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Biomedical subjects

Masahiko Kawaguchi

Publications and source records attributed to Masahiko Kawaguchi.

At least 19 recordsLinked to original sources
PubMed2006

Delta opioid receptors stimulation with [D-Ala2, D-Leu5] enkephalin does not provide neuroprotection in the hippocampus in rats subjected to forebrain ischemia.

It has been reported that delta opioid agonists can have neuroprotective efficacy in the central nervous system. This study was conducted to test the hypothesis that a delta opioid receptor (DOR) agonist, [D-Ala2, D-Leu5] enkephalin (DADLE), can improve neuron survival against experimental forebrain ischemia in rats. Using male rats (n=125), intraperitoneal injection of DADLE (0, 0.25, 1, 4, 16 mg kg-1) was performed 30 min before ischemia. Ten minutes interval forebrain ischemia was provided by the bilateral carotid occlusion combined with hypotension (35 mm Hg) under isoflurane (1.5%) anesthesia. All animals were neurologically and histologically evaluated after a recovery period of 1 week. As histological evaluation, percentages of ischemic neurons in the CA1, CA3, dentate gyrus (DG) were measured. During the recovery period, 27 rats died because of apparent upper airway obstruction, seizure, or unidentified causes. There were no differences in the motor activity score among the groups. Ten minutes forebrain ischemia induced approximately 75, 20, and 10% neuronal death in the CA1, CA3, and DG, respectively. Any doses of DADLE did not attenuate neuronal injury in the hippocampus after ischemia. Pre-ischemic treatment of DORs agonism with DADLE did not provide any neuroprotection to the hippocampus in rats subjected to forebrain ischemia.

Analgesics, Opioid↗
PubMed2006

Effects of neuromuscular block on systemic and cerebral hemodynamics and bispectral index during moderate or deep sedation in critically ill patients.

OBJECTIVE: To investigate whether neuromuscular block can affect bispectral index (BIS) or cerebral hemodynamics under moderate or deep sedation produced by propofol. DESIGN AND SETTING: Prospective, controlled study in a university hospital affiliated intensive care unit. PATIENTS: Seventeen surgical patients undergoing elective esophagectomy. INTERVENTIONS: After stabilization with either light or deep sedation we investigated whether the BIS, electromyographic activity (EMG), or cerebral and systemic hemodynamic parameters were affected by administration of muscle relaxant. MEASUREMENTS AND MAIN RESULTS: Neuromuscular block reduced the BIS during moderate sedation but not during deep sedation although the EMG at both levels of sedation was significantly reduced. No positive effects of neuromuscular block on cerebral hemodynamics were obtained with monitoring of regional cerebral oxygen saturation and middle cerebral artery blood velocity; however, significant effects on systemic hemodynamic parameters were observed only at moderate propofol sedation. The values of BIS and systemic hemodynamic variables with moderate sedation were also very similar to those with deep sedation and neuromuscular block although these values differed without neuromuscular block. CONCLUSIONS: Neuromuscular block altered the BIS score in moderately sedated patients but not in deeply sedated patients although cerebral hemodynamics was not affected by neuromuscular block during either moderate or deep sedation. Muscular relaxant also enhanced cardiovascular stability with moderate sedation. These results suggest that level of consciousness may be decreased by neuromuscular block during moderate sedation but not affected during deep sedation.

Aged↗
PubMed2006

Effects of increasing concentrations of propofol on jugular venous bulb oxygen saturation in neurosurgical patients under normothermic and mildly hypothermic conditions.

BACKGROUND: Recent evidence suggested that propofol can deteriorate the cerebral oxygen balance compared with inhalational anesthetics. However, dose-related influences of propofol on cerebral oxygen balances were not clearly investigated. In the current study, the authors investigated the effects of increasing concentrations of propofol on jugular venous bulb oxygen saturation (Sj(O2)) in neurosurgical patients under normothermic and mildly hypothermic conditions. METHODS: After institutional approval and informed consent were obtained, 30 adult patients undergoing elective craniotomy were studied. Patients were randomly allocated to either normothermic or hypothermic group (n = 15 in each group). In the normothermic and hypothermic groups, tympanic membrane temperature was maintained at 36.5 degrees and 34.5 degrees C, respectively. Sj(O2) was measured at predicted propofol concentrations of 3, 5, and 7 microg/ml using a target-controlled infusion system in both groups. RESULTS: At a predicted propofol concentration of 3 microg/ml, there were no significant differences in Sj(O2) values between the normothermic and hypothermic groups, although the incidence of desaturation (Sj(O2) < 50%) was significantly higher in the normothermic group than in the hypothermic group (30% vs. 13%; P < 0.05). Sj(O2) values and the incidence of desaturation remained unchanged during the changes in predicted propofol concentration from 3 to 7 microg/ml both in the normothermic and hypothermic groups. CONCLUSION: The results indicated that the increasing concentrations of propofol did not affect Sj(O2) values in neurosurgical patients under normothermic and mildly hypothermic conditions.

Adult↗
PubMed2006

Reevaluation of gray and white matter injury after spinal cord ischemia in rabbits.

BACKGROUND: Although gray matter injury has been well characterized, the available data on white matter injury after spinal cord ischemia (SCI) in rabbits are limited. The current study was conducted to investigate the evolution of ischemia induced injury to gray and white matter and to correlate this damage to hind-limb motor function in rabbits subjected to SCI. METHODS: Thirty-eight rabbits were randomly assigned to 24-h, 4-day, or 14-day reperfusion groups or a sham group (n = 9 or 10 per group). SCI was induced by occlusion of the infrarenal aorta for 16 min. Hind-limb motor function was assessed using the Tarlov scale (0 = paraplegia, 4 = normal). The gray matter damage was assessed on the basis of the number of normal neurons in the anterior spinal cord. White matter damage was assessed on the basis of the extent of vacuolation and accumulation of amyloid precursor protein immunoreactivity. RESULTS: Tarlov scores gradually decreased and reached a nadir 14 days after reperfusion. There were no significant differences in the number of normal neurons among the 24-h, 4-day, and 14-day groups. The extent of vacuolation, expressed as a percent of total white matter area, was significantly greater in the 4-day and 14-day groups in comparison with the sham group. By contrast, there was no difference in vacuolation between the sham and 24-h groups. Amyloid precursor protein immunoreactivity was greater in the 4-day and 14-day groups. CONCLUSION: The results in the current study show that SCI induced white matter injury as well as gray matter injury in a rabbit model of SCI. The time course for 14 days after reperfusion may differ among the gray and white matter damages and hind-limb motor function in rabbits subjected to SCI.

Amyloid beta-Protein Precursor↗
PubMed2006

The effects of xenon on myogenic motor evoked potentials in rabbits: a comparison with propofol and isoflurane.

We compared the effects of xenon on myogenic motor evoked potentials (MEPs) with those of propofol and isoflurane in rabbits under ketamine/fentanyl anesthesia. Thirty animals were randomly allocated to one of 3 groups (n = 10 in each group). In the propofol group, propofol was administered at a rate of 0.4 mg x kg(-1) x min(-1) (small) and 0.8 mg x kg(-1) x min(-1) (large). In the isoflurane group, isoflurane was administered at 0.8% (small) and 1.6% (large). In the xenon group, xenon was administered at 35% (small) and 70% (large). Myogenic MEPs in response to stimulation with single pulse and a train of 5 pulses were recorded from the soleus muscle before, during (at small and large doses), and after the administration of each anesthetic. With single-pulse stimulation, MEPs were recorded in 90% and 50% of animals at small and large doses of xenon, respectively, and MEP amplitudes in the xenon and isoflurane groups were significantly lower compared with those in the propofol group. With train pulse stimulation, MEPs were recorded in 100% and 90% of animals at small and large doses of xenon, respectively, and a reduction in MEP amplitudes by xenon was more prominent than by propofol but less than isoflurane at large doses. These results suggest that MEP recording may be feasible under xenon anesthesia if multipulse stimulation is used, although xenon has suppressive effects on myogenic MEPs.

Anesthetics, Inhalation↗
PubMed2006

[Motor evoked potentials].

Motor dysfunction following spinal surgery and thoracoabdominal aortic surgery remain as one of their devastating complications. Since the development of postoperative motor dysfunction can deteriorate quality of life of patients, the prevention of such complications is an important clinical challenge. Recently, advances in stimulation technique using multipulse made intraoperative monitoring of functional integrity of motor pathways possible by recording myogenic motor evoked potentials (MEPs). However, myogenic MEPs can be affected by most of anesthetic agents and muscle relaxants. Anesthesiologists are therefore required to properly understand MEPs and to manage anesthesia carefully. We summarize the methods for monitoring of myogenic MEPs and anesthetic techniques during intraoperative MEP monitoring.

Anesthesia↗
PubMed2005

Neuroprotective effects of anesthetic agents.

Ischemic neuronal injury is characterized by early death mediated by excitotoxicity and by delayed death caused by apoptosis. Current evidence indicates that volatile agents, barbiturates, and propofol can protect neurons against ischemic injury caused by excitotoxicity. In the case of volatile agents and propofol, neuroprotection may be sustained if the ischemic insult is relatively mild; however, with moderate to severe insults, this neuronal protection is not sustained after a prolonged recovery period. This suggests that volatile agents and propofol do not reduce delayed neuronal death caused by apoptosis. The long-term effects of barbiturates on ischemic cerebral injury are not yet defined. Cerebral ischemia is characterized by continued neuronal loss for a long time after the initial ischemic insult. Therefore, in investigations of cerebral ischemia, the duration of the recovery period should be taken into consideration in the analysis of the neuroprotective effects of anesthetic agents. A combination of different approaches that target specific stages of the evolution of ischemic injury may be required for sustained neuroprotection.

Anesthetics↗
PubMed2005

Tetanic stimulation of the peripheral nerve before transcranial electrical stimulation can enlarge amplitudes of myogenic motor evoked potentials during general anesthesia with neuromuscular blockade.

BACKGROUND: Neuromuscular blockade can suppress myogenic motor evoked potentials (MEPs). The authors hypothesized that tetanic stimulation (TS) of the peripheral nerve before transcranial stimulation may enhance myogenic MEPs during neuromuscular blockade. In the current study, the authors evaluated MEP augmentations by TS at different levels of duration, posttetanic interval, neuromuscular blockade, and stimulus intensity. METHODS: Thirty-two patients undergoing propofol-fentanyl-nitrous oxide anesthesia were examined. Train-of-five stimulation was delivered to C3-C4, and MEPs were recorded from the abductor hallucis muscle. In study 1, TS with a duration of 1, 3, or 5 s was delivered at 50 Hz to the tibial nerve 1, 3, or 5 s (interval) before transcranial stimulation, and the effects of TS on MEP amplitude were evaluated. In study 2, TS-induced MEP augmentations were evaluated at the neuromuscular blockade level (%T1) of 50% or 5%. In study 3, MEP augmentations by TS at stimulus intensities of 0, 5, 25, and 50 mA were evaluated. RESULTS: The application of TS significantly enlarged the amplitudes of MEPs at the combinations of duration (3, 5 s) and interval (1, 3, 5 s) compared with those without TS. TS-induced MEP augmentations were similarly observed at %T1 of both 50% and 5%. TS-induced MEP augmentations were observed at stimulus intensities of 25 and 50 mA. CONCLUSIONS: The results indicate that TS of the peripheral nerve before transcranial stimulation can enlarge the amplitude of MEPs during general anesthesia with neuromuscular blockade. TS of the peripheral nerve can be intraoperatively applied as a method to augment myogenic MEP responses.

Aged↗
PubMed2005

Effects of nitrous oxide on spike activity on electrocorticogram under sevoflurane anesthesia in epileptic patients.

We sought to investigate the effects of nitrous oxide on intraoperative electrocorticogram (ECoG) spike activities in 11 patients with intractable epilepsy. Grid electrodes were placed on the brain surface, and ECoG was recorded under the following conditions: 1.5 minimal alveolar anesthetic concentration (MAC) sevoflurane without nitrous oxide and 1.5 MAC sevoflurane with 50% nitrous oxide. The number of spikes for 5 minutes and the percentage of leads with spikes of total leads measured were assessed in each condition. The median numbers (25-75th) of spikes without and with nitrous oxide were 127 (87-368) and 61 (43-247), respectively. The numbers of spikes with nitrous oxide were significantly lower than those without nitrous oxide (P<0.05). The median percentages of leads with spikes without and with nitrous oxide were 68 (25-81) and 61 (28-70), respectively, and there were no significant differences in percentages of leads with spikes between the conditions. These results indicate that nitrous oxide attenuated the frequency of spikes on ECoG in epileptic patients, although it did not affect the extent of areas with spike activity.

Adult↗
PubMed2005

Evaluation of relatively low dose of oral transmucosal ketamine premedication in children: a comparison with oral midazolam.

BACKGROUND: Oral Transmucosal ketamine (lollipop) has been shown to be an effective, harmless preoperative medication for children. However, its efficacy was not compared with commonly used premedication drugs. We, therefore, compared the efficacy of oral transmucosal ketamine with oral midazolam for premedication in children. METHODS: Fifty-five children (2-6 years of age) were randomized to receive orally either a lollipop containing 50 mg of ketamine (the group K; n = 27) or syrup containing 0.5 mg.kg(-1) of midazolam (the group M; n = 28) before minor surgery. A five points-sedation score (1 = asleep to 5 = agitated; scores 2 and 3 were defined as 'effective') on arrival in the operating room and a three points-acceptance score of separation from the parents and a three points-mask cooperation score at induction of anesthesia (1 = easy to 3 = markedly resistant; score 3 was defined as 'poor') were used. RESULTS: Sedation scores in group K were significantly higher than those in group M (P = 0.012), and the incidence of 'effective' in sedation was significantly lower in group K than in group M (P = 0.036). The incidence of 'poor' at separation from the parents and for mask cooperation was significantly higher in group K than in group M (P = 0.017, P = 0.019, respectively). CONCLUSION: These results indicate that a relatively low dose of oral transmucosal ketamine premedication provides no benefits over oral midazolam in children.

Administration, Buccal↗
PubMed2005

An evaluation of white matter injury after spinal cord ischemia in rats: a comparison with gray matter injury.

We quantitatively assessed both gray and white matter injury after spinal cord ischemia in rats, and the relationship between the magnitude of gray and white matter injury was determined. Twenty-five male rats were anesthetized with isoflurane, and spinal cord ischemia (SCI) was induced by balloon intraaortic occlusion combined with hypotension. The animals were randomly allocated to one of the following three groups: animals with SCI for 12 min (SCI-12; n = 8), 15 min (SCI-15; n = 9), or those with sham operation (n = 8). Twenty-four hours after reperfusion, hindlimb motor function was assessed using the Basso-Beattie-Bresnahan scale scoring. Gray matter damage was assessed on the basis of the number of normal neurons in the ventral horn. White matter damage was assessed on the basis of the extent of vacuolation and amyloid precursor protein immunoreactivity in the ventral and ventrolateral white matter. There were significantly less normal neurons in the SCI-15 group compared with those in the SCI-12 and sham groups (P < 0.05). There was a significant positive correlation between the Basso-Beattie-Bresnahan scores and the number of normal neurons. The percentages of vacuolation areas in the SCI-15 group were significantly larger compared with those in the SCI-12 and sham groups (30% +/- 10% versus 9% +/- 7%, 0% +/- 0%, P < 0.05). Immunohistochemical analysis revealed increased amyloid precursor protein immunoreactivity in the swollen axons, especially in the SCI-15 group. There was a significant negative correlation between the number of normal neurons and percentages of vacuolation areas. These results indicate that both gray and white matter were injured after SCI in rats and the degree of white mater injury was correlated with the severity of gray matter injury after a relatively short recovery period.

Amyloid beta-Protein Precursor↗
PubMed2005

The effects of sevoflurane and hyperventilation on electrocorticogram spike activity in patients with refractory epilepsy.

UNLABELLED: We investigated the effects of sevoflurane and hyperventilation on intraoperative electrocorticogram (ECoG) spike activity in 13 patients with intractable epilepsy. Grid electrodes were placed on the brain surface and ECoG was recorded under the following conditions: 1) 0.5 minimal alveolar anesthetic concentration (MAC) sevoflurane, 2) 1.5 MAC sevoflurane, and 3) 1.5 MAC sevoflurane with hyperventilation. The number of spikes per 5 min and the percentage of leads with spikes were assessed in each condition. In 4 patients with chronically implanted-subdural electrodes, the leads with seizure onset and with spikes during the interictal periods in the awake state were compared with those during sevoflurane anesthesia at 0.5 MAC and 1.5 MAC. The number of spikes and the percentage of leads with spikes were significantly more under 1.5 MAC sevoflurane anesthesia compared with those under 0.5 MAC sevoflurane (P < 0.05). The induction of hyperventilation significantly increased the number of spikes and percentage of leads with spikes (P < 0.05). With 0.5 MAC sevoflurane, the leads with spikes were similar to those at seizure onset in the awake state, whereas with 1.5 MAC sevoflurane, spikes were similar to those occurring during interictal periods in the awake state. These results indicate that sevoflurane and hyperventilation can affect the frequency and extent of ECoG spike activity in patients with intractable epilepsy. Careful attention should be paid to the concentration of sevoflurane used and ventilatory status when intraoperative EcoG is used to localize epileptic lesions. IMPLICATIONS: Electrocorticogram can be used to define the location and extent of epileptic foci during epilepsy surgery. However, electrocorticogram can be affected by anesthetic technique. The present study found that sevoflurane concentration and hyperventilation affected the frequency and the extent of electrocorticogram spike activity in epileptic patients.

Adult↗
PubMed2004

Cyclooxygenase-2 expression in Schwann cells and macrophages in the sciatic nerve after single spinal nerve injury in rats.

Recent evidence suggested that cyclooxygenase-2 (COX-2) expression in the peripheral nerve early after nerve injury might be involved in the development of neuropathic pain. Although previous investigators have demonstrated that COX-2 is expressed in peripheral nerve at a late phase (2-4 weeks) after nerve injury, COX-2 up-regulation at an early phase after nerve injury has not been determined. Using immunohistochemistry, we observed biphasic increases of COX-2 expression after L5 single spinal nerve injury. The first increment of COX-2 positive cells was noted 1 day after nerve injury and these cells co-expressed the Schwann cell marker S-100. A second increment was noted after 7-14 days and these cells co-expressed the macrophage marker ED-1. These results suggested that the cellular sources of COX-2 expression might be different between the early and late phases after nerve injury.

Animals↗
PubMed2004

Peri-sciatic administration of indomethacin early after nerve injury can attenuate the development of tactile allodynia in a rat model of L5 single spinal nerve injury.

To clarify the role of cyclooxygenase in the peripheral nerve on the development of neuropathic pain, we investigated the effects of peri-sciatic administration of indomethacin on the development of allodynia in a model of L5 single spinal nerve injury. Peri-sciatic administration of indomethacin (1 mg/kg) was performed 3, 24, or 72 h after nerve injury (n=6/each). In rats with indomethacin 3 or 24 h after nerve injury, ipsi-lateral paw withdrawal thresholds 7-35 days after nerve injury were significantly higher compared with those in the control group (n=6: without peri-sciatic treatment) (P<0.05). However, such efficacy was no longer apparent when indomethacin was administered 72 h after nerve injury. These results suggest that peri-sciatic administration of indomethacin early (less than 24 h) after nerve injury can attenuate the development of allodynia.

Animals↗
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↗
PubMed2004

Intravenous administration of flurbiprofen does not affect cerebral blood flow velocity and cerebral oxygenation under isoflurane and propofol anesthesia.

UNLABELLED: Flurbiprofen, a nonsteroidal antiinflammatory drug (NSAID), has been used to treat rheumatic and osteoarthritic pain and to reduce postoperative pain. Although other NSAIDs, such as indomethacin, reduce cerebral blood flow (CBF), the effect of flurbiprofen on CBF is unknown. In the present study, we investigated the effects of flurbiprofen on cerebral blood flow velocity (CBFV) and cerebral oxygenation under isoflurane or propofol anesthesia. Forty-eight patients undergoing orthopedic or abdominal surgery were enrolled. Patients were randomly allocated to receive either propofol (target control infusion: target site effect concentration 3 microg/mL) or isoflurane (1 MAC) for maintenance of anesthesia. In each group (n = 12), 1 mg/kg of flurbiprofen (PROP-F and ISO-F groups) or 0.1 mL/kg saline (PROP-S and ISO-S groups) was administered i.v. for 5 min. During and after the administration of flurbiprofen or saline, cerebral oxygenation variables (tissue oxygen index [TOI], total hemoglobin change [Delta cHb], oxygenated hemoglobin changes [Delta O(2)Hb], and deoxygenated hemoglobin changes [Delta HHb]), and middle cerebral artery flow velocity (Vmca) were measured using a cerebral oximeter (NIRO 300) and transcranial Doppler, respectively, from 5 min before study drug administration to 60 min post-administration. Before the administration of flurbiprofen, control values of TOI in the ISO-S and ISO-F groups were significantly higher than those in the PROP-S and PROP-F groups, respectively (ISO-S versus PROP-S, 67% +/- 4% versus 60% +/- 7%; IOS-F versus PROP-F, 69% +/- 4% versus 63% +/- 8%; P < 0.05). However, values of TOI, Delta cHb, Delta O(2)Hb, Delta HHb, and Vmca did not change significantly during and after the administration of flurbiprofen under propofol or isoflurane anesthesia, and these values were similar to those during and after the administration of saline in the same anesthesia group. These data indicate that flurbiprofen does not affect CBFV and cerebral oxygenation under propofol or isoflurane anesthesia. IMPLICATIONS: Indomethacin, a nonsteroidal antiinflammatory drug (NSAID), has been demonstrated to reduce cerebral blood flow (CBF). The CBF effects of flurbiprofen, another NSAID, are unknown. We investigated cerebral blood flow velocity (CBFV) and cerebral oxygenation during and after the administration of flurbiprofen under isoflurane and propofol anesthesia. We found that flurbiprofen had no effect on CBFV and cerebral oxygenation.

Adult↗