group LE' (n = 6) received intravenous lidocaine (5 mg/kg/min) and epinephrine (2.5 μg/kg/min). Brain tissue oxygen partial pressure (PtO2) was monitored during infusion, and arterial and sagittal sinus blood samples were obtained immediately after the onset of EEG spike activity to determine plasma lidocaine concentration. The convulsive dose of lidocaine was significantly decreased when lidocaine was administered with epinephrine (Group L: 61.5 ± 5.3 mg/kg (mean ± SD); Group LE: 30.1 ± 4.0 mg/kg) (p < 0.05), but there were no significant differences in plasma lidocaine concentration among these groups. R-CBF, CSF pressure, and CPP immediately before EEG spike activity were higher in Group LE than in Group L. Neither decreased PtO2nor extravasation of EB was observed in rats treated with epinephrine and lidocaine, excluding cerebral ischemia and BBB breakdown from possible mechanisms by which epinephrine decreased the convulsive dose of lidocaine. None of the rats in Group E exhibited EEG findings suggestive of a preconvulsive state, ruling out a convulsive effect of epinephrine itself. The results suggest that an increase in lidocaine supply to the brain caused by increased CBF causes the low cumulative dose of lidocaine at the onset of convulsion in rats given lidocaine plus epinephrine.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID

摘要:

Hypertonic saline was recently introduced as a new hyperosmolar agent for treatment of intracranial hypertension and cerebral edema. It has the potential to cause a rebound phenomenon similar to other osmotic agents. The authors report on two patients with cerebral edema caused by hypertensive intracerebral hemorrhage who were treated with hypertonic saline infusion. Both patients improved clinically after 24 hours of hypertonic saline administration. However, both patients deteriorated clinically, 48 and 96 hours after initiation of therapy, despite continued hypertonic saline administration. Compared with pre-treatment computed tomographic scans, edema volume on repeat scans increased from 131 cc to 262 cc, and from 171 cc to 239 cc in the first and second patients, respectively, despite the lack of change in hematoma volume. Malignant edema formation late in the course of intracerebral hemorrhage after prolonged administration of hypertonic saline may represent a rebound phenomenon of hyperosmolar therapy. Further studies are warranted to identify the occurrence of this phenomenon and the subset of patients susceptible to it.

ISSN:0898-4921    

出版商:OVID    

年代:1998

数据来源: OVID