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Biomedical subjects

Koh Shingu

Publications and source records attributed to Koh Shingu.

At least 37 records · Page 2Linked to original sources
PubMed2005

[Appropriate dose of isobaric bupivacaine with fentanyl in spinal anesthesia for cesarean section].

BACKGROUND: Spinal anesthesia combined with fentanyl is commonly used for cesarean section. We studied the appropriate dose of isobaric bupivacaine for spinal anesthesia when combined with a fixed dose of 20 microg fentanyl. METHODS: Forty-seven women scheduled for cesarean section were allocated into four-groups according to the dose of 0.5% isobaric bupivacaine with 20 microg fentanyl; 1.0 ml (n=5), 1.5 ml (n=11), 2.0 ml (n=11), and 2.5 ml (n=20). RESULTS: The requirement of epidural anesthesia for pain relief or muscle relaxant was less in the 2.0 ml and 2.5 ml groups than the other groups. However, dyspnea due to high spinal anesthesia developed in 3 subjects out of 20 in the 2.5 ml group. CONCLUSIONS: Two ml of 0.5% isobaric bupivacaine was the most appropriate dose for cesarean section, when combined with 20 microg of fentanyl.

Adult↗
PubMed2005

[Laryngeal mask during emergence from anesthesia in intubated patients with asthmatic attack or ischemic heart disease].

We report two patients in whom the presence of a tracheal tube induced asthmatic attack or hemodynamic instability and the laryngeal mask was useful during emergence from anesthesia. Case 1:A 24-year-old man with asthma was scheduled for reconstruction of an amputated finger. After induction of anesthesia and neuromuscular blockade, the trachea was intubated without complications. At the end of 9.5-h uneventful operation under anesthesia with sevoflurane, nitrous oxide and oxygen, inhalational anesthetics were turned off. During emergence from anesthesia, bucking with asthmatic attack occurred. Sevoflurane and theophilline resolved the attack, which recurred after termination of sevoflurane. Under deep anesthesia with sevoflurane, the laryngeal mask was placed, and then the tracheal tube removed without complications. The laryngeal mask was removed when the patient awoke uneventfully. Case 2: A 69-year-old man with a recent history of myocardial infarction was scheduled for skin grafting. After uneventful operation, sevoflurane and nitrous oxide were turned off. Multiple premature ventricular contractions (PVCs) with hypertension and tachycardia occurred, and necessitated the restart of sevoflurane. Under deep anesthesia, the laryngeal mask was inserted and the trachea extubated, and the patient regained consciousness without complications.

Adult↗
PubMed2005

[Brain protection with mild hypothermia during carotid artery clamping].

A 71-year-old man was scheduled for removal of a Kirchner wire malpositioned in the mediastinum, which had been placed for fixing the fractured right clavicle five months before. Anesthesia was induced and maintained with propofol, fentanyl and vecuronium. The wire was found to be penetrating the brachiocephalic artery after sternotomy. An emergency angiography performed in the operating room showed that Willis arterial circle was sufficiently developed for clamping the brachiocephalic artery. The wire was removed under clamping the brachiocephalic artery for 9 minutes, but massive bleeding from the left common carotid artery continued, then the left common carotid artery was clamped and injured region was resected and reconstructed for 68 minutes. The body temperature was reduced to 32.5-33 degree with a cooling water mattress for brain protection and prostaglandin E1 was infused for vasodilation during hypothermia. Monitoring with somatosensory evoked potential was added during anesthesia. The surgery was performed uneventfully and the patient showed no neurological sequelae postoperatively.

Aged↗
PubMed2004

The intravenous anesthetic propofol inhibits hypoxia-inducible factor 1 activity in an oxygen tension-dependent manner.

Hypoxia elicits a wide range of responses that occur at different organizational levels in the body. Hypoxia is not only a signal for energy conservation and metabolic change, but triggers expression of a select set of genes. The transcription factor hypoxia-inducible factor 1 (HIF-1) is now appreciated to be a master factor of the gene induction. Although knowledge on molecular mechanisms of HIF-1 activation in response to hypoxia is accumulating, the molecular mechanism of maintenance of HIF-1 activity under normoxic conditions remains to be elucidated. We demonstrate that the intravenous anesthetic propofol reversibly inhibits HIF-1 activity and the gene expression mediated by HIF-1 by blocking the synthesis of the HIF-1alpha subunit under 20% or 5% O2 conditions, but not under 1% O2 conditions.

Anesthetics, Intravenous↗
PubMed2004

The inhibitory effect of sodium nitroprusside on HIF-1 activation is not dependent on nitric oxide-soluble guanylyl cyclase pathway.

Adaptation to hypoxia and maintenance of O(2) homeostasis involve a wide range of responses that occur at different organizational levels in the body. One of the most important transcription factors that activate the expression of O(2)-regulated genes is hypoxia-inducible factor 1 (HIF-1). Nitric oxide (NO) mediates a variety of biological effects including relaxation of blood vessels and cytotoxicity of activated macrophages. We investigated the effect of the clinically used nitrates nitroglycerin (NTG), isosorbide dinitrate (ISDN), and sodium nitroprusside (SNP) on HIF-1-mediated transcriptional responses to hypoxia. We demonstrate that among the three nitrates, only SNP inhibits HIF-1 activation in response to hypoxia. In contrast, NTG or ISDN does not affect HIF-1 activity. SNP inhibits the accumulation of HIF-1alpha, the regulatory subunit of HIF-1, and the transcriptional activation of HIF-1alpha via a mechanism that is not dependent on either NO or soluble guanylate cyclase.

Animals↗
PubMed2004

Ketamine attenuates hypocapnia-induced neuronal damage in the caudoputamen in a rat model of chronic cerebral hypoperfusion.

We previously demonstrated that the caudoputamen was exclusively further damaged by hypocapnia in a rat with chronic cerebral hypoperfusion which is characterized by white matter lesions (WML) and a well-established model for patients with cerebrovascular diseases and/or dementia, and suggest that this process may be the cause of long lasting postoperative delirium or brain dysfunction in such patients. In the present study, we investigated whether ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, could attenuate the neuronal damage in the caudoputamen. Ketamine, at doses of 10 and 20 mg/kg, which was given intraperitoneally before hypocapnia induction, attenuated the aggravation of WML score, neuronal damage, and astroglial proliferation in the rat caudoputamen. These results suggest that ketamine may be beneficial for preventing postoperative brain dysfunction, especially in patients with cerebrovascular diseases and/or dementia induced by hypocapnia, which is likely to occur in the mechanical ventilation used during surgery.

Animals↗
PubMed2004

A new method using flow cytometry to measure the effects of drugs on gastric emptying and gastrointestinal transit in mice.

The use of radiolabelled markers is considered to be a gold standard for assessing gastric emptying and gastrointestinal transit in mice and rats, but their use has increasingly been restricted due to health concern. Therefore, a new method using fluorescent polystyrene microbeads and flow cytometry was devised. Saline containing fluorescent markers (together with non-fluorescent microbeads) was infused into the stomach of each mouse and gastric emptying and gastrointestinal transit were calculated by measuring the quantity of the fluorescent microbeads in the gastrointestinal tract using flow cytometer. The effects of saline (as a control), morphine (CAS 52-26-6) and dexmedetomidine (CAS 113775-47-6) were tested. Both gastric emptying and gastrointestinal transit measured with this method (after i.p. injection of saline) were similar to those reported previously using the conventional radiolabelled methods. Morphine significantly inhibited both gastric emptying and gastrointestinal transit in a dose-dependent manner. Dexmedetomidine did not significantly inhibit gastric emptying but inhibited gastrointestinal transit. These results were also similar to those obtained using the conventional radiolabelled method. The method using fluorescent microbeads and flow cytometry may be a reliable alternative to the methods using radioisotope for studying the effects of drugs on gastric emptying and gastrointestinal transit.

Analgesics, Non-Narcotic↗
PubMed2004

Adenosine and a nitric oxide donor enhances cardioprotection by preconditioning with isoflurane through mitochondrial adenosine triphosphate-sensitive K+ channel-dependent and -independent mechanisms.

BACKGROUND: Preconditioning with isoflurane has been shown to confer cardioprotection via activation of mitochondrial adenosine triphosphate-sensitive K+ (mito K(ATP)) channels. However, the relative contribution of mito K(ATP) channel and non-mito K(ATP) channel mechanisms to isoflurane-mediated cardioprotection has not been investigated. METHODS: Isolated and buffer-perfused rat hearts were used. Flavoprotein fluorescence was monitored as an index for mito K(ATP) channel activity. Isovolumic left ventricular function and infarct size were measured as indices for cardioprotection. RESULTS: Flavoprotein fluorescence, which was monitored as an index for mito K(ATP) channel activity, was increased by isoflurane and a known mito K(ATP) channel opener, diazoxide, in a 5-hydroxydecanoate-sensitive manner. Although flavoprotein oxidation induced by diazoxide was dissipated soon after its removal from the buffer, flavoprotein oxidation induced by isoflurane was sustained after cessation of the treatment. The sustained increase in flavoprotein oxidation was associated with a significant reduction in infarct size after 30 min of ischemia followed by 120 min of reperfusion. Although adenosine and S-nitroso-N-acetyl-penicillamine each alone did not increase flavoprotein fluorescence, nor did they confer significant cardioprotection, coadministration of adenosine and S-nitroso-N-acetyl-penicillamine with isoflurane conferred a highly significant reduction of infarct size and improvement of left ventricular function without increasing flavoprotein oxidation over isoflurane alone. The early treatment with 5-hydroxydecanoate before and during preconditioning completely reversed flavoprotein oxidation and inhibited the infarct-sparing effect of isoflurane and combined preconditioning with isoflurane, adenosine, and S-nitroso-N-acetyl-penicillamine. The late treatment with 5-hydroxydecanoate after preconditioning abolished flavoprotein oxidation and the infarct-sparing effect of isoflurane but only partially inhibited cardioprotection conferred by the combined preconditioning, despite complete abrogation of flavoprotein oxidation. CONCLUSIONS: Mito K(ATP) channel activation is the essential trigger of both preconditioning with isoflurane and combined preconditioning with isoflurane, adenosine, and S-nitroso-N-acetyl-penicillamine. Mito K(ATP) channel activation is also a crucial mediator of cardioprotection afforded by preconditioning with isoflurane. However, enhanced cardioprotection conferred by combined preconditioning is mediated through both mito K(ATP) channel-dependent and -independent mechanisms.

Adenosine↗
PubMed2004

Time-related cuff pressures of the laryngeal tube with and without the use of nitrous oxide.

UNLABELLED: The Laryngeal tube (VBM Medizintechnik, Sulz, Germany), a new supraglottic airway, consists of an airway tube, two cuffs, and two distal apertures between the two cuffs. One concern with the use of this device is ischemic change to the oropharyngeal mucosa. We studied the time-course change of the intracuff pressure (which reflects the pharyngeal pressure) of the laryngeal tube during anesthesia with and without nitrous oxide. After insertion of a laryngeal tube, 24 patients were randomly allocated to 1 of 2 groups. In one group (group N or nitrous oxide group), 66% nitrous oxide was used, whereas in the other group nitrous oxide was not used (group A or air group). In both groups, sevoflurane was used to maintain anesthesia. Time-course changes of the intracuff pressure and postoperative airway complications were recorded. In group N, the intracuff pressure significantly increased over time (P < 0.001; the maximal pressure: 120 cm H(2)O), whereas in group A the intracuff pressure remained stable. The intracuff pressure was significantly higher in group N than in group A (P < 0.0001; 95% confidence intervals for difference: 6-20 cm H(2)O at 30 min). Postoperatively, two patients in group A and one patient in group N complained of mild sore throat. IMPLICATIONS: Nitrous oxide may increase pharyngeal pressure by the cuffs of the laryngeal tube, and thus it is advisable to monitor and adjust the intracuff pressure of the laryngeal tube during anesthesia to minimize possible ischemic changes to the oropharynx.

Adolescent↗
PubMed2004

Propofol and midazolam inhibit gastric emptying and gastrointestinal transit in mice.

We studied the effect of propofol and midazolam on gastric emptying and gastrointestinal transit in mice. Ten minutes after intraperitoneal injection of propofol or midazolam, 0.2 mL of saline containing fluorescent microbeads was infused into the stomach. Thirty minutes later, the gastrointestinal tract was excised, and gastric emptying and gastrointestinal transit were calculated by measuring the quantity of fluorescent microbeads in the gastrointestinal tract by using a flow cytometer. At a dose that produced a light level of sedation (mice righted themselves within 2 s), both drugs significantly, but weakly, inhibited gastric emptying to a similar degree (propofol: P < 0.001 versus control value; 95% confidence interval [CI] for difference, 4.9%-20.2%; midazolam: P < 0.001 versus control value; 95% CI for difference, 7.8%-14.7%). Midazolam, but not propofol, delayed gastrointestinal transit (P < 0.001). At a larger dose that produced a deeper level of sedation (absence of righting reflex >10 s), both drugs significantly inhibited gastric emptying (propofol: P < 0.001; 95% CI for difference, 31.4%-61.2%; midazolam: P < 0.001; 95% CI for difference, 30.8%-61.1%) and gastrointestinal transit (P < 0.001 for both drugs).

Algorithms↗
PubMed2004

[Propofol anesthesia for fetal sedation].

We were requested to reduce neonatal respiratory effort at delivery in anesthetic management for Cesarean section. A 26-year-old pregnant woman was suspected through abdominal ultrasound examination and amniotic fluid test, of her baby having immature lungs associated with remarkable pleural effusion. Lungs could be damaged by respiratory effort after delivery, and respiratory management immediately after delivery was planned. Anesthesia was induced with propofol and fentanyl 300 micrograms. Propofol was administered with a target controlled infusion setting with the target blood concentration of 10 micrograms.ml-1. Fetal electrocardiogram was monitored for detecting fetal sedation. The concentrations of propofol at delivery were 10.7 and 4.1 micrograms.ml-1 in maternal arterial and umbilical venous blood, respectively, and the baby was apneic. Respiration of the baby was managed with a high frequency jet ventilation mode, and 160 ml of pleural effusion was aspirated immediately after the delivery. The baby was discharged from the hospital 5 weeks afterward.

Adult↗
PubMed2004

[Airway obstruction during one-lung ventilation using a bronchial blocker and a tracheostomy tube].

We describe our experience with a 60-year-old man who had severe airway obstruction during one-lung ventilation with the tracheostomy tube using a bronchial blocker. The blocker, deriving from Univent tube, was passed through the tracheostomy tube and placed in the right main bronchus. We checked that the blocker was in appropriate place with a bronchofiberscope and obtained good one-lung ventilation with the patient in the left lateral position. However, just after the start of operation, when the skin was incised, sever hypoxia and resultant bradycardia and hypotension occurred, probably because of not only malposition of blocker but also atelectasis in the upper lobe of the dependent lung by secretion.

Airway Obstruction↗
PubMed2003

Integrated pharmacological preconditioning in combination with adenosine, a mitochondrial KATP channel opener and a nitric oxide donor.

BACKGROUND: Mitochondrial K(ATP) channel activation is an essential component of ischemic preconditioning. These channels are selectively opened by diazoxide and may be up-regulated by adenosine and nitric oxide. Therefore, pharmacological preconditioning with diazoxide in combination with adenosine and a nitric oxide donor (triple-combination pharmacological preconditioning) may enhance cardioprotection. METHODS AND RESULTS: Isolated and perfused rat hearts underwent ischemic preconditioning with 3 cycles of 5 minutes of ischemia and 5 minutes of reperfusion before 5 minutes of oxygenated potassium cardioplegia and 35 minutes of ischemia. Pharmacological preconditioning was performed by adding adenosine, diazoxide, and a nitric oxide donor S-nitroso-N-acetyl-penicillamine each alone or in combinations for 25 minutes followed by 10 minutes washout before cardioplegic arrest. Only triple-combination pharmacological preconditioning conferred significant cardioprotection as documented by highly improved left ventricular function and limited creatine kinase release during reperfusion that was comparable to that afforded by ischemic preconditioning. Mitochondrial K(ATP) channel activity assessed by flavoprotein oxidation was increased by diazoxide, but no further increase in flavoprotein oxidation was obtained by ischemic preconditioning and triple-combination pharmacological preconditioning. Significant activation of protein kinase C-epsilon was observed in only ischemic preconditioning and triple-combination pharmacological preconditioning. Pretreatment with the mitochondrial K(ATP) channel inhibitor 5-hydroxydecanoate or the protein kinase C inhibitor chelerythrine abrogated activation of protein kinase C-epsilon and cardioprotection afforded by ischemic preconditioning and triple-combination pharmacological preconditioning. CONCLUSIONS: Integrated pharmacological preconditioning is not simply mediated by enhanced mitochondrial K(ATP) channel activation, but is presumably mediated through amplified protein kinase C signaling promoted by coordinated interaction of adenosine, mitochondrial K(ATP) channel activation, and nitric oxide.

Adenosine↗
PubMed2003

Regulation of Vav localization in membrane rafts by adaptor molecules Grb2 and BLNK.

Despite the importance of the Vav family proteins for B cell receptor (BCR) signaling, their activation mechanisms remain poorly understood. We demonstrate here that adaptor molecules Grb2 and BLNK, in addition to Vav, are required for efficient Rac1 activation in response to BCR stimulation. Loss of either Grb2 or BLNK results in decreased translocation of Vav3 to membrane rafts. By expression of Vav3 as a raft-targeted construct, the defective Rac1 activation in Grb2- or BLNK-deficient B cells is restored. Hence, our findings suggest that Grb2 and BLNK cooperate to localize Vav into membrane rafts, thereby contributing to optimal activation of Vav in B cells.

Adaptor Proteins, Signal Transducing↗
PubMed2003

Pentobarbital inhibits ketamine-induced dopamine release in the rat nucleus accumbens: a microdialysis study.

UNLABELLED: Dopamine release in the nucleus accumbens (NAC) plays a crucial role in the actions of various psychotropic and addictive drugs. Ketamine and barbiturates have psychotropic effects and addictive properties, but barbiturates prevent ketamine's psychotomimetic effects. We investigated the effects of ketamine and pentobarbital on dopamine release in the NAC. A microdialysis probe was implanted in the NAC in 35 rats, which were randomly assigned to seven groups: a normal saline intraperitoneal injection (ip) group, 50 and 100 mg/kg of ketamine ip groups, 25 and 50 mg/kg of pentobarbital ip groups, and a normal saline or 25 mg/kg of pentobarbital ip followed by 50 mg/kg of ketamine ip groups. Perfusate samples were collected every 20 min, and dopamine concentration was measured by high-performance liquid chromatography. Ketamine at doses of 50 mg/kg and 100 mg/kg significantly increased dopamine release in the NAC. Conversely, pentobarbital significantly decreased dopamine release in the NAC and inhibited the ketamine-induced dopamine release. These data suggest that the dopamine release in the NAC may be involved in ketamine-induced, but not barbiturate-induced, psychotropic effects and addiction. Inhibition of ketamine-induced dopamine release by barbiturates may be a mechanism by which they prevent ketamine emergence reactions. IMPLICATIONS: Ketamine increased dopamine release in the nucleus accumbens, which was inhibited by pentobarbital. The mesolimbic dopamine system may be involved in the psychotomimetic effects of ketamine, and the suppression of ketamine emergence reactions by barbiturates may be because of the inhibition of ketamine-induced dopamine release in the nucleus accumbens.

Anesthetics, Dissociative↗
PubMed2003

[Difficult tracheal intubation in a patient suspected of malignant hyperthermia].

We report anesthetic management of a patient suspected of malignant hyperthermia with difficult tracheal intubation. A 64-year-old man was scheduled for a fixation of humerus bone fractures in prone position. He had a history of difficult tracheal intubation due to masseter spasm, and his niece was suspected to be malignant hyperthermia. Anesthesia was induced with propofol using a target controlled infusion. No muscle relaxant was given and spontaneous breathing was maintained. Trials for tracheal intubation failed whenever using a standard laryngoscope, a bronchofiberscope, a laryngeal mask airway or an intubating laryngeal mask airway. Resecting the epiglottic elevating bar of an intubating laryngeal mask airway enabled fiberoptic tracheal intubation. No symptom suggesting malignant hyperthermia developed.

Anesthesia↗
PubMed2003

[Anesthetic management of therapeutic angiogenesis with autologous bone marrow cells for medically intractable angina pectoris].

We report anesthetic management of therapeutic angiogenesis with autologous marrow cells for medically intractable angina pectoris. A 64-year-old man suffering from severe angina after multiple bypass surgery was presented for this novel procedure. Under general anesthesia with propofol, about 650 ml of bone marrow was aspirated from his ilium in prone position. Hypotension was treated with volume infusion and the use of vasoactive drugs. Next, left thoracotomy was performed with the patient in right lateral position. With the aid of one lung ventilation, the apex and the posterior wall of the heart, where ischemia had been localized, was exposed. An epicardial stabilizer was used to immobilize the apex where purified marrow cells were manually injected. Ventricular premature beats occurred when marrow cells were injected, but they were self-limited. The procedure was completed without any serious complications. Prevention of perioperative myocardial ischemia, volume supplementation during bone marrow aspiration and preparation for ventricular arrhythmia during injection were suggested to be the key issues in the management of this procedure.

Anesthesia↗