Biomedical subjects

Kenji Takeda

Publications and source records attributed to Kenji Takeda.

18 recordsLinked to original sources

PubMed2006

Major histocompatibility complex haplotype is associated with postherpetic pain in mice.

BACKGROUND: Postherpetic neuralgia is one of the major complications of herpes zoster caused by the reactivation of varicella-zoster virus and is characterized by severe pain. The authors previously showed the association of a human major histocompatibility complex (MHC) haplotype with postherpetic neuralgia. This study was performed to experimentally confirm the role of MHC haplotype in the development of postherpetic pain using a mouse model of postherpetic pain, which corresponds to postherpetic neuralgia. METHODS: BALB/c mice (MHC haplotype: H-2), C57BL/6 mice (MHC haplotype: H-2), and BALB/b mice, a congenic BALB/c strain with H-2, were used. Herpes simplex virus type I was transdermally inoculated on the hind paw. Unilaterally zosteriform skin lesion and pain-related responses (acute herpetic pain) were caused, and some mice showed pain-related responses (postherpetic pain) after the cure of skin lesions. Herpes simplex virus type I antigen and CD3-positive cells were immunostained in the dorsal root ganglion in the acute phase. RESULTS: The incidence (78%) of postherpetic pain in C57BL/6 mice was significantly higher than that (35%) in BALB/c mice (P = 0.004, odds ratio = 6.7). Furthermore, the incidence of postherpetic pain in BALB/b (H-2) was similar to that in C57BL/6. Herpes simplex virus type I antigen-positive cells were less in the dorsal root ganglion of C57BL/6 mice than that of BALB/c mice. CD3-positive T cells were more in the dorsal root ganglion of C57BL/6 mice than BALB/c mice. CONCLUSIONS: These results suggest that the MHC haplotype (H-2) is involved in the incidence of postherpetic pain, and CD3-positive T cells may play a role in its pathogenesis.

Animals↗

PubMed2005

Heavy photon states in photonic chains of resonantly coupled cavities with supermonodispersive microspheres.

We propose and demonstrate a "bottom-up" approach to constructing photonic structures for photon manipulation. Supermonodispersive polymer microspheres are used as building blocks and a size uniformity better than 0.05% could be obtained by sorting the spheres using spectroscopic methods. The spheres are positioned in a V groove on a silicon substrate and form a photonic chain with resonant coupling of the optical whispering-gallery modes. Photonic band modes are clearly observed in fluorescence and resonant scattering spectra, and an excellent agreement with a tight-binding model calculation is found. Heavy photon states and a group index as high as 40 are obtained.

Journal Article↗

PubMed2005

Anti-allodynic and anti-hyperalgesic effects of nociceptin receptor antagonist, JTC-801, in rats after spinal nerve injury and inflammation.

The effects of nociceptin/orphanin FQ (N/OFQ) peptide receptor antagonist JTC-801 on allodynia and hyperalgesia were examined in rats in order to explore the involvement of N/OFQ system in these pathological pain states. Tactile allodynia induced by L5/L6 spinal nerve ligation was reversed by both systemic (3-30 mg/kg) and spinal (22.5 and 45 pg) JTC-801 in a dose-dependent manner. Concerning hyperalgesia induced by formalin injection into the hindpaw, JTC-801 dose-dependently suppressed the second phase, but not the first phase, of the licking behavior. Furthermore, systemic JTC-801 reduced Fos-like immunoreactivity in the dorsal horn of the spinal cord (laminae I/II). In conclusion, N/OFQ receptor antagonist JTC-801 exerted anti-allodynic and anti-hyperalgesic effects in rats, suggesting that N/OFQ system might be involved in the modulation of neuropathic pain and inflammatory hyperalgesia.

Aminoquinolines↗

PubMed2005

Role for cyclooxygenase 2 in the development and maintenance of neuropathic pain and spinal glial activation.

BACKGROUND: Lines of evidence have indicated that cyclooxygenase 2 plays a role in the pathophysiology of neuropathic pain. However, the site and mechanism of its action are still unclear. Spinal glia has also been reported to mediate pathologic pain states. The authors evaluated the effect of continuous intrathecal or systemic cyclooxygenase-2 inhibitor on the development and maintenance of neuropathic pain and glial activation in a spinal nerve ligation model of rats. METHODS: Continuous intrathecal infusion of meloxicam (32 or 320 mug . kg . day) or saline was started immediately after L5-L6 spinal nerve ligation. Mechanical allodynia and thermal hyperalgesia were evaluated on days 4 and 7 postoperatively. Spinal astrocytic activation was evaluated with glial fibrially acidic protein immunoreactivity on day 7. In other groups of rats, continuous intrathecal meloxicam was started 7 days after spinal nerve ligation, and effects on established neuropathic pain and glial activation were evaluated. Last, effects of continuous systemic meloxicam (16 mg . kg . day) on existing neuropathic pain and glial activation were examined. RESULTS: Intrathecal meloxicam prevented the development of mechanical allodynia and thermal hyperalgesia induced by spinal nerve ligation. It also inhibited spinal glial activation responses. In contrast, when started 7 days after the nerve ligation, intrathecal meloxicam did not reverse established neuropathic pain and glial activation. Systemic meloxicam started 7 days after ligation partially reversed neuropathic behaviors but not glial activation. CONCLUSIONS: Spinal cyclooxygenase 2 mediates the development but not the maintenance of neuropathic pain and glial activation in rats. Peripheral cyclooxygenase 2 plays a part in the maintenance of neuropathic pain.

Animals↗

PubMed2005

The electrical properties of epidural catheters: what are the requirements for nerve stimulation guidance?

We designed the present study to investigate the electrical resistance of commercially available epidural catheters and to search for products and procedures suitable for nerve stimulation-guided insertion. Four types of epidural catheters were evaluated: 2 nonwire-reinforced catheters (19-gauge and 20-gauge nylon) and 2 wire-reinforced catheters (19-gauge without stylet and 20-gauge with stylet). The resistance of a catheter was calculated from the voltage level proportional to the fixed resistance in series circuit. In case of physiologic saline, the resistance of nonreinforced catheters was more than 700 kOmega, whereas the wire-reinforced catheter was 14.4 +/- 0.20 kOmega without stylet and 10.1 +/- 0.42 kOmega with stylet. When the stylet was passed through a 20-gauge nylon catheter, the resistance decreased to 49.2 +/- 1.96 kOmega. When catheters were primed with 10% hypertonic saline, the resistance of both nonreinforced catheters decreased by one third compared with physiologic saline. The electrical resistance of the saline-filled epidural catheters significantly differed among products tested. We conclude that epidural catheterization that is guided by electrical stimulation should be performed only with catheters equipped with spiral stainless steel wire reinforcement or with a stainless steel stylet.

Anesthesia, Epidural↗

PubMed2005

Statin response and pharmacokinetics variants.

Despite statin therapy being effective in the primary and secondary prevention of coronary heart disease, the benefit of treatment varies between individuals. Interindividual variations in pharmacokinetics play a central role in the cause of variability of drug disposition, and, in turn, the drug's clinical efficacy. Exploring genetic variations that influence pharmacokinetics may lead clinicians to apply the most efficient and safe drug therapy. So far, variants in eight candidate genes related to pharmacokinetics of statins have been investigated as the potential determinant of drug responsiveness or adverse event risk. All reported data remains inconclusive, but it has been suggested that combined analysis of more than two different polymorphisms, or a combination of genetic association and studies using in vitro recombinant expression techniques, may be more informative in predicting the specific phenotype of a genetic variant. Future studies using these approaches could provide more striking evidence, which may be sufficient to justify genetic analysis regarding pharmacokinetic variants in the clinical practice of statin therapy.

Cytochrome P-450 Enzyme System↗

PubMed2005

[General anesthesia for a patient with Noonan's syndrome and long-term antidepressant therapy].

Noonan's syndrome is associated with cardiovascular, spinal and airway abnormalities. We experienced general anesthesia for a patient with Noonan's syndrome and long-term antidepressant therapy. A 42-year-old man was scheduled for radical operation for ventral hernia. He had been diagnosed as Noonan's syndrome by his facial and spinal abnormalities. He was intubated under bronchofiberscopy for his previous general anesthesia. He had received amitriptyline 50 mg daily for ten years. Anesthesia was induced with midazolam 3 mg, fentanyl 50 microg, droperidol 1.25 mg. He was intubated under bronchofiberscopy after topical lidocaine 400 mg application. Then thiopental 125 mg and sevoflurane 0.4% was administered. Blood pressure decreased after intubation to 70/40 mmHg, which was resistant to ephedrine 10 mg. After starting surgery, blood pressure increased to 100/70 mmHg and was stable until the end of surgery. This patient presented a problem of difficult intubation as Noonan's syndrome and had a history of a long-term use of antidepressant, which might induce sympathomimetic resistant hypotension.

Adult↗

PubMed2004

General anesthetics inhibit the nitrous-oxide-induced activation of corticotropin releasing factor containing neurons in rats.

The activation of intracerebral corticotropin releasing factor (CRF) system is involved in nitrous oxide analgesia. We evaluated the effect of general anesthetics on nitrous-oxide-induced CRF activation and antinociception. Male Sprague-Dawley rats inhaled isoflurane (0%, 0.6%, 1.0% and 1.5%) or were administered with intravenous propofol (0, 0.1 and 0.2 mg/kg/min), with or without 75% nitrous oxide inhalation, for 90 min. The brain was fixed with fixative, and brain sections, including the paraventricular nucleus of the hypothalamus, were double immunostained with c-Fos and CRF antibodies to assess the activation of CRF-containing neurons. In other groups of rats, the effect of propofol on nitrous oxide antinociception was evaluated with tail flick latency tests. Both inhaled isoflurane and intravenous propofol inhibited nitrous-oxide-induced activation of CRF neurons, suggesting that these general anesthetics may inhibit one of the analgesic mechanisms of nitrous oxide. Indeed, propofol inhibited the antinociceptive action of nitrous oxide, as evaluated with tail flick latencies (TFL).

Anesthetics, General↗

PubMed2004

Ischemic preconditioning and morphine attenuate myocardial apoptosis and infarction after ischemia-reperfusion in rabbits: role of delta-opioid receptor.

We examined whether ischemic preconditioning (IPC) attenuates ischemia-reperfusion injury, in part, by decreasing apoptosis and whether the delta-opioid receptor (DOR) plays a pivotal role in the regulation of apoptosis. Rabbits were subjected to 30-min coronary artery occlusion (CAO) and 180 min of reperfusion. IPC was elicited with four cycles of 5-min ischemia and 10-min reperfusion before CAO. Morphine (0.3 mg/kg iv) was given 15 min before CAO. Naloxone (Nal; 10 mg/kg iv) and naltrindole (Nti; 10 mg/kg iv), the respective nonselective and selective DOR antagonists were given 10 min before either morphine or IPC. Infarct size (%risk area) was reduced from 46 +/- 3.8 in control to 11.6 +/- 1.0 in IPC and 19.5 +/- 3.8 in the morphine group (means +/- SE; P < 0.001 vs. control). Nal blocked the protective effects of IPC and morphine, as shown by the increase in infarct size to 38.6 +/- 7.2 and 44.5 +/- 1.8, respectively. Similarly, Nti blocked IPC and morphine-induced protection. The percentage of apoptotic cells (revealed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) decreased in IPC (3.6 +/- 1.9) and morphine groups (5.2 +/- 1.2) compared with control group (12.4 +/- 1.6; P < 0.001). Nti pretreatment increased apoptotic cells 11.2 +/- 2.2% in IPC and 12.1 +/- 0.8% in morphine groups. Nal failed to block inhibition of apoptosis in the IPC group (% of cells: 5.7 +/- 1.3 vs. 3.6 +/- 1.9 in IPC alone; P > 0.05). These results were also confirmed by nucleosomal DNA laddering pattern. We conclude that IPC reduces lethal injury, in part, by decreasing apoptosis after ischemia-reperfusion and activation of the DOR may play a crucial role in IPC or morphine-induced myocardial protection.

Analgesics, Opioid↗

PubMed2004

Transient glucose deprivation causes upregulation of heme oxygenase-1 and cyclooxygenase-2 expression in cardiac fibroblasts.

Transient glucose deprivation (TGD) has been shown to induce a resistance to a subsequent ischemia and reperfusion injury in the heart. Induction of cyclooxygenase-2 (COX-2) and heme oxygenase-1 (HO-1) is known to mediate the powerful defensive adaptation of the heart against oxidative stress. In this study, we found that a 30-min incubation in the absence of glucose resulted in a rapid increased expression of COX-2 and HO-1 in cardiac fibroblasts as examined by real-time quantitative polymerase chain reaction (PCR) and western blot analysis. Interestingly, TGD increased the generation of reactive oxygen species (ROS) and caused the transient phosphorylation of p38 mitogen-activated protein kinase (MAPK) as well as the translocation of protein kinase C (PKC)- from the cytosolic to the membrane fraction. However, no significant change in the distribution of PKC-delta isoform was observed compared with the control. Pretreatment of the cells with an antioxidant, N-acetylcysteine (NAC), resulted in the inhibition of p38 MAPK phosphorylation and PKC- translocation during TGD. In addition, the induction of COX-2 and HO-1 expression by TGD was prevented by pretreatment with NAC or SB203580, a p38 MAPK inhibitor. Surprisingly, pretreatment with chelerythrine, an inhibitor of PKC, strongly augmented the HO-1 mRNA expression but blocked the COX-2 mRNA induction by TGD. These results demonstrate that briefly removing glucose from cultured cardiac fibroblasts induces COX-2 and HO-1 expression via generation of ROS and p38 MAPK phosphorylation, while the translocation of PKC- to the membrane fraction may participate in the induction of COX-2 but not in the HO-1 expression.

Alkaloids↗

PubMed2004

Effect of methylprednisolone on neuropathic pain and spinal glial activation in rats.

BACKGROUND: Basic data are lacking regarding the efficacy and mechanisms of action of corticosteroids in neuropathic pain. Because recent studies indicate that spinal glial activation mediates the pathologic pain states, the authors sought to determine the effects of systemic and intrathecal methylprednisolone on the development and maintenance of neuropathic pain and spinal glial activation in a rat model. METHODS: Rats were anesthetized, and L5 and L6 spinal nerves were tightly ligated. Then, continuous infusion of systemic (4 mg x kg(-1) x day(-1)) or intrathecal (80 microg x kg(-1) x day(-1)) methylprednisolone or saline was started. Mechanical allodynia and thermal hyperalgesia were evaluated on days 4 and 7 postoperatively with von Frey and Hargreaves tests, respectively. Spinal astrocytic activation was evaluated with glial fibrillary acidic protein immunoreactivity on day 7. In other groups of rats, continuous 3-day treatment with intrathecal methylprednisolone or saline was started 7 days after spinal nerve ligation, when neuropathic pain had already developed. Behavioral tests and immunostaining were performed up to 3 weeks after the treatment. RESULTS: Spinal nerve ligation induced mechanical allodynia and thermal hyperalgesia on days 4 and 7 postoperatively. Glial fibrillary acidic protein immunoreactivity was remarkably enhanced on day 7. Both systemic and intrathecal methylprednisolone inhibited the development of neuropathic pain states and glial activation. Three-day treatment with intrathecal methylprednisolone reversed existing neuropathic pain state and glial activation up to 3 weeks after the treatment. CONCLUSION: : Systemic and intrathecal methylprednisolone inhibited spinal glial activation and the development and maintenance of a neuropathic pain state in a rat model of spinal nerve ligation.

Animals↗

PubMed2004

Pretreatment with tyrosine kinase inhibitor attenuates the reduction of apoptosis 24 h after ischemic preconditioning.

We investigated whether ischemic preconditioning (PC) attenuates ischemia/reperfusion-induced injury in part by decreasing apoptosis and whether tyrosine kinase (TK) can regulate the signaling pathway leading to apoptosis in delayed cardioprotection. Six groups of rabbits were studied in the early phase (EP) and in the delayed phase (DP): (1) sham-operated control animals were received vehicle only (Veh-sham); (2) rabbits that received I.V. genistein (a nonspecific TK inhibitor) 10 min before ischemia (Gen-sham); (3) rabbits that received I.V. daidzein (an inactive structural analog of genistein) 10 min before ischemia (Dzn-sham); (4) rabbits preconditioned with 4 cycles of 5-min occlusion of left anterior descending coronary artery (LAD) and 10-min reperfusion (PC); (5) rabbits that received I.V. genistein, 10 min before PC (Gen-PC); (6) rabbits that received I.V. daidzein 10 min before PC (Dzn-PC). All rabbits underwent 30-min ischemia followed by 180-min reperfusion. Infarct size in the PC, Gen-PC, and Dzn-PC groups in the EP was significantly (p < 0.0001) reduced relative to controls Gen and Dzn. Delayed cardioprotection was blocked significantly (p < 0.0001) by genistein. In the EP, apoptosis was significantly (p < 0.0001) decreased in PC, Gen-PC, and Dzn-PC groups relative to controls Gen and Dzn. In the DP, a reduction of apoptosis was not seen in the Gen-PC group. This study suggests that PC reduces ischemic injury in part by decreasing apoptosis after ischemia/reperfusion and also that TK phosphorylation is involved in the signal transduction cascade leading to the decline of apoptosis in the DP.

Animals↗

PubMed2004

Imbalance of sex hormone levels in men with coronary artery disease.

OBJECTIVE: Sex hormones are thought to play a key role in atherogenesis, but the available evidence is inconclusive, partly because of a lack of accuracy in measurement. The aim of the study was to investigate the potential role of sex hormones in coronary atherosclerosis. METHODS: We prospectively applied a simple highly-sensitive method using solid-phase extraction followed by radioimmunoassay. Both phases were carried out using commercially available kits to determine levels of estradiol (E2). We also measured the levels of free testosterone (FT), dehydroepiandrosterone sulfate, luteinizing hormone, follicle-stimulating hormone, and progesterone in 236 consecutive male patients with angiographically-defined stable coronary artery disease and in 143 disease-free and age-matched controls. RESULTS: The levels of highly-sensitive E2 and FT in patients and controls differed slightly in opposing directions, but neither difference reached statistical significance. However, the ratio of FT to highly-sensitive E2 in patients was significantly higher than in the controls (mean +/- SD; 2.50 +/- 1.89 versus 2.06 +/- 1.14, P = 0.018), and this difference remained significant after adjustments for age and body mass index had been made. Multiple regression analysis revealed that age, the association of diabetes, and the presence of coronary atherosclerosis were significantly and independently associated with the values of the FT/highly-sensitive E2 ratio. Other hormones examined did not differ significantly between the patients and the controls. CONCLUSIONS: Highly-sensitive E2 measurement demonstrated a significant imbalance of FT to E2 in male patients with coronary artery disease, but individual sex hormone levels did not differ between the patients and the controls.

Coronary Angiography↗

PubMed2003

Photonic molecule lasing.

Lasing at resonantly coupled whispering-gallery mode frequencies is observed in photonic molecules consisting of bispheres of 4.2 and 5.1 microm in diameter placed in a silicon V-groove. We examine spatial profiles of photonic molecule modes by use of frequency-resolved imaging and reveal bonding and antibonding mode features. From the lasing threshold characteristics, we quantitatively measure the quality factor and the spontaneous-emission coupling ratio of the photonic molecule modes and confirm that strong coherent coupling leads to photonic molecule modes.

Journal Article↗

PubMed2003

Corticotropin-releasing factor mediates the antinociceptive action of nitrous oxide in rats.

BACKGROUND: Exposure to nitrous oxide activates brainstem noradrenergic nuclei and descending inhibitory pathways, which produce the acute antinociceptive action of nitrous oxide. Because corticotropin-releasing factor (CRF) can produce activation of noradrenergic neurons in the locus ceruleus, the authors sought to determine whether it might be responsible for the antinociceptive action of nitrous oxide. METHODS: Male Sprague-Dawley rats (250-300 g) were exposed for 60 min to room air or 25, 50 or 70% nitrous oxide in oxygen. Brain sections including the hypothalamus were immunostained for both c-Fos (a marker of neuronal activation) and CRF and the percentage of CRF-positive neurons expressing c-Fos was determined. The functional consequences of changes in CRF were investigated by assessing the effect of intracerebroventricular administration of a CRF antagonist (alpha-helical CRF9-41, 20 microg/10 microl) on both activation of locus ceruleus noradrenergic neurons and the antinociception (with the tail-flick latency test) produced by nitrous oxide. RESULTS: Inhalation of nitrous oxide induced a dose-dependent increase in c-Fos expression in CRF-positive neurons in the paraventricular nucleus of the hypothalamus. Intracerebroventricular administration of CRF antagonist inhibited nitrous oxide-induced c-Fos expression in the locus ceruleus and the antinociceptive effect of nitrous oxide. CONCLUSIONS: Nitrous oxide activates the CRF system in the brain, which results in stimulation of noradrenergic neurons in the locus ceruleus and its consequent antinociceptive effect.

Analgesics, Non-Narcotic↗

PubMed2003

Differential activation of protein kinase C between ischemic and pharmacological preconditioning in the rabbit heart.

The objective of the present study was to investigate the differential activation of protein kinase C between ischemic (IPC) and pharmacological preconditioning (PPC) in the rabbit heart. Control, IPC, diazoxide (Diaz), and chelerythrine (Chel)+IPC groups underwent prolonged coronary artery occlusion (CAO) for 30 minutes followed by 180 minutes' reperfusion (protocol I). In protocol II, sham, IPC-only, Diaz-only, and Chel+IPC-only groups did not undergo prolonged CAO. IPC was induced with 4 cycles of 5-min regional ischemia and 10-min reperfusion before prolonged CAO. Diaz (5 mg/kg) was administered 30 min before prolonged CAO. Chel (5 mg/kg) was administered 5 min before the IPC procedure. Infarct size was determined by tetrazolium staining. Assessment of protein kinase C (PKC) isoforms from a left ventricular (LV) sample was conducted by western blotting. Apoptosis in situ was determined by TUNEL assay. The infarction area in the IPC (11.6 +/- 1.0%) and Diaz (19.5 +/- 3.8%) groups was reduced significantly (p< 0.01, p< 0.05) relative to the control group (40.0 +/- 3.8%). The reduction by IPC was abolished by pretreatment with Chel. Apoptosis was significantly decreased (p< 0.01) in the IPC and diazoxide groups compared with the control and Chel+IPC groups (control: 4.78 +/- 0.56% vs. IPC: 2.00 +/- 0.38% vs. Diaz: 2.20 +/- 0.32% vs. Chel+IPC: 4.32 +/- 0.41%) and DNA laddering was attenuated in the IPC and Diaz groups. Membrane PKC-epsilon levels in the IPC and Diaz groups increased significantly relative to the control and Chel+IPC groups. Membrane PKC-epsilon levels in the IPC-only group showed greater increases than the Diaz-only and Chel+IPC-only groups. These findings suggest that whereas PPC suppresses apoptosis when diazoxide opens mitochondrial K(ATP) channels and then activates PKC-epsilon through ischemia-reperfusion, IPC activates PKC-epsilon in the particulate fraction prior to continuous ischemia-reperfusion. We concluded that the difference between IPC and PPC appears to consist in the difference in the timing of PKC-epsilon activation, though both IPC and PPC provide the cardioprotection in ischemia-reperfusion injury.

Alkaloids↗

PubMed2002

[Relationship between activities of daily living and residential environment for patients receiving home oxygen therapy].

PURPOSE: The purpose of this study was to investigate the relationship between ADL and residential environment for patients receiving home oxygen therapy. METHODS: We interviewed 27 HOT patients with chronic respiratory failure, aged 53-85, at an internal medicine outpatient clinic of a national hospital in Yokohama city, using a questionnaire focusing on physical condition, dyspnea, ADL, and residential environment. RESULTS: 1. Of the patients 21 (78%) were III-IV level by Hugh-Jones classification. HOT patients experienced severe dyspnea when climbing stairs and bathing. Their ADL was limited to within their own homes. HOT patients opt to use taxies more often than facilities such as buses and trains. 2. Out of 20 patients living in a two-story house, the ADL of 16 (80%) were limited to downstairs. Two patients living in apartment houses without an elevator complained of great difficulties in going down stairs to go out. Twelve of the patients (44%) interviewed resided in hillside area, the distance to the nearest bus stop being greater than in flat area. 3. A public financial support for house innovation has been offered for some time, but most of the patients did not have any information about this system. They had not realized how their residential environment might affect their ADL. CONCLUSION: These results suggest that more education for HOT patients is needed. They should be clearly shown the importance of the residential environment in enhancers their ADL.

Activities of Daily Living↗

PubMedDate not supplied

Thoracic epidural catheter insertion using the caudal approach assisted with an electrical nerve stimulator in young children.

OBJECTIVES: We evaluated whether thoracic epidural catheter placement using the caudal approach and assisted with an electrical stimulator could be performed in young children. METHODS: Ten young children (1-4 years) who underwent abdominal surgeries were studied. Under general anesthesia without muscle relaxants, caudal catheter placement was performed using an 18-gauge Crawford-type needle and a 20-gauge radiopaque epidural catheter with a stainless-steel stylet. A metal adapter and a 3-way stopcock were attached to the catheter to connect to an electrical stimulator and to inject physiological saline. Electrical stimulation was performed intermittently while advancing the catheter until it reached the target length. The catheter position was confirmed on postoperative roentgenogram. RESULTS: The mean age of the subjects was 32.2 +/- 10.1 months (13-48 months), and the height was 85.3 +/- 6.1 cm (72-93 cm). In 9 of 10 patients, an epidural catheter could be placed at the first insertion. In 1 patient, the catheter could be placed successfully at the second insertion. The electrical current required for muscle contraction at the target length was 5.8 +/- 1.5 mA. CONCLUSION: Electrical stimulation reliably indicated the location of the catheter tip. This technique for thoracic epidural catheter insertion was easy to perform and could be used in young children.

Analgesia, Epidural↗