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1.
Anesth Prog ; 61(3): 107-10, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25191984

RESUMEN

Difficulties with airway management are often caused by anatomic abnormalities due to previous oral surgery. We performed general anesthesia for a patient who had undergone several operations such as hemisection of the mandible and reconstructive surgery with a deltopectoralis flap, resulting in severe maxillofacial deformation. This made it impossible to ventilate with a face mask and to intubate in the normal way. An attempt at oral awake intubation using fiberoptic bronchoscopy was unsuccessful because of severe anatomical abnormality of the neck. We therefore decided to perform retrograde intubation and selected the cuffed oropharyngeal airway (COPA) for airway management. We inserted the COPA, not through the patient's mouth but through the abnormal oropharyngeal space. Retrograde nasal intubation was accomplished with controlled ventilation through the COPA, which proved to be very useful for this difficult airway management during tracheal intubation even though the method was unusual.


Asunto(s)
Manejo de la Vía Aérea/instrumentación , Intubación Intratraqueal/instrumentación , Orofaringe , Anciano , Manejo de la Vía Aérea/métodos , Anestesia General , Broncoscopía/métodos , Sedación Consciente/métodos , Humanos , Intubación Intratraqueal/métodos , Masculino , Mandíbula/cirugía , Fibras Ópticas , Procedimientos de Cirugía Plástica/métodos , Respiración Artificial/métodos , Colgajos Quirúrgicos/trasplante
2.
Pain Med ; 14(3): 351-7, 2013 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-23240990

RESUMEN

BACKGROUND: Burning mouth syndrome (BMS) is characterized by the following subjective complaints without distinct organic changes: burning sensation in mouth or chronic pain of tongue. BMS is also known as glossodynia; both terms are used equivalently in Japan. Although the real cause of BMS is still unknown, it has been pointed out that BMS is related to some autonomic abnormality, and that stellate ganglion near-infrared irradiation (SGR) corrects the autonomic abnormality. Frequency analysis of heart rate variability (HRV) is expected to be useful for assessing autonomic abnormality. OBJECTIVES: This study investigated whether frequency analysis of HRV could reveal autonomic abnormality associated with BMS, and whether autonomic changes were corrected after SGR. SUBJECTS AND METHODS: Eight subjects received SGR; the response to SGR was assessed by frequency analysis of HRV. RESULTS: No significant difference of autonomic activity concerning low-frequency (LF) norm, high-frequency (HF) norm, and low-frequency/high-frequency (LF/HF) was found between SGR effective and ineffective groups. Therefore, we proposed new parameters: differential normalized low frequency (D LF norm), differential normalized high frequency (D HF norm), and differential low-frequency/high-frequency (D LF/HF), which were defined as differentials between original parameters just before and after SGR. These parameters as indexes of responsiveness of autonomic nervous system (ANS) revealed autonomic changes in BMS, and BMS seems to be related to autonomic instability rather than autonomic imbalance. CONCLUSIONS: Frequency analysis of HRV revealed the autonomic instability associated with BMS and enabled tracing of autonomic changes corrected with SGR. It is suggested that frequency analysis of HRV is very useful in follow up of BMS and for determination of the therapeutic efficacy of SGR.


Asunto(s)
Enfermedades del Sistema Nervioso Autónomo/diagnóstico , Síndrome de Boca Ardiente/complicaciones , Frecuencia Cardíaca , Ganglio Estrellado , Adulto , Anciano , Anciano de 80 o más Años , Enfermedades del Sistema Nervioso Autónomo/complicaciones , Enfermedades del Sistema Nervioso Autónomo/radioterapia , Femenino , Humanos , Masculino , Persona de Mediana Edad , Resultado del Tratamiento
3.
Biol Cell ; 103(2): 69-86, 2011 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-21138418

RESUMEN

BACKGROUND INFORMATION: AQPs (aquaporins) are water channel proteins that are expressed in almost all living things. In mammalians, 13 members of AQPs (AQP0-12) have been identified so far. AQP5 is known to be expressed mostly in the exocrine cells, including the salivary gland acinar cells. A naturally occurring point mutation (G308A, Gly103 > Asp103) was earlier found in the rat AQP5 gene [Murdiastuti, Purwanti, Karabasil, Li, Yao, Akamatsu, Kanamori and Hosoi (2006) Am. J. Physiol. 291, G1081-G1088]; in this mutant, the rate of initial saliva secretion under stimulated and unstimulated conditions is less than that for the wt (wild-type) animals. RESULTS: Here the mutant molecule was characterized in detail. Using the Xenopus oocyte system, we demonstrated the mutant AQP5 to have water permeability almost the same as that of the wt molecule. Mutant and wt AQP5s, tagged with GFP (green fluorescent protein; GFP-AQP5s) and expressed in polarized MDCK-II (Madin-Darby canine kidney II) cells, first appeared in the vesicular structure(s) in the cytoplasm, and were translocated to the upper plasma membrane or apical membrane during cultivation, with the mutant GFP-AQP5 being translocated less efficiently. Thapsigargin and H-89 both induced translocation in vitro of either molecule, whereas colchicine inhibited this activity; the fraction of cells showing apical localization of mutant GFP-AQP5 was less than that showing that of the wt molecule under any of the experimental conditions used. In the mutant SMG (submandibular gland) tissue, localization of AQP5 in the apical membrane of acinar cells was extremely reduced. Vesicular structures positive for AQP5 and present in the cytoplasm of the acinar cells were co-localized with LAMP2 (lysosome-associated membrane protein 2) or cathepsin D in the mutant gland, whereas such co-localizations were very rare in the wt gland, suggesting that the mutant molecules largely entered lysosomes for degradation. CONCLUSION: Replacement of highly conserved hydrophobic Gly103 with strongly hydrophilic Asp103 in rat AQP5, though it did not affect water permeability, may possibly have resulted in less efficient membrane trafficking and increased lysosomal degradation, leading to its lower expression in the apical membrane of the acinar cells in the SMG.


Asunto(s)
Acuaporina 5/genética , Acuaporina 5/metabolismo , Mutación Puntual , Glándula Submandibular/metabolismo , Agua/metabolismo , Secuencia de Aminoácidos , Animales , Acuaporina 5/química , Línea Celular , Membrana Celular/química , Membrana Celular/genética , Membrana Celular/metabolismo , Perros , Datos de Secuencia Molecular , Mutación Missense , Permeabilidad , Transporte de Proteínas , Ratas , Alineación de Secuencia , Glándula Submandibular/química , Xenopus
4.
Neuro Endocrinol Lett ; 33(2): 177-82, 2012.
Artículo en Inglés | MEDLINE | ID: mdl-22592198

RESUMEN

OBJECTIVE: Nerve growth factor (NGF) triggers long-term neuronal excitability. We examined its effect on murine bone marrow stromal cells (BMSC)-derived neurons. METHODS: With an optimal differentiation protocol, BMSCs were differentiated into neurons in culture. To confirm the probability of differentiation of BMSC into neuron, the expression of neuronal marker protein, neurofilament, was examined by immunocytochemistry. To examine the electrophysiological properties of BMSC-derived neurons, the field potentials were recorded either from nontreated (control) BMSC-derived neurons or from BMSC-derived neurons after the treatment with NGF by using extracellular recording techniques. RESULTS: Most BMSC-derived neurons showed spontaneous discharges whose amplitudes were up to 2 mV. When NGF at a concentration of 100 ng/ml was applied to BMSC-derived neurons, the amplitudes of discrete field potentials were gradually enlarged within 1 min after NGF application and peaked 3 min later (20-fold the size of control). However, the enlargement of the amplitudes of field potentials almost disappeared 5 min after NGF application. CONCLUSION: This finding indicates that neuronal cells derived from murine BMSCs generate discrete field potential activities spontaneously and that NGF has the effect of enlarging transient, but not sustained, electrical activity of BMSC-derived neurons.


Asunto(s)
Potenciales de Acción/fisiología , Células de la Médula Ósea/fisiología , Factor de Crecimiento Nervioso/fisiología , Neuronas/fisiología , Células del Estroma/fisiología , Potenciales de Acción/efectos de los fármacos , Animales , Células de la Médula Ósea/efectos de los fármacos , Diferenciación Celular/efectos de los fármacos , Diferenciación Celular/fisiología , Células Cultivadas , Masculino , Ratones , Ratones Endogámicos C57BL , Factor de Crecimiento Nervioso/farmacología , Proteínas de Neurofilamentos/metabolismo , Neuronas/metabolismo , Células del Estroma/efectos de los fármacos
6.
Biochem Biophys Res Commun ; 388(1): 141-5, 2009 Oct 09.
Artículo en Inglés | MEDLINE | ID: mdl-19646954

RESUMEN

We investigated the effects of ketamine on the type 3 facilitative glucose transporter (GLUT3), which plays a major role in glucose transport across the plasma membrane of neurons. Human-cloned GLUT3 was expressed in Xenopus oocytes by injection of GLUT3 mRNA. GLUT3-mediated glucose uptake was examined by measuring oocyte radioactivity following incubation with 2-deoxy-d-[1,2-(3)H]glucose. While ketamine and S(+)-ketamine significantly increased GLUT3-mediated glucose uptake, this effect was biphasic such that higher concentrations of ketamine inhibited glucose uptake. Ketamine (10microM) significantly increased V(max) but not K(m) of GLUT3 for 2-deoxy-d-glucose. Although staurosporine (a protein kinase C inhibitor) increased glucose uptake, no additive or synergistic interactions were observed between staurosporine and racemic ketamine or S(+)-ketamine. Treatment with ketamine or S(+)-ketamine partially prevented GLUT3 inhibition by the protein kinase C activator phorbol-12-myrisate-13-acetate. Our results indicate that ketamine increases GLUT3 activity at clinically relevant doses through a mechanism involving PKC inhibition.


Asunto(s)
Transportador de Glucosa de Tipo 3/metabolismo , Glucosa/metabolismo , Ketamina/farmacología , Proteína Quinasa C/fisiología , Animales , Transporte Biológico/efectos de los fármacos , Transportador de Glucosa de Tipo 3/genética , Ketamina/química , Oocitos , Proteína Quinasa C/antagonistas & inhibidores , Estereoisomerismo , Xenopus laevis
7.
Masui ; 54(6): 676-9, 2005 Jun.
Artículo en Japonés | MEDLINE | ID: mdl-15966390

RESUMEN

A 17-year-old man with fracture of the mandible underwent open fixation under general anesthesia. He was an athlete of the rugby suffering the fracture in a match. His preoperative physical examinations were normal except for I degrees atrioventricular block on electrocardiogram (ECG). During anesthesia, atrioventricular dissociation and frequent premature ventricular contractions were induced by the stimulation of nasotracheal intubation and the administration of atropine for the reversal of muscle relaxation. We thought the cause of the arrhythmia is the athlete's heart which may be vagotonic and may induce vagal reflex or fatal arrhythmia. This case demonstrates that it is necessary to pay attention to chronotropic action associated with the intubation of nasopharynx, the handling of laryngoscope and the usage of drugs for the anesthetic management of the athlete.


Asunto(s)
Anestesia General/efectos adversos , Fútbol Americano/lesiones , Fracturas Mandibulares/cirugía , Complejos Prematuros Ventriculares/etiología , Adolescente , Electrocardiografía , Frecuencia Cardíaca , Humanos , Técnicas de Fijación de Maxilares , Masculino
8.
Case Rep Dent ; 2014: 656045, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25045545

RESUMEN

This is the first case report of orthostatic dysregulation (OD) manifested during postural change on the dental chair and intraoperatively monitored by heart rate variability (HRV) analysis. OD-associated autonomic dysfunction is induced by postural changes and easily leads to disturbance in circulatory dynamics; however, most dental practices have not yet realized the importance of managing OD. We measured autonomic activity in a patient with OD during dental therapy and assessed the clinical significance of HRV analysis for OD. The patient was a 17-year-old Japanese female. She was diagnosed with impacted wisdom teeth and had no previous history of a distinct systemic disease. A surgical procedure to extract the teeth was safely performed under both local anesthesia and sedation with nitrous oxide and midazolam. After the surgery, her postural change to sitting induced orthostatic hypotension. HRV variables showed parasympathetic dominance due to the upright position. Subsequently, her posture was returned to supine, and atropine sulfate administration for the immediate treatment of OD returned her blood pressure to normal levels. HRV variables showed relative sympathetic dominance due to an atropine-derived parasympathetic blockade. HRV analysis revealed OD-associated autonomic dysfunction and should become a standard tool for safe and secure dental management of OD.

9.
Case Rep Dent ; 2014: 171657, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25386367

RESUMEN

The purpose of this study was to apply high-wattage pulsed irradiation of linearly polarized near-infrared light to the stellate ganglion area for burning mouth syndrome (BMS) and to assess the efficacy of the stellate ganglion area irradiation (SGR) on BMS using differential time-/frequency-domain parameters (D parameters). Three patients with BMS received high-wattage pulsed SGR; the response to SGR was evaluated by visual analogue scale (VAS) representing the intensity of glossalgia and D parameters used in heart rate variability analysis. High-wattage pulsed SGR significantly decreased the mean value of VAS in all cases without any adverse event such as thermal injury. D parameters mostly correlated with clinical condition of BMS. High-wattage pulsed SGR was safe and effective for the treatment of BMS; D parameters are useful for assessing efficacy of SGR on BMS.

10.
Neuroreport ; 23(1): 21-5, 2012 Jan 04.
Artículo en Inglés | MEDLINE | ID: mdl-22113212

RESUMEN

The hypothesis that the facilitative glucose transporter type 3 (GLUT3) in the brain also exhibits water channel properties similar to that of GLUT1 was tested in Xenopus oocytes expressing human GLUT3 or GLUT1. The volume of oocytes expressing GLUT3 exposed to hypotonic medium increased in an exponential manner. The osmotic water permeability (Pf) for GLUT3 or GLUT1 increased significantly compared with that for oocytes-injected water. The osmotic water transport by GLUT3 was completely inhibited by treatment with a selective GLUT inhibitor, cytochalasin B. The Pf values for GLUT3 significantly increased with increasing temperature of the extracellular medium and the activation energy for GLUT3 was almost the same as that for GLUT1. Thus, GLUT3 in the brain also exhibits water channel properties.


Asunto(s)
Acuaporinas/metabolismo , Transportador de Glucosa de Tipo 3/metabolismo , Agua/metabolismo , Animales , Transporte Biológico , Citocalasina B/farmacología , Femenino , Glucosa/metabolismo , Transportador de Glucosa de Tipo 1/metabolismo , Transportador de Glucosa de Tipo 3/genética , Humanos , Oocitos/metabolismo , Temperatura , Xenopus laevis
11.
Neuroreport ; 23(11): 687-91, 2012 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-22692552

RESUMEN

To understand the mechanisms underlying the neuroprotective efficacy of barbiturates, the effect of pentobarbital on glucose uptake and water transport was determined in Xenopus oocytes expressing glucose transporter type 3 (GLUT3). Pentobarbital induced a 50% concentration-dependent inhibition in glucose uptake, but exerted no effect on water transport by GLUT3. Eadie-Hofstee analysis showed that pentobarbital decreased Vmax significantly, but not Km of GLUT3 for 2-deoxy-D-glucose. Although the protein kinase C (PKC) activator significantly decreased glucose uptake by GLUT3, no additive or synergistic interactions were observed between the PKC activator and pentobarbital. Our results suggest that pentobarbital may play an important role in neuroprotection by inhibition of glucose uptake by GLUT3 by a mechanism involving PKC.


Asunto(s)
Moduladores del GABA/farmacología , Transportador de Glucosa de Tipo 3/efectos de los fármacos , Glucosa/metabolismo , Fármacos Neuroprotectores/farmacología , Pentobarbital/farmacología , Proteína Quinasa C/metabolismo , Animales , Transporte Biológico/efectos de los fármacos , Transportador de Glucosa de Tipo 3/metabolismo , Oocitos/efectos de los fármacos , Oocitos/metabolismo , Agua/metabolismo , Xenopus laevis
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