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Biomedical subjects

Junichi Ogata

Publications and source records attributed to Junichi Ogata.

At least 19 recordsLinked to original sources
PubMed2005

The effects of the neurosteroids: pregnenolone, progesterone and dehydroepiandrosterone on muscarinic receptor-induced responses in Xenopus oocytes expressing M1 and M3 receptors.

The neurosteroids pregnenolone, progesterone, and dehydroepiandrosterone (DHEA) occur naturally in the nervous system. They act on neural tissues, participate in neuronal signaling, and are reported to alter neuronal excitability via nongenomic mechanisms. Muscarinic receptors have important roles in neuronal functions in the brain and autonomic nervous system. In this study, we investigated the effects of pregnenolone, progesterone, and DHEA on M(1) and M(3) muscarinic receptors using the Xenopus oocyte expression system. Pregnenolone and progesterone inhibited the acetylcholine (ACh)-mediated responses of M(1) and M(3) receptors expressed in Xenopus oocytes, whereas DHEA did not. The half-maximal inhibitory concentrations (IC(50)) for pregnenolone inhibition of M(1) receptor- and M(3) receptor-mediated currents were 11.4 and 6.0 microM respectively; the IC(50) values for progesterone inhibition of M(1) receptor- and M(3) receptor-mediated currents were 2.5 and 3.0 microM respectively. The selective protein kinase C (PKC) inhibitor GF109203X had little effect on the pregnenolone or progesterone inhibition of the ACh-induced currents in Xenopus oocytes expressing M(1) or M(3) receptors. The inhibitory effects of pregnenolone and progesterone were overcome at higher concentrations of ACh. Pregnenolone and progesterone inhibited the [(3)H]quinuclidinyl benzilate (QNB) binding to M(1) and M(3) receptor expressed in Xenopus oocytes, and Scatchard plot analysis of [(3)H]QNB binding revealed that pregnenolone and progesterone altered the K(d) value and the B(max), indicating noncompetitive inhibition. In conclusion, pregnenolone and progesterone inhibited M(1) and M(3) receptor functions noncompetitively by the mechanism independent of PKC and by interfering with ACh binding to the receptors.

Acetylcholine↗
PubMed2005

The effects of the tramadol metabolite O-desmethyl tramadol on muscarinic receptor-induced responses in Xenopus oocytes expressing cloned M1 or M3 receptors.

O-desmethyl tramadol is one of the main metabolites of tramadol. It has been widely used clinically and has analgesic activity. Muscarinic receptors are involved in neuronal functions in the brain and autonomic nervous system, and much attention has been paid to these receptors as targets for analgesic drugs in the central nervous system. We have reported that tramadol inhibits the function of type-1 muscarinic (M(1)) receptors and type-3 muscarinic (M(3)) receptors, suggesting that muscarinic receptors are sites of action of tramadol. However, the effects of O-desmethyl tramadol on muscarinic receptor functions have not been studied in detail. In this study, we investigated the effects of O-desmethyl tramadol on M(1) and M(3) receptors, using the Xenopus oocyte expression system. O-desmethyl tramadol (0.1-100 microM) inhibited acetylcholine (ACh)-induced currents in oocytes expressing the M(1) receptors (half-maximal inhibitory concentration [IC(50)] = 2 +/- 0.6 microM), whereas it did not suppress ACh-induced currents in oocytes expressing the M(3) receptor. Although GF109203X, a protein kinase C inhibitor, increased the ACh-induced current, it had little effect on the inhibition of ACh-induced currents by O-desmethyl tramadol in oocytes expressing M(1) receptors. The inhibitory effect of O-desmethyl tramadol on M(1) receptor was overcome when the concentration of ACh was increased (K(D) with O-desmethyl tramadol = 0.3 microM). O-desmethyl tramadol inhibited the specific binding of [(3)H]quinuclidinyl benzilate ([(3)H]QNB) to the oocytes expressed M(1) receptors (IC(50) = 10.1 +/- 0.1 microM), whereas it did not suppress the specific binding of [(3)H]QNB to the oocytes expressed M(3) receptors. Based on these results, O-desmethyl tramadol inhibits functions of M(1) receptors but has little effect on those of M(3) receptors. This study demonstrates the molecular action of O-desmethyl tramadol on the receptors and may help to explain its neural function.

Acetylcholine↗
PubMed2005

[Complications related to anesthesia method in the University of Occupational and Environmental Health Hospital].

BACKGROUND: Complications related to anesthesia remain a problem. We studied the incidence of complications during anesthesia in 2758 patients who had undergone anesthesia in the University of Occupational and Environmental Health Hospital. METHODS: We checked the anesthesia records retrospectively and analyzed the collected data for the incidence of complications during anesthesia. RESULTS: The total incidence of complications during anesthesia was 12.2%. The incidences of complication are estimated to be 13.4% in inhalation anesthesia, 11.9% in inhalation anesthesia plus epidural, spinal or conduction block, 8.9% in CSEA, zero % in epidural anesthesia and 7.5% in spinal anesthesia. CONCLUSIONS: The incidence of complications in inhalation anesthesia was almost as same as that in inhalation anesthesia plus epidural, spinal or conduction block. More study should be necessary to prevent complications related to anesthesia.

Anesthesia↗
PubMed2005

[Complications related to anesthesia in the University of Occupational and Environmental Health Hospital].

BACKGROUND: Complications related to anesthesia remain a problem. We studied the incidence of complications during anesthesia in 2688 patients who had undergone anesthesia in the University of Occupational and Environmental Health Hospital. METHODS: We checked the anesthesia records retrospectively and analyzed the collected data for the incidence of complications during anesthesia. RESULTS: The total incidence of complications during anesthesia was 8.7%:5.5% related to circulation and 1.9% to respiration. CONCLUSIONS: Complications related to anesthesia should be prevented as much as possible through anesthesiologists' efforts in protocol development and skilled assistance.

Adolescent↗
PubMed2004

Gargling with povidone-iodine reduces the transport of bacteria during oral intubation.

PURPOSE: Nosocomial pneumonia remains a common complication in patients undergoing endotracheal intubation. This study examined the transport of bacteria into the trachea during endotracheal intubation, and evaluated the effects of gargling with povidone-iodine on bacterial contamination of the tip of the intubation tube. METHODS: In the gargling group, patients gargled with 25 mL of povidone-iodine (2.5 mg.mL(-1)). In the control group, patients gargled with 25 mL of tap water. Before tracheal intubation, microorganisms were obtained from the posterior wall of the patient's pharynx using sterile cotton swabs. After anesthesia, all patients were extubated and bacteria contaminating the tip of the tracheal tube were sampled and cultured. RESULTS: Before orotracheal intubation, all 19 patients who gargled with tap water (control group) had bacterial colonization on the posterior walls of the pharynx. This group included five patients who had methicillin-resistant staphylococcus aureus (MRSA) in their nasal cavity preoperatively and MRSA was also detected in the pharynx of four patients. Bacterial colonization was observed in all 19 patients who gargled with povidone-iodine (gargling group) and four patients carried MRSA in their nasal cavity, although no MRSA was detected in the pharynx. In the control group, all the patients had bacterial colonization at the tip of the tube after extubation. Additionally, MRSA was detected in two of the four patients. In the gargling group, povidone-iodine eradicated general bacteria and MRSA colonies in the pharynx before intubation and at the tip of the tube after extubation. CONCLUSION: Gargling with povidone-iodine before oral intubation reduces the transport of bacteria into the trachea.

Anti-Infective Agents, Local↗
PubMed2004

A forskolin derivative, colforsin daropate hydrochloride, inhibits the decrease in cortical renal blood flow induced by noradrenaline or angiotensin II in anesthetized rats.

A forskolin derivative, colforsin daropate hydrochloride (CDH), acts directly on adenylate cyclase to increase the intracellular cyclic adenosine monophosphate levels which produce a positive inotropic effect and a lower blood pressure. However, little is known about the effects of CDH on the renal function. We used laser Doppler flowmetry to measure the cortical renal blood flow (RBF) in male Wistar rats given a continuous intravenous infusion of CDH and evaluated the effects of CDH on the noradrenaline (NA) and angiotensin II (AngII) induced increases in blood pressure and reductions in RBF. Continuous intravenous administration of CDH at 0.25 microg/kg/min did not affect the mean arterial pressure (MAP), but increased heart rate and RBF. Continuous intravenous administration of CDH at high doses (0.5-0.75 microg/kg/min) decreased the MAP, with little effect on the RBF. The administration of exogenous NA (1.7 microg/kg) increased the MAP and decreased the RBF. However, a bolus injection of NA did not decrease the RBF during continuous intravenous administration of CDH, and CDH did not affect the NA-induced increase in MAP. The administration of exogenous AngII (100 ng/kg) increased MAP and decreased RBF and heart rate, but a bolus injection of AngII did not decrease RBF during continuous intravenous administration of CDH. These results suggest that CDH plays a protective role against the pressor effects and the decrease in RBF induced by NA or AngII.

Anesthesia↗
PubMed2004

The inhibitory effects of tramadol on 5-hydroxytryptamine type 2C receptors expressed in Xenopus oocytes.

UNLABELLED: Although tramadol is widely available as an analgesic, its mechanism of antinociception remains unresolved. Serotonin (5-hydroxytryptamine, 5-HT) is a monoaminergic neurotransmitter that modulates numerous sensory, motor, and behavioral processes. The 5-HT type 2C receptor (5-HT(2C)R) is one of the major 5-HT receptor subtypes and is implicated in many important effects of 5-HT, including pain, feeding, and locomotion. In this study, we used a whole-cell voltage clamp to examine the effects of tramadol on 5-HT-induced Ca(2+)-activated Cl(-) currents mediated by 5-HT(2C)R expressed in Xenopus oocytes. Tramadol inhibited 5-HT-induced Cl(-) currents at pharmacologically relevant concentrations. The protein kinase C (PKC) inhibitor, bisindolylmaleimide I (GF109203x), did not abolish the inhibitory effects of tramadol on the 5-HT(2C)R-mediated events. We also studied the effects of tramadol on [(3)H]5-HT binding to 5-HT(2C)R expressed in Xenopus oocytes, and found that it inhibited the specific binding of [(3)H]5-HT to 5-HT(2C)R. Scatchard analysis of [(3)H]5-HT binding revealed that tramadol altered the apparent dissociation constant for binding without changing maximal binding, indicating competitive inhibition. The results suggest that tramadol inhibits 5-HT(2C)R function, and the mechanism of this inhibitory effect seems to involve competitive displacement of the 5-HT binding to the 5-HT(2C)R, rather than via activation of the PKC pathway. IMPLICATIONS: We examined the effects of tramadol on 5-hydroxytryptamine type 2C receptor (5-HT(2C)R) expressed in Xenopus oocytes. Tramadol inhibited 5-HT(2C)R function and the specific binding of [(3)H]5-HT to 5-HT(2C)R in a competitive manner. From these data, the mechanism of the inhibitory effect on 5-HT(2C)R might involve the competitive displacement of 5-HT binding to the 5-HT(2C)R.

Analgesics, Opioid↗
PubMed2004

Anesthetic management of patients with severe peripheral ischemia due to calciphylaxis.

Calciphylaxis is a small-vessel disease associated with renal failure. Here, we report the management of a 43-yr-old man with calciphylaxis who received left lower leg amputation with prostaglandin E(1) (PGE(1)) under monitoring by laser Doppler blood flowmetry in the left second and third fingers. Anesthesia was induced with midazolam, fentanyl, and vecuronium and was maintained with oxygen, nitrous oxide, and sevoflurane. The peripheral blood flow varied and decreased gradually; therefore, we added PGE(1) 20 ng. kg(-1). min(-1), which increased blood flow of the tissues. Three weeks after the operation, we again anesthetized the patient. We maintained the blood flow with PGE(1) throughout anesthesia. Monitoring by laser Doppler blood flowmetry and PGE(1) 20 ng. kg(-1). min(-1) could be useful for patients with impaired peripheral circulation, as in calciphylaxis.

Adult↗
PubMed2004

[The airway management using laryngeal mask airway and tracheal fiberscopy in a pediatric patient with tracheal stenosis after tracheostomy].

A 9-year-old boy was scheduled for excision of tracheal granuloma which had developed at the tip of a tracheostomy tube. Instead of a tracheostomy tube, a 4 mm ID tracheal tube was inserted via the tracheostomy beyond the tracheal constriction because of rapid development of respiratory failure. General anesthesia was induced and maintained with sevoflurane and oxygen via the tube, and a size 2.5 laryngeal mask airway (LMA) was inserted without muscle relaxant. Spontaneous respiration remained. Under monitoring by fiberoptic tracheoscopy via the LMA, the tracheal tube was extubated carefully. An 8 Fr. suction tube was indwelled via the tracheostomy beyond the stenosis for oxygen supply. After sealing the tracheostomy, he could breath spontaneously through the LMA. During the excision of tracheal granuloma by holmium:YAG laser, fiberoptic observation was continued via the LMA, and the procedure was performed without any complication. We conclude that the tracheal stenosis can be managed using the LMA, continuous fiberoptic monitoring and additional option of keeping spontaneous ventilation.

Anesthesia, General↗
PubMed2004

[The management of extirpation of chronic expanding hematoma after thoracoplasty in the chest].

A 71-year-old man was scheduled for an extirpation of chronic expanding hematoma (CEH) of his right thorax. He had a history of right thoracoplasty for tuberculosis 37 years previously. He complained of dyspnea that had deteriorated over three months. His inflammatory responses including general fatigue and fever due to chronic empyema remained to be resolved. The chest computed tomography revealed that the CEH remarkably compressed the trachea and the heart resulting in the cause of left mediastinal deviation. General anesthesia was induced with fentanyl and propofol, and maintained with sevoflurane. During general anesthesia, mean central venous pressure (CVP) via the right femoral vein and arterial blood pressure (ABP) via the left radial artery were monitored. Bilateral peripheral vein catheters with 16 G could effectively provide huge amount of transfusion. Although his blood loss was 10,000 ml because of superior vena caval rupture and oozing from pleura, prompt and adequate management of hemodynamics could be maintained using CVP and ABP monitoring. The CEH is known as a specific type of chronic empyema and its extraction would require ingenuity since there are number of factors associated with diagnosis, indication and prevention. Each case is to be evaluated individually and managed carefully.

Aged↗
PubMed2003

A forskolin derivative, colforsin daropate hydrochloride, inhibits rat mesangial cell mitogenesis via the cyclic AMP pathway.

A forskolin derivative, colforsin daropate hydrochloride (CDH), has been introduced as an inotropic agent that acts directly on adenylate cyclase to increase intracellular cyclic AMP (cAMP) levels and ventricular contractility, resulting in positive inotropic activity. We investigated the effects of CDH on rat mesangial cell (MC) proliferation. CDH (10(-7)-10(-5) mol/l) inhibited [(3)H]thymidine incorporation into cultured rat MCs in a concentration-dependent manner. CDH (10(-7)-10(-5) mol/l) also decreased cell numbers in a similar manner, and stimulated cAMP accumulation in MCs in a concentration-dependent manner. A protein kinase A inhibitor, H-89, abolished the inhibitory effects of CDH on MC mitogenesis. These findings suggest that CDH would inhibit the proliferation of rat MCs via the cAMP pathway.

Animals↗
PubMed2003

The inhibitory effects of ketamine and pentobarbital on substance p receptors expressed in Xenopus oocytes.

UNLABELLED: Substance P receptors (SPR) modulate nociceptive transmission within the spinal cord. The effects of IV anesthetics on SPR are not clear. In this study, we investigated the effects of IV anesthetics on SPR expressed in Xenopus oocytes. We examined the effects of ketamine, pentobarbital, propofol, and tramadol on SP-induced Ca(2+)-activated Cl(-) currents mediated by SPR expressed in Xenopus oocytes using a whole-cell voltage clamp. Ketamine and pentobarbital inhibited the SPR-induced currents at pharmacologically relevant concentrations, but propofol and tramadol had little effect on the currents. We also studied the effects of ketamine and pentobarbital on [(3)H]-SP to SPR. Ketamine and pentobarbital inhibited the specific binding of [(3)H]-SP to SPR expressed in Xenopus oocytes. Scatchard analysis of [(3)H]-SP binding revealed that ketamine and pentobarbital decreased the apparent dissociation constant for binding and maximal binding, indicating noncompetitive inhibition. The protein kinase C (PKC) inhibitor bisindolylmaleimide I did not abolish the inhibitory effects of ketamine and pentobarbital on SP-induced Ca(2+)-activated Cl(-) currents. The results suggest that ketamine and pentobarbital inhibit SPR function. The mechanism of their inhibition on SPR function could not be through activation of the PKC pathway and may be due to noncompetitive displacing the SP binding. IMPLICATIONS: We investigated the effects of IV anesthetics on substance P receptors (SPR) expressed in Xenopus oocytes. Ketamine and pentobarbital inhibit SPR function via noncompetitive displacing SP binding. The findings imply that the inhibition of SPR function by these compounds may play a role in the analgesic effects of these IV anesthetics.

Aluminum Compounds↗
PubMed2003

Sino-atrial block during anesthesia in a patient with breast cancer being treated with the anticancer drug epirubicin.

IMPLICATIONS: Epirubicin, an anticancer drug, causes cardiotoxicity. We reported a case of sino-atrial block during general anesthesia in a woman with breast cancer who had received epirubicin. Anesthesiologists should be aware of the possible occurrence of sino-atrial block with epirubicin, and planting a pacemaker might be considered even in asymptomatic patients.

Anesthesia, General↗
PubMed2003

The inhibitory effects of alphaxalone on M1 and M3 muscarinic receptors expressed in Xenopus oocytes.

UNLABELLED: Alphaxalone is a neurosteroid anesthetic, but its mechanisms of action are not completely understood. Muscarinic receptors are involved in a variety of neuronal functions in the brain and autonomic nervous system, and much attention has been paid to them as targets of anesthetics. In this study, we investigated the effects of alphaxalone on M(1) and M(3) muscarinic receptors using the Xenopus oocyte expression system. Alphaxalone inhibited acetylcholine-induced currents in oocytes expressing M(1) receptors at clinically relevant concentrations. Alphaxalone also suppressed acetylcholine-induced currents in oocytes expressing M(3) receptors. The half-maximal inhibitory concentration values for the inhibition of M(1)- and M(3)-mediated currents were 1.8 +/- 0.6 micro M and 5.3 +/- 1.0 micro M, respectively. GF109203X, a selective protein kinase C inhibitor, had little effect on the inhibition of acetylcholine-induced currents by alphaxalone in oocytes expressing these receptors. Alphaxalone inhibited the specific binding of [(3)H]quinuclidinyl benzilate to oocytes expressing M(1) or M(3) receptors. These findings suggest that alphaxalone at clinically relevant concentrations inhibits the function of M(1) and M(3) receptors through a protein kinase C-independent mechanism by interfering with the [(3)H]quinuclidinyl benzilate binding sites on the receptors. IMPLICATIONS: Alphaxalone, a neurosteroid anesthetic, inhibited the function of muscarinic M(1) and M(3) receptors and the specific binding of [(3)H]quinuclidinyl benzilate ([(3)H]QNB) to oocytes expressing these receptors. These findings suggest that alphaxalone inhibits these receptors by interfering with the QNB binding sites.

Acetylcholine↗
PubMedDate not supplied

Intramuscular tramadol increases gastric pH during anesthesia.

PURPOSE: Tramadol, [(1RS, 2RS)-2-dimethylamino) methyl-1-(3-methoxyphenyl)-cyclohexanol hydrochloride], is an analgesic in clinical use. It has been reported that tramadol inhibits muscarinic type 3 receptor function, which primarily mediates smooth muscle contraction and glandular secretion. We investigated the effects of tramadol on the pH of gastric juices during anesthesia to determine whether tramadol inhibits secretion from the gastric glands. METHODS: ASA physical status I or II adult patients (n = 30) presenting for major elective orthopedic surgery of the upper extremities or mastectomy were enrolled. Patients were randomly assigned to receive treatment with tramadol (n = 10), famotidine (n = 10), or saline (n = 10). General anesthesia was then induced using propofol, vecuronium bromide, and fentanyl. After inducing anesthesia, the gastric pH was measured using pH test paper and, then, 100 mg tramadol, 20 mg famotidine, or saline were injected into the deltoid muscle. Three hours after starting the operation, gastric juice was again aspirated and its gastric pH measured. RESULTS: There were no differences in the pH before anesthesia between the three groups. By contrast, gastric pH was increased in the tramadol group by the same amount as it was in the famotidine group three hours after administering the drugs. Gastric pH of the saline, famotidine, and tramadol groups was 2.6 +/- 2.5, 6.3 +/- 2.0, and 6.4 +/- 0.8, respectively. CONCLUSION: These results suggest that tramadol inhibits the secretion of gastric acid.

Adult↗