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Biomedical subjects

Toshisuke Sakaki

Publications and source records attributed to Toshisuke Sakaki.

At least 19 recordsLinked to original sources
PubMed2004

Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild hypothermia in neurosurgical patients.

Sevoflurane and propofol have been widely used as anesthetic agents for neurosurgery. Recent evidence has suggested that the influence of these anesthetics on cerebral oxygenation may differ. In the present study, the authors investigated jugular bulb oxygen saturation (SjO2) during propofol and sevoflurane/nitrous oxide anesthesia under mildly hypothermic conditions. After institutional approval and informed consent, 20 patients undergoing elective craniotomy were studied. Patients were randomly divided to the group S/N2O (sevoflurane/nitrous oxide/fentanyl anesthesia) or the group P (propofol/fentanyl anesthesia). After induction of anesthesia, the catheter was inserted retrograde into the jugular bulb and SjO2 was analyzed. During the operation, patients were cooled and tympanic membrane temperature was maintained at 34.5 degrees C. SjO2 was measured at normocapnia during mild hypothermia and at hypocapnia during mild hypothermia. There were no statistically significant differences in demographic variables between the groups. During mild hypothermia, SjO2 values were significantly lower in group P than in group S/N2O. The incidence of SjO2 less than 50% under mild hypothermic-hypocapnic conditions was significantly higher in group P than in group S/N2O. These results suggest that hyperventilation should be more cautiously applied during mild hypothermia in patients anesthetized with propofol and fentanyl versus sevoflurane/nitrous oxide/fentanyl.

Analysis of Variance↗
PubMed2003

Novel tumor suppressor loci on 6q22-23 in primary central nervous system lymphomas.

Deletions on the long arm of chromosome 6 (6q) are one of the most common chromosomal alterations in systemic high-grade non-Hodgkin's lymphomas. However, the locations of allelic deletions and their roles have not yet been reported in primary central nervous system lymphomas (PCNSLs), most of which are classed as non-Hodgkin's lymphoma. We thus performed fine loss of heterozygosity (LOH) mapping of 6q in 29 samples of surgically resected PCNSLs using 39 microsatellite markers to identify commonly deleted regions. LOH was found at 1 or more loci at 6q22-23 in 19 samples (66%); furthermore, 18 of these samples shared a deletion in the same small ( approximately 140 kb) region flanked by D6S1030 and D6S1690, a region in which the human R-PTP-kappa gene (PTPRK) is reported to be located. Reverse transcription-PCR analysis of the mRNA from 4 cases with 6q deletions confirmed loss of this gene, and loss of PTPRK expression was observed in 76% (22 of 29) of tumors with immunohistochemistry. In addition, LOH on 6q22-q23 significantly correlated to shorter patient survival (12.8 +/- 4.3 versus 23.4 +/- 3.5 months; P < 0.0001). Our results suggest that a 140-kb deletion located at 6q22-23 may contain the putative tumor suppressor, PTPRK, that appears to be relevant to the pathogenesis and prognosis of PCNSLs.

Central Nervous System Neoplasms↗
PubMed2003

Magnetic resonance imaging shows delayed ischemic striatal neurodegeneration.

Brief focal ischemia leading to temporary neurological deficits induces delayed hyperintensity on T1-weighted magnetic resonance imaging (MRI) in the striatum of humans and rats. The T1 hyperintensity may stem from biochemical alterations including manganese (Mn) accumulation after ischemia. To clarify the significance of this MRI modification, we investigated the changes in the dorsolateral striatum of rats from 4 hours through 16 weeks after a 15-minute period of middle cerebral artery occlusion (MCAO), for MRI changes, Mn concentration, neuronal number, reactivities of astrocytes and microglia/macrophages, mitochondrial Mn-superoxide dismutase (Mn-SOD), glutamine synthetase (GS), and amyloid precursor protein. The cognitive and behavioral studies were performed in patients and rats and compared with striatal T1 hyperintensity to show whether alteration in brain function correlated with MRI and histological changes. The T1-weighted MRI signal intensity of the dorsolateral striatum increased from 5 days to 4 weeks after 15-minute MCAO, and subsequently decreased until 16 weeks. The Mn concentration of the dorsolateral striatum increased after ischemia in concert with induction of Mn-SOD and GS in reactive astrocytes. The neuronal survival ratio in the dorsolateral striatum decreased significantly from 4 hours through 16 weeks, accompanied by extracellular amyloid precursor protein accumulation and chronic glial/inflammatory responses. The patients and rats with neuroradiological striatal degeneration had late-onset cognitive and/or behavioral declines after brief focal ischemia. This study suggests that (1) the hyperintensity on T1-weighted MRI after mild ischemia may involve tissue Mn accumulation accompanied by Mn-SOD and GS induction in reactive astrocytes, (2) the MRI changes correspond to striatal neurodegeneration with a chronic inflammatory response and signs of oxidative stress, and (3) the subjects with these MRI changes are at risk for showing a late impairment of brain function even though the transient ischemia is followed by total neurological recovery.

Aged↗
PubMed2003

Noxious stimuli do not modify myogenic motor evoked potentials by electrical stimulation during anesthesia with propofol-based anesthesia.

PURPOSE: To investigate whether motor evoked potentials (MEP) to transcranial electrical stimulation under constant blood propofol concentration are affected by the arousing effect of surgical noxious stimuli. METHODS: Twenty patients who underwent elective spinal surgery were studied. Patients were anesthetized with 50% nitrous oxide in oxygen, fentanyl, and propofol to maintain the bispectral index (BIS) score around 50. MEP in response to a multipulse transcranial electrical stimulation at stimulus sites of C3-C4 were recorded over the right abductor pollicis brevis muscle. Changes of peak-to-peak amplitude and onset latency of MEP, BIS score before and after surgical stimuli were evaluated. Propofol plasma concentration was measured at the same time points. RESULTS: Both MEP amplitude and latency did not change significantly after surgical stimuli although BIS increased significantly (48 +/- 6 to 58 +/- 5; P < 0.05). Plasma propofol concentration was maintained at the same level between the two measurement points (3.3 +/- 0.7 to 3.3 +/- 0.7 micro g*mL(-1)). There was no relation between BIS change and changes of MEP amplitude and latency, and propofol plasma concentration. CONCLUSION: MEP to the transcranial electrical stimulation under a constant and clinically appropriate blood propofol concentration are not affected by surgical noxious stimuli.

Anesthesia, General↗
PubMed2003

Chemical preconditioning prevents paradoxical increase in glutamate release during ischemia by activating ATP-dependent potassium channels in gerbil hippocampus.

Ischemic tolerance induced by pretreatment with a low dose of 3-nitropropionic acid (3-NPA), called chemical preconditioning, prolongs the delay to hypoxic depolarization and improves the recovery of synaptic transmission (Exp. Neurol. 166 (2000), 385-391). We studied the effect of chemical preconditioning on the presynaptic site by analyzing spontaneous excitatory postsynaptic currents (sEPSCs) and miniature EPSCs (mEPSCs) with a whole cell patch-clamp technique in gerbil hippocampal slices. The frequency of sEPSCs decreased first and then dramatically increased during ischemia (10 min in duration, low pO(2), and deprivation of glucose) up to 200-300%. This increase was apparently a paradox, since synaptic transmission evoked by electrical stimulation diminished when the sEPSC frequency started to increase. The frequency of mEPSCs also increased in the same time course. Increases in sEPSC and mEPSC frequencies were prevented by chemical preconditioning with 3-NPA (4 mg/kg) administered intraperitoneally 3 h before the preparation of brain slices. These effects of chemical preconditioning were abolished by glibenclamide (5 microM), a blocker of ATP-dependent potassium (K(ATP)) channels, applied in vitro before the ischemic insult. The application of diazoxide (500 microM), an opener of K(ATP) channels, produced the same preventive effects on sEPSC and mEPSC frequencies. These results suggested that chemical preconditioning acted on presynaptic terminals to prevent the paradoxical increase in glutamate release during ischemia through the activation of K(ATP) channels.

Adenosine Triphosphate↗
PubMed2003

Brain metastases from urachal carcinoma.

We present a case of brain metastases of the urachal carcinoma, which is extremely rare and malignant. Contrast-enhanced MRI was employed to detect them. A large mass was removed surgically and 4 other small metastases were treated by gamma knife radiosurgery. Six weeks after radiosurgery, the 4 lesions had disappeared on MRI. We emphasise the importance of early diagnosis using MRI and treatment by radiosurgery for this rare condition.

Adenocarcinoma↗
PubMed2003

Protective effect of C1 esterase inhibitor on reperfusion injury in the rat middle cerebral artery occlusion model.

OBJECTIVE: The complement system is thought to play a major role in initiating some of the inflammatory events that occur during reperfusion injury. The aim of this study was to assess the effects of C1 esterase inhibitor (C1-INH) on ischemic injury in the rat model of middle cerebral artery suture occlusion and reperfusion. METHODS: Thirty-six male Wistar rats were used. Intraluminal middle cerebral artery occlusion was performed for 60 minutes. Just before reperfusion, C1-INH (50 international units/kg) (C1-INH group, n = 19) or saline solution (control group, n = 17) was administered. Physiological parameters (arterial blood gas values, mean arterial blood pressure, and heart rate) and local cerebral blood flow were recorded during the experiment. Forty-eight hours after reperfusion, all rats were killed, and assessments of leukocyte infiltration with a myeloperoxidase activity assay and histological analyses with 2,3,5-triphenyl tetrazolium chloride staining were performed. RESULTS: The physiological parameters and local cerebral blood flow values were not significantly different in the two groups. The infarction volume was significantly smaller and the myeloperoxidase activity was significantly lower in the C1-INH group (84.9 +/- 69.1 mm(3) and 0.40 +/- 0.29 units/g, respectively) than in the control group (202.3 +/- 98.3 mm(3) and 1.41 +/- 0.44 units/g, respectively) (P < 0.01). Myeloperoxidase activities were strongly correlated with infarction volumes (r = 0.73, P < 0.01). CONCLUSION: The results of this study indicated that C1-INH reduced polymorphonuclear leukocyte accumulation and neuronal damage in focal ischemia and reperfusion.

Animals↗
PubMed2003

Potential use of embryonic stem cells for the treatment of mouse parkinsonian models: improved behavior by transplantation of in vitro differentiated dopaminergic neurons from embryonic stem cells.

BACKGROUND: and Aims. The purpose of the present study was to examine the efficacy of transplantation of mouse embryonic-stem-(ES)-cell-derived tyrosine hydroxylase-positive (TH(+)) cells into Parkinsonian mice using behavioral tests and immunohistochemical evaluation. METHODS: Undifferentiated ES cells carrying the enhanced green fluorescent protein (EGFP) gene were differentiated into a cell population containing TH(+) neurons using a five-step in vitro differentiation method. These ES-cell-derived cells were used as allografts in Parkinsonian mice, made by administering injections of 6-hydroxydopamine (6-OHDA). Fifteen hemiparkinsonian mice were divided into three groups. Four weeks after 6-OHDA injection, mice in groups 1, 2, and 3 received phosphate-buffered saline, 1 x 10(4) graft cells, and 1 x 10(5) graft cells, respectively, into their dopamine-denervated striata. RESULTS: Improved rotational behavior was observed in the graft-transplanted groups (groups 2 and 3) 2 weeks after transplantation. Mice in group 2 displayed a continuous maintenance of reduced rotational behavior, while those in group 3 showed ipsilateral rotation toward the lesioned side at 4, 6, and 8 weeks after transplantation. Tumor formation was observed in one mouse in group 3. TH(+) cells were found at the grafted sites 8 weeks after transplantation in mice in groups 2 and 3, some of which were immunopositive to GFP, demonstrating the presence of dopaminergic neurons derived from the ES cells. CONCLUSION: Transplantation of in vitro differentiated ES cells changed rotational behavior in Parkinsonian mice. Our results suggest the potential availability of ES cells for Parkinson's disease.

Animals↗
PubMed2003

[Vascular endothelial growth factor expression in the rat dural arteriovenous fistula model].

UNLABELLED: Although various mechanisms of the development of dural arteriovenous fistula (DAVF) have been proposed, the pathogenesis of these lesions are still unclear. Recent experimental evidence suggested a role of angiogenic growth factors in the genesis of vascular malformations of the central nervous system. To further investigate the pathogenesis of DAVF, we examined the expression of the angiogenic growth factor, vascular endothelial growth factor (VEGF), in rat DAVF model. MATERIAL AND METHODS: Male Wistar rats (weighting 280 to 300 g, n = 40) were used. Each rat was mounted on a stereotaxic frame under general anesthesia. DAVF model (Spetzler et al.) was made by common carotid artery-external jugular vein anastomosis, bipolar coagulation of the vein draining the transverse sinus, and superior sagittal sinus thrombosis (SSS). SSS was thrombosed by a hemostatic agent through 16-gauge needle. Venous hypertension was induced in 30 rats, which were divided into two experimental groups; (1) immunohistological study group (n = 15) and (2) angiography group (n = 15). Immunohistological analysis was performed by VEGF antibody 1 week after, and angiography was done 90 days after the surgery. Developing of angiographical DAVF was observed with the magnifying X-ray camera. Each 5 rats served as sham-operated controls, which received a similar surgery without induction of venous hypertension. RESULTS: VEGF expression and DAVF were not observed in sham group. In immunohistological study group, VEGF expression in the endothelium and the connective tissues of the dura mater in the five rats (33%) and in the neurons in the eleven rats (73%) of the cerebral cortex and the basal ganglia were identified. In angiography group, DAVF formed in 6 among 15 rats (40%). CONCLUSION: The findings of this study provide the first experimental evidence that angiogenic growth factors VEGF may participate in the genesis of DAVF. These results suggest a novel strategy for the management and prevention of DAVF and related disorders.

Animals↗
PubMed2002

Intraoperative monitoring of myogenic motor-evoked potentials from the external anal sphincter muscle to transcranial electrical stimulation.

STUDY DESIGN: Motor-evoked potentials from the external anal sphincter were analyzed using transcranial electrical stimulation during spinal surgery in patients under general anesthesia. OBJECTIVE: To investigate whether motor-evoked potentials from the external anal sphincter could be elicited by transcranial electrical stimulation under general anesthesia. SUMMARY OF BACKGROUND DATA: Lumbosacral surgery often places nerve rootlets at risk for injury during operative dissection. Specifically, injury for sacral rootlets can result in bowel and bladder dysfunction, but the techniques for monitoring bowel and bladder function are limited. METHODS: Thirty patients who underwent elective spinal surgery were studied. Patients were anesthetized with 50% nitrous oxide in oxygen, fentanyl, and 4 mg/kg/h of propofol (n = 19) or 1 mg/kg/h of ketamine (n = 11). The level of neuromuscular blockade, assessed by recording the M-response from the right abductor pollicis brevis muscle, was maintained at an M-response amplitude of 40-50% of control. Motor-evoked potentials in response to a multipulse transcranial electrical stimulation at stimulus sites of C3-C4 or Fz-Cz were recorded from the skin over the subcutaneous part of the external anal sphincter using a plug-type electrode probe. The success rate of motor-evoked potentials' recording and peak-to-peak amplitude and the onset latency of motor-evoked potentials were evaluated. RESULTS: Success rates of motor-evoked potentials from the external anal sphincter were 73% and 53% after transcranial stimulation at stimulus sites of C3-C4 and Cz-Fz, respectively. Amplitudes of motor-evoked potentials after C3-C4 stimulation were significantly greater than those after Cz-Fz stimulation. Motor-evoked potential latency from the external anal sphincter was 18.6 +/- 1.5 and 19.0 +/- 2.7 msec after C3-C4 and Cz-Fz stimulation, respectively. CONCLUSIONS: The results suggest that, using a transcranial multipulse stimulation, monitoring of motor-evoked potentials from the external anal sphincter is feasible during ketamine- and propofol-based anesthesia. However, further improvement of techniques would be required for intraoperative elicitation of motor-evoked potentials from the external anal sphincter.

Adolescent↗
PubMed2002

Expression of c-Jun N-terminal kinases after axotomy in the dorsal motor nucleus of the vagus nerve and the hypoglossal nucleus.

c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases (SAPKs) are a subgroup of mitogen-activated protein kinases (MAPKs), and important mediators of signal transduction from the cell surface to the nucleus. JNK phosphorylates the transcription factor c-Jun. c-Jun is one of the earliest and most consistent markers for neurons that respond to nerve-fiber transection. To elucidate the c-Jun metabolism after axotomy, we investigated the expression of JNKs mRNA and of JNKs and c-Jun proteins following vagus and hypoglossal nerve transection. We found that JNK 1, JNK 2 and JNK 3 mRNA were positive in the cytoplasm of neuronal and glial cells. JNK 1 and JNK 2 protein were distributed mainly in the cytoplasm of neurons and glial cells, while only JNK 3 immunoreactivity was observed intensely in the nuclei of neuronal cells. Activated JNK was also observed intensely in the nuclei of neuronal cells. In sham-operated animals, the cytoplasm of a few glial cells showed moderate immunoreactivity for activated JNK, while after axotomy the cytoplasm of all perineuronal microglial cells were stained intensely. Up-regulated c-Jun and phosphorylated c-Jun immunoreactivities were found in the nuclei of neuronal cells in the severed side of both the dorsal motor and hypoglossal nuclei. These results indicate that the principal activity of JNKs in neurons is contributed largely by JNK 3 under both normal and axotomized conditions, and that JNKs play an important role in signal transduction of perineuronal microglial cells after axotomy.

Animals↗
PubMed2002

ATP-dependent potassium channel mediates neuroprotection by chemical preconditioning with 3-nitropropionic acid in gerbil hippocampus.

Chemical preconditioning with low dose of 3-nitropropionic acid (3-NPA) prolongs the latency to hypoxic depolarization (HD), which triggers cell death, and also restores the synaptic transmission which disappears during hypoxia in gerbil hippocampal slices. Here we show that these neuroprotective effects are mediated by the activation of K(ATP) channels. Diazoxide, a K(ATP) channel opener, prolonged the latency to HD dose-dependently to the same extent as that of the chemical preconditioning with 3-NPA. Glibenclamide, a K(ATP) channel blocker, abrogated the prolongation of HD with 3-NPA. The hypoxic tolerance of synaptic transmission with 3-NPA was also abolished by glibenclamide. Diazoxide also induced the hypoxic tolerance of synaptic transmission. Theses results suggest that K(ATP) channel is involved in the neuroprotection afforded by the chemical preconditioning.

Adenosine Triphosphate↗
PubMed2002

Changes in expression of p38 mitogen-activated protein kinase in the dorsal motor nucleus of the vagus nerve and hypoglossal nucleus after axotomy in adult rats.

Mitogen-activated protein (MAP) kinase cascades are activated in response to various extracellular stimuli. P38 MAP kinase is one of the MAP kinase family and is activated by proinflammatory cytokines and environmental stresses. Activating transcription factor-2 (ATF-2) is one of the targets for p38 MAP kinase. To obtain information on the role of the p38 MAP kinase in the neurons and glial cells after axotomy, we investigated changes of expression of p38 MAP kinase, MAP kinase kinase (MKK) 3, MKK4, MKK6 and ATF-2 in the dorsal motor nucleus of the vagus nerve and the hypoglossal nucleus following axotomy in rats using in situ hybridization and immunohistochemical techniques. Expression of p38 MAP kinase mRNA was observed in the neurons in control rats and showed no remarkable changes after axotomy in both nuclei. On the other hand, expression of p38 MAP kinase mRNA was observed in the perineuronal microglias after axotomy. The expression of p38 MAP kinase, activated p38 MAP kinase, MKK3 and ATF-2 were immunohistochemically observed in neurons of control rats in both nuclei. After axotomy, the expression of p38 MAP kinase, active and inactive, and ATF-2 in neurons were reduced in both nuclei, while expression of mRNA of p38 MAP kinase showed no reduction in neurons. These findings indicate that p38 MAP kinase is functionally regulated not by synthesis but by phosphorylation and regulates the activation of ATF-2 in neurons, and this cascade plays some role in retrograde neuronal reactions. Moreover, perineuronal microglial cells showed strong expression of p38 MAP kinase, active and inactive, after axotomy in both nuclei. These findings suggest that p38 MAP kinase is related to microglial cell reactions after axotomy.

Activating Transcription Factor 2↗
PubMed2002

Giant frontal mucocele extending into the anterior cranial fossa.

The authors report a patient with a huge frontal mucocele presenting with transient left hemiparesis. Magnetic resonance imaging and computed tomography showed the huge frontal mucocele arising from the frontal sinus extending to the anterior cranial fo ssa. Right middle cerebral artery stenosis was seen on the carotid angiography. The mucocele was treated with Killian's surgery. On the postoperative seventh day, the patient showed massive cerebrospinal fluid leakage that ceased with conservative management. The patient was discharged from the hospital without any neurological deficit. We discuss the clinical symptoms and postoperative course of the huge frontal mucocele with intracranial extension.

Aged↗
PubMed2002

High-dose amrinone is required to accelerate rewarming from deliberate mild intraoperative hypothermia for neurosurgical procedures.

BACKGROUND: Since the time available to provide the cooling and rewarming is limited during deliberate mild hypothermia, the technique to accelerate the cooling and rewarming rate of core temperature has been studied. Amrinone has been reported to accelerate the cooling rate but not the rewarming rate of core temperature during deliberate mild hypothermia. The failure of amrinone effect on the rewarming rate might be due to an insufficient dose of amrinone during hypothermic conditions. The authors therefore tested whether higher doses of amrinone can accelerate the rewarming rate of core temperature during deliberate mild hypothermia for neurosurgery. METHODS: After institutional approval and informed consent, 30 patients were randomly assigned to one of three groups. Patients in the control group (n = 10) did not receive amrinone; patients in the AMR 15 group (n = 10) received 15 microg x kg(-1) x min(-1) amrinone with a 1.0-mg/kg loading dose of amrinone at the beginning of cooling; and patients in the ReAMR group (n = 10) received 5 microg x kg(-1) x min(-1) amrinone with 1.0-mg/kg loading and reloading doses of amrinone at the beginning of cooling and rewarming, respectively. Administration of amrinone was started just after the induction of cooling and continued until the end of anesthesia. Anesthesia was maintained with nitrous oxide in oxygen, propofol, and fentanyl. After induction of anesthesia, patients were cooled, and tympanic membrane temperature was maintained at 34.5 degrees C. After completion of the main surgical procedures, patients were actively rewarmed and extubated in the operating room. RESULTS: The cooling and rewarming rates of core temperature were both significantly faster in both amrinone groups than in the control group. During the cooling and rewarming periods, forearm minus fingertip temperature gradient was significantly smaller in both amrinone groups than in the control group. During the rewarming period, heart rate and mean arterial pressure in the AMR 15 group were significantly faster and lower, respectively, than in the control group. Systemic vascular resistance in the AMR 15 group was smaller than in the control group throughout the study; on the other hand, only the value after the start of rewarming in the ReAMR group was smaller than in the control group. CONCLUSIONS: Amrinone at an infusion rate of 15 or 5 microg x kg(-1) x min(-1) with a reloading at the beginning of rewarming accelerated the rewarming rate of core temperature during deliberate mild hypothermia. This suggests that high-dose amrinone is required to accelerate rewarming from deliberate mild intraoperative hypothermia for neurosurgical procedures.

Adult↗
PubMed2002

Effects of anti-intercellular adhesion molecule-1 antibody on reperfusion injury induced by late reperfusion in the rat middle cerebral artery occlusion model.

OBJECTIVE: Inflammatory processes have been implicated in the mechanisms of reperfusion injury. The migration of leukocytes into ischemic tissue on reperfusion, which involves binding to the intercellular adhesion molecule (ICAM) of the endothelial cell, is thought to exacerbate tissue injury. The aim of the present study was to assess the effects of an anti-ICAM-1 antibody on reperfusion-induced injury after late reperfusion in a rat middle cerebral artery occlusion (MCAO) suture model. METHODS: The animals were divided into four groups: 1) Group 1 (n = 7), 6 hours of permanent MCAO; 2) Group 2 (n = 7), 3 hours of MCAO followed by 3 hours of reperfusion; 3) Group 3 (n = 6), 6 hours of permanent MCAO and treatment with anti-ICAM-1 antibody (designated 1A29, 1 mg/kg) at 2 hours after onset of MCAO; and 4) Group 4 (n = 6), 3 hours of MCAO followed by 3 hours of reperfusion and 1A29 treatment. During the experiment, regional cerebral blood flow was measured by a laser Doppler flowmetric scanning technique. At the 6-hour time point, all rats were killed, and the results of leukocyte infiltration by myeloperoxidase activity and histological analysis using 2,3,5-triphenyltetrazolium chloride staining were examined. RESULTS: Regional cerebral blood flow values before and after MCAO were not significantly different among the four groups. Regional cerebral blood flow values after reperfusion were not significantly different in the two reperfused groups. The percentage brain injury volumes in both the total and cortical areas and the myeloperoxidase activity in the latter were significantly larger in Group 2 (the reperfused group) than in the other groups (P < 0.05) but were decreased by anti-ICAM-1 antibody treatment (Group 2 versus Group 4, P < 0.05). However, there were no differences between Groups 1 and 3 without reperfusion. Myeloperoxidase activities correlated positively with infarct volumes (P < 0.01). CONCLUSION: The findings of this study demonstrate that the anti-ICAM antibody treatment is effective at inhibiting early inflammatory processes and reperfusion-induced injury caused by late arterial recanalization, which would contribute to widening the therapeutic window of thrombolytic therapy.

Animals↗
PubMed2002

Amplitudes and intrapatient variability of myogenic motor evoked potentials to transcranial electrical stimulation during ketamine/N2O- and propofol/N2O-based anesthesia.

The aim of the current study was to investigate whether there are differences in amplitudes and intrapatient variability of motor evoked potentials to five pulses of transcranial electrical stimulation between ketamine/N2O- and propofol/N2O-based anesthesia. Patients in the propofol group (n = 13) and the ketamine group (n = 13) were anesthetized with 50% N2O in oxygen, fentanyl, and 4 mg/kg/hr of propofol or 1 mg/kg/hr of ketamine, respectively. The level of neuromuscular blockade was maintained at an M-response amplitude of approximately 50% of control. Motor evoked potentials in response to multipulse transcranial electrical stimulation were recorded from the right adductor pollicis brevis muscle, and peak-to-peak amplitude and onset latency of motor evoked potentials were evaluated. To estimate intrapatient variability, the coefficient of variation (standard deviation/mean x 100%) of 24 consecutive responses was determined. Motor evoked potential amplitudes in the ketamine group were significantly larger than in the propofol group (mean, 10th-90th percentile: 380 microV, 129-953 microV; 135 microV, 38-658 microV, respectively; P <.05). There were no significant differences in motor evoked potential latency (mean +/- standard deviation: 20.9 +/- 2.2 msec and 21.4 +/- 2.2 msec, respectively) and coefficient of variation of amplitudes (median [range]: 32% [22-42%] and 26% [18-41%], respectively) and latencies (mean +/- standard deviation: 2.1 +/- 0.7% and 2.1 +/- 0.7%, respectively) between the ketamine and propofol groups. In conclusion, intrapatient variability of motor evoked potentials to multipulse transcranial stimulation is similar between ketamine/N2O- and propofol/N2O-based anesthesia, although motor evoked potential amplitudes are lower during propofol/N2O-based anesthesia than ketamine/N2O-based anesthesia.

Anesthesia↗