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Naoko Kurita

Publications and source records attributed to Naoko Kurita.

11 recordsLinked to original sources

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↗

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↗

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↗

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↗

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↗

The effects of the delta-opioid agonist SNC80 on hind-limb motor function and neuronal injury after spinal cord ischemia in rats.

Recent investigation suggested neuroprotective efficacy of a delta-opioid agonist in the brain. We investigated the effects of intrathecal treatment with a delta-opioid agonist (SNC80) on spinal cord ischemia (SCI) in rats. SCI was induced with an intraaortic balloon catheter. The animals were randomly allocated to one of the following five groups: 1) SNC80 before 9 min of SCI (SNC-9; n = 12), 2) vehicle before 9 min of SCI (V-9; n = 12), 3) SNC80 before 11 min of SCI (SNC-11; n = 10), 4) vehicle before 11 min of SCI (V-11; n = 12), or 5) sham (n = 12). SNC80 (400 nmol) or vehicle was administered 15 min before SCI. Forty-eight hours after reperfusion, hind-limb motor function was assessed by using the Basso, Beattie, Bresnahan (BBB) scale (0 = paraplegia; 21 = normal) and histological assessment of the L4 and L5 spinal segments was performed. BBB scores in the SNC-9 group were higher compared with those in the V-9 group (P < 0.05), whereas there were no differences in BBB scores between the SNC-11 and V-11 groups. There were significantly more normal neurons in the SNC-9 and SNC-11 groups than in the V-9 and V-11 groups (P < 0.05). The results indicate that intrathecal treatment with the delta-opioid agonist SNC80 can attenuate hind-limb motor dysfunction and neuronal injury after SCI in rats.

Animals↗

[Retrospective analysis of postoperative nausea and vomiting after craniotomy].

BACKGROUND: Postoperative nausea and vomiting are important complications after craniotomy. METHODS: One hundred and seventy eight patients who had undergone brain tumor resection at Nara Medical University were retrospectively divided to one of two groups; with or without PONV within 24 hours postoperatively. Variables compared between the groups include gender, age, weight, height, site of surgery (supratentorial versus infratentorial craniotomy), size of brain tumor, type of anesthesia (inhalation versus intravenous anesthesia with nitrous oxide), intraoperative fentanyl dose, duration of surgery as well as anesthesia, and intraoperative posture. RESULTS: PONV occurred in 87 patients (49%). The incidence of PONV in patients undergoing infratentorial craniotomy was significantly higher than that in patients undergoing supratentorial craniotomy (75% vs 45%, P = 0.0011). There were no significant associations between PONV and other variables analyzed. CONCLUSIONS: These results indicate that the incidence of PONV after brain tumor resection is high and infratentorial surgery is a risk factor for PONV. Strategies for the prevention of PONV after craniotomy are required.

Anesthesia, General↗

Long-term assessment of hind limb motor function and neuronal injury following spinal cord ischemia in rats.

Recent evidence suggests that brain injury caused by ischemia is a dynamic process characterized by ongoing neuronal loss for at least 14 days after ischemia. However, long-term outcome following spinal cord ischemia has not been extensively examined. Therefore, we investigated the changes of hind limb motor function and neuronal injury during a 14-day recovery period after spinal cord ischemia. Male Sprague-Dawley rats received spinal cord ischemia (n = 64) or sham operation (n = 21). Spinal cord ischemia was induced by inflation of a 2F Fogarty catheter placed into the thoracic aorta for 6, 8, or 10 minutes. The rats were killed 2, 7, or 14 days after reperfusion. Hind limb motor function was assessed with the 21-point Basso, Beattie, and Bresnahan (BBB) scale during the recovery period. The number of normal and necrotic neurons was counted in spinal cord sections stained with hematoxylin/eosin. Longer duration of spinal cord ischemia produced severer hind limb motor dysfunction at each time point. However, BBB scores gradually improved during the 14-day recovery period. Neurologic deterioration was not observed between 7 and 14 days after reperfusion. The number of necrotic neurons peaked 2 days after reperfusion and then decreased. A small number of necrotic neurons were still observed 7 and 14 days after reperfusion in some of the animals. These results indicate that, although hind limb motor function may gradually recover, neuronal loss can be ongoing for 14 days after spinal cord ischemia.

Animals↗

[Effects of amrinone in patients undergoing off-pump coronary artery bypass grafting].

We evaluated the effect of amrinone in 41 patients undergoing off-pump coronary artery bypass grafting(CABG) retrospectively. Amrinone was intravenously administered at the rate of 5 mcg.kg-1.min-1 after coronary artery anastomosis (A 1 group: 11 cases) or after induction of anesthesia(A 2 group: 13 cases). The hemodynamic variables and use of concomitant drugs were compared among A 1, A 2 and the non-amrinone group (control group: 17 cases). Hemodynamics was measured before, during, after coronary artery anastomosis, and after the chest closure. Catecholamine and vasodilator were used to maintain mean arterial pressure (> 60 mmHg) and cardiac index(> 3.0 l.min-1.m-2). Mean pulmonary artery pressure, right atrial pressure and pulmonary artery wedge pressure were significantly higher during anastomosis than before anastomosis in control and A 1 group, but no significant changes in these parameters were observed in A 2 group. In addition, these variables increased significantly after chest closure in control group, but were unchanged in A 1 and A 2 groups. Patients with concomitant use of catecholamine and vasodilator in A 2 group were fewer than those in control and A 1 group. In conclusion, in the patients undergoing off-pump CABG, infusion of amrinone was recommended from the end of the induction of anesthesia.

Aged↗

[Paradoxical embolism during MIDCAB surgery].

A 36-year-old woman underwent MIDCAB surgery. During the exposure of LAD, the right ventricular wall was injured. The bleeding was controlled by compression. After that, she developed hypotension followed by cardiac arrest. At the same time, TEE showed bubbles in all of the right ventricle. The open chest massage and epinephrine 1 mg restored the heart beat. It was thought that bubbles were brought to the right ventricle via the injured wall by the blower. A few minutes after the cardiac arrest, bubbles were detected in the left atrium by TEE. This phenomenon was suspected as transpulmonary paradoxical embolism because no cardiac shunt could be detected by TEE.

Adult↗

[Incidence and duration of hoarseness following endotracheal intubation].

The incidence and duration of hoarseness following tracheal intubation with general anesthesia were studied retrospectively from November 1998 to October 2000 in postanesthetic clinic of Nara Medical University. Total number of patients was 3977 and 37.1% of them complained of hoarseness. Most of there patients recovered within three days after surgery but in 4.2% the hoarshness persisted over ten days and in 0.7% persisted over one month after surgery. Most of these persistent hoarseness were considered to have originated from surgical procedures (such cervical, pulmonary, cardioaortic operation, etc.) and those following only tracheal intubation recovered within two months after surgery. The hoarseness decreased the satisfactory level for anesthesia in 1.0% of total patients and 12.8% of patients with persistent hoarseness. We consider that preoperative explanation and postoperative communication by anesthesiologists are important.

Adult↗