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Biomedical subjects

I Yoshiya

Publications and source records attributed to I Yoshiya.

At least 55 records · Page 3Linked to original sources
PubMed1998

[Total intravenous anesthesia with propofol is advantageous than thiopental-sevoflurane anesthesia in the recovery phase].

A randomized, prospective and multi-institutional study was performed to investigate whether different anesthetic methods affected differently the quality of recovery from anesthesia. Two hundred and eleven patients were allocated to one of two groups; total intravenous anesthesia (TIVA) with propofol and fentanyl (group P, n = 107) and general anesthesia with thiopental, sevoflurane and nitrous oxide (group TS, n = 104). The rapidity of emergence from anesthesia and postoperative incidence of nausea, vomiting, and headache were compared between the two groups. The group P showed significantly shorter emergence times for verbal command responses (7.4 +/- 5.6 min), extubation (10.0 +/- 6.0 min) and orientation (13.1 +/- 7.8 min) than the group TS (9.1 +/- 5.0 min, 11.7 +/- 6.2 min, 16.4 +/- 7.9 min, respectively). The postoperative incidence of vomiting was not significantly different between the two groups (3.7% in the group P and 9.6% in the group TS), but the postoperative incidences of nausea and headache were significantly lower in the group P compared with the group TS (10.3%, 17.8%, respectively in the group P and 34.6%, 29.8%, respectively in the group TS). We conclude that TIVA with propofol is advantageous than thiopental-sevoflurane anesthesia in the recovery phase.

Adult↗
PubMed1997

Intrathecal administration of a new nitric oxide donor, NOC-18, produces acute thermal hyperalgesia in the rat.

A nitric oxide releasing compound, NOC-18, was injected intrathecally in order to determine the role of NO in spinal nociceptive mechanisms in rats. The nociceptive threshold was evaluated by the radiant heat tail-flick test. The effects of intrathecal injection of N-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor; methylene blue (MB), a soluble guanylate cyclase inhibitor and hemoglobin (Hb), an NO scavenger, on the nociceptive threshold were measured in the presence and absence of 0.1, 1 and 10 microg of NOC-18. The results were compared with a control group of rats which were injected with the same volume of normal saline. NOC-18 caused a dose-dependent curtailment of the tail-flick latency during the period from 15 to 150 min. L-NAME, MB and Hb all produced prolongation of the tail-flick latency during the same time period. The hyperalgesia induced by this concentration range of NOC-18 was completely blocked by Hb, but was not affected by either L-NAME or MB. These findings indicate that NO plays a direct role in thermal hyperalgesia in the spinal cord, and that an another pathway in addition to the NO-cGMP pathway may be involved.

Animals↗
PubMed1997

Expression of beta-calcitonin gene-related peptide in axotomized rubrospinal neurons and the effect of brain derived neurotrophic factor.

The mRNA levels for alpha- and beta-calcitonin gene-related peptide (CGRP) in rat rubrospinal neurons were studied by in situ hybridization 3, 7, 14, 28 and 56 days following cervical spinal hemisection. CGRP-like immunoreactivity (LI) in the rubrospinal neurons and the rubrospinal tract in cervical spinal cords were examined using immunohistochemistry. There was almost no signal for alpha- and beta-CGRP mRNAs and undetectable level of CGRP-LI in the rubrospinal neurons ipsilateral to cervical spinal hemisection (control side). Fourteen days after spinal hemisection, the rubrospinal neurons contralateral to cervical hemisection (axotomized side) showed CGRP-LI in their cell bodies, and CGRP containing fibers were observed in the lateral funiculi just proximal, but not distal, to the injury sites. In situ hybridization showed upregulation of beta-CGRP mRNA in a subpopulation of the rubrospinal neurons on the axotomized side. The proportion of beta-CGRP mRNA-expressing neurons reached its maximum (approximately 19%) 4 days following axotomy and slowly decreased to about 5% 56 days after axotomy. The percentage of alpha-CGRP mRNA-expressing neurons was much lower than that of beta-CGRP mRNA (maximum about 2.6% 4 days after axotomy) and not significantly different from the control side throughout the time period studied. These data indicate that axotomy induces de novo synthesis of the CGRP beta-subtype in rubrospinal neurons and that the beta-CGRP is transported to the injury site through the rubrospinal tract. In addition, we studied the effect of the intracerebral injections of brain derived neurotrophic factor (BDNF). BDNF treatment fully reversed the severe cell atrophy that followed axotomy and increased the number of neurons labeled for beta-CGRP mRNA, but did not increase the percentage of rubrospinal neurons expressing beta-CGRP mRNA. Thus, topical application of BDNF does not have direct modulatory effect on CGRP induction in axotomized neurons in the red nucleus.

Animals↗
PubMed1997

Inhalation anesthetics suppress the expression of c-Fos protein evoked by noxious somatic stimulation in the deeper layer of the spinal cord in the rat.

The effects of inhalation anesthetics, nitrous oxide (N2O) and halothane, on the expression of c-Fos protein evoked by formalin injection were studied in the spinal cord in the rat. The expression of c-Fos protein was detected by immunocytochemistry following the injection of formalin (5%, 100 microliters) into the plantar surface of the left hindpaw. After 15 min of halothane (F) anesthesia, the anesthetics was switched to 40% or 70% of N2O, 0.5% or 1.5% of F or room air (for control) immediately following the formalin injection. Two hours later the rats were sacrificed and perfused. Sections of the L4 level of spinal cord were immunostained with anti c-Fos antibody. We counted the number of Fos-like immunoreactive (FLI) cells in every specific lamina as follows: superficial layer (laminae I and II), nucleus proprius (laminae III and IV), neck of the dorsal horn (laminae V and VI) and ventral gray (laminae VII-X). Then we compared the results of each category of sample. Both N2O and halothane suppressed the expression of c-Fos in the neck of the dorsal horn and ventral gray in a dose-dependent manner, but no effects were seen at the superficial layer or nucleus proprius. Suppression of c-Fos expression was greater under N2O than halothane anesthesia. This finding suggests that N2O had a stronger analgesic effect than halothane. The current study indicates that inhalation anesthetics do not act equally on every kind of spinal neurons. Both N2O and halothane have effects on spinal neurons in the deeper layers but not on the neurons existed in laminae I-II, some of which directly receive noxious inputs. Pretreatment with 2 mg/kg of naloxone, which completely reversed the effects of morphine, did not alter the effect of 70%N2O, suggesting that the analgesic effect of N2O is not mediated by an intrinsic opioid mechanism at the spinal cord level.

Analgesia↗
PubMed1997

Effects of vasodilators guanethidine, nicardipine, nitroglycerin, and prostaglandin E1 on primary afferent nociceptors in humans.

Although vasodilator agents have been used to alleviate the pain of complex regional pain syndromes, the precise mechanism of pain relief is not well known. In this study the effects of various kinds of vasodilators on primary afferent nociceptors were investigated by measuring the thermal pain threshold. Evaluated in the study were the effects of guanethidine (2 mg/mL), nicardipine (0.2 mg/mL). Nitroglycerin (0.3 mg/mL), and prostaglandin E1 (1 microgram/mL) on the cutaneous pain threshold and blood flow at 7-day intervals in six healthy volunteers. Each aliquot of 0.5 mL of the test vasodilator or lidocaine (10 mg/mL) and saline (control) were intradermally injected at three sites each on both forearms. The pricking-pain threshold and skin tissue blood flow were determined using a radiant heat-stimulating system and a laser-Doppler tissue-blood flowmeter, respectively. The pain threshold increased with lidocaine, guanethidine, and nicardipine; remained unchanged with Nitroglycerin; but decreased with prostaglandin E1. In contrast, the skin tissue blood flow increased by four to nine times with all vasodilators. These results indicate that the effect of vasodilators on primary afferent nociceptors is not related to the vasodilating effect and may not involve a common mechanism of action for pain relief in complex regional pain syndromes.

Adult↗
PubMed1997

Arterial oxygenation during one lung ventilation.

PURPOSE: To compare the effects of isoflurane and sevoflurane on arterial oxygenation and middle cerebral artery blood flow velocity during one lung ventilation. METHODS: This was a randomized, crossover study in 20 patients undergoing thoracotomy for oesophageal cancer and scheduled for long term one lung ventilation (OLV). They were randomized to one of two groups: group A, firstly isoflurane was administered followed by sevoflurane, and then isoflurane was resumed; group B, the order of the administration was reversed. Arterial blood gas samples were drawn at the start of OLV, 30 and 60 min after the initiation of OLV and the end of OLV (the change of volatile anesthetics was done 30 and 60 min after the start of OLV). Middle cerebral artery (MCA) was monitored continuously with the probe positioned over the temporal bone window. This probe transmitted 2 MHZ wave Doppler signals. Time-averaged MCA blood flow velocity was calculated from the signals. RESULTS: The PaO2 values decreased 30 min after the start of OLV (364.4 +/- 33.4 mmHg vs 179.0 +/- 19.5, and 338.7 +/- 24.8 mmHg vs 139.7-19.9 in groups A and B respectively), but there was no difference between the groups. Blood flow velocity of MCA did not change after the start of OLV (53.1 +/- 3.2, 55.9 +/- 3.0, 56.4 +/- 2.4, and 54.1 +/- 1.9 vs 50.8 +/- 2.1, 50.7 +/- 2.4, 53.7 +/- 1.5, 50.8 +/- 2.2 cm.sec-1 in groups A and B respectively): there was no difference between the groups. (P < 0.05). CONCLUSION: In clinical practice, the selection of either isoflurane and sevoflurane for OLV was of no difference in terms of the arterial blood oxygenation. With both agents MCA blood flow velocity was maintained during OLV.

Adult↗
PubMed1997

Differential expression patterns of GABA transporters (GAT1-3) in the rat olfactory bulb.

The localization of GABA transporters 1-3 (GAT1-3) was investigated in the rat olfactory bulb by using in situ hybridization and immunohistochemistry. In the glomerular and the internal granular layers, GAT1 mRNA was expressed in most of periglomerular and granule cells, which are known to be GABAergic. In addition, we compared GAT1 mRNA expression with that of glutamic acid decarboxylase67 (GAD67) mRNA. The expressions were very similar in these two layers, indicating that GAT1 mRNA is mainly expressed in GABAergic neurons. However, in the external plexiform and the olfactory nerve layers, we observed more GAT1 mRNA-positive cells than GAD67 ones, suggesting that GAT1 mRNA is also expressed in non-GABAergic neurons and in glial cells. GAT3 mRNA expression was observed in small glial-like cells which might be involved in GABAergic neurotransmission throughout the olfactory bulb. This was confirmed by double-immunostaining studies which showed the expression of both GAT3 and glial fibrillary acidic protein (GFAP) mRNAs in astrocytes. Moreover, GAT2 mRNA was expressed only in the ependyma and arachnoid. These findings suggest that the expression patterns of GABA transporters differ with the type of cells in the rat olfactory bulb where GAT1 and GAT3 may play an imporatant role in GABA-mediated transmission, such as lateral inhibition.

Animals↗
PubMed1997

Localization of molecules involved in cytokine receptor signaling in the rat trigeminal ganglion.

The localization of some cytokine receptors and their downstream intracellular signaling molecules was examined in the trigeminal ganglia of rats. Among cytokine receptor components, we examined signal transduction subchain, gp130, IL-2Rgamma and IL-5Rbeta, which are common to respective groups of cytokine receptors. Most of the sensory ganglion neurons expressed gp130, but not IL-2Rgamma nor IL-5Rbeta. We further examined the localization of Janus kinase (JAK) family members which were reported to be associated with various kind of cytokine receptors and are thought to be implicated in major cytokine receptor-signaling pathways [6,9,11,13]. While JAK1 and Tyk2 were expressed in all the type of neurons, JAK2 was predominantly expressed in the small neurons. In addition, JAK3 immunoreactivity was only found in satellite cells. The present results indicate that most of neurons express gp130, and that the localization of JAK family members differs with the cell type. This also suggests that the cytokine receptor-signaling pathway may be different in neuronal and glial cells.

Animals↗
PubMed1997

Critical care in Japan and Korea. The market of excellence.

Medical services in general are well advanced in Japan and Korea. However, intensive and critical care medicine is still on its way to further developments. One particular problem in both countries is the shortage of positions for intensive care physicians and nurses. Although they are well equipped with therapeutic and monitoring devices, there are a limited number of ICU beds. In Korea, the estimated number of ICUs is 122 or more. In Japan, the number of ICUs is estimated to be between 229 and 944.

Critical Care↗
PubMed1997

The involvement of pertussis toxin-sensitive G proteins in the post receptor mechanism of central I1-imidazoline receptors.

1. To elucidate the possible involvement of pertussis toxin (PTX)-sensitive G proteins in the post receptor mechanism of alpha 2-adrenoceptors and imidazoline receptors, we examined the effect of pretreatment of the central nervous system with PTX on the antidysrhythmic effect of dexmedetomidine, a selective alpha 2-adrenoceptor agonist, and rilmenidine, a selective I1-imidazoline receptor agonist on halothane-adrenaline dysrhythmias in rats. 2. Dexmedetomidine (0, 1.0, 2.0, 5.0 micrograms kg-1 min-1.i.v.) and rilmenidine (0, 1.0, 3.0, 10, 20 micrograms kg-1, i.v.) prevented the genesis of halothane-adrenaline dysrhythmias in a dose-dependent fashion. Both idazoxan (10, 20 micrograms kg-1, intracerebroventricularly (i.c.v.)), an alpha 2-adrenoceptor antagonist with high affinity for imidazoline receptors, and rauwolscine, (40 micrograms kg-1, i.c.v.), an alpha 2-adrenoceptor antagonist with low affinity for imidazoline receptors inhibited the action of dexmedetomidine (5.0 micrograms kg-1, min-1, i.v.), but the inhibitory potency of idazoxan was much greater than that of rauwolscine. While the pretreatment with PTX (0.1, 0.5, 1.0 micrograms kg-1, i.c.v.) did not change the dysrhythmogenecity of adrenaline, this treatment completely blocked the antidysrhythmic property of rilmenidine (20 micrograms kg-1, i.v.) as well as dexmedetomidine (5.0 micrograms kg-1 min-1, i.v.). 3. It is suggested that central I1-imidazoline receptors as well as alpha 2-adrenoceptors may be functionally coupled to PTX-sensitive G proteins.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1997

Interactions between neuronal histamine and halothane anesthesia in rats.

Using an in vivo microdialysis method, we measured the release of histamine in the anterior hypothalamic area (AHy) of rats under several concentrations of halothane anesthesia (1, 0.5, and 0.2%). The release of histamine increased to 341 and 325% at halothane concentrations of 0.5 and 0.2%, compared with the basal level at anesthesia induced by 1% halothane. alpha-Fluoromethylhistidine (100 mg/kg i.v.), a specific and irreversible inhibitor of histidine decarboxylase, reduced the histamine release to <35% of the basal value at 1% halothane anesthesia in the AHy, and also decreased the anesthetic requirement for halothane, evaluated as the minimum alveolar concentration (MAC), by 26%. Furthermore, pyrilamine (20 mg/kg i.v.), a brain-penetrating H1 antagonist, and zolantidine (20 mg/kg i.v.), a brain-penetrating H2 antagonist, reduced the MAC for halothane by 28.5 and 16%, respectively. Although thioperamide (5 mg/kg i.v.), an antagonist of presynaptic H3 autoreceptor, induced an approximate twofold increase in the level of histamine release in conscious freely moving rats, the same dose of thioperamide had little effect on the release of histamine under 1% halothane anesthesia in the AHy. Furthermore, thioperamide did not change the anesthetic requirement (MAC) for halothane. The present findings indicate that halothane anesthesia inhibits the release of neuronal histamine and that histaminergic neuron activities change the anesthetic requirement (MAC) for halothane through H1 as well as H2 receptors.

Anesthetics, Inhalation↗
PubMed1997

Laser Doppler skin blood flow and sympathetic nervous responses to surgical incision during halothane and isoflurane anesthesia.

The aim of the present study was to evaluate whether a sudden decrease in skin blood flow measured using a laser Doppler velocimeter reflects sympathetic nervous response to surgical skin incision during halothane (n = 17) and isoflurane (n = 16) anesthesia in 33 ASA physical status I or II patients scheduled for laparotomy. Plasma norepinephrine concentrations in the responding patients who showed a sudden decrease in the skin blood flow after surgical incision increased significantly and continued to increase 1-10 min after skin incision under halothane and isoflurane anesthesia. Although plasma norepinephrine concentrations in the nonresponders did not increase after surgical incision with halothane, the concentrations increased significantly at 1 min, but not at 3 and 10 min, after skin incision with isoflurane. The results indicate that the sudden decrease in laser Doppler flow reflects the sympathetic response to surgical incision. However, these also suggest that the factors that control the skin blood flow may not be simply sympathetic but may reflect other modulators as well. Plasma epinephrine concentration increased during skin incision, but the concentrations did not differ between the patients with and without a sudden decrease in skin blood flow. Increases in systolic blood pressure and rate-pressure product on skin incision were also significantly more in patients with skin blood flow response compared with those without the response. The magnitude of changes in plasma norepinephrine concentration and hemodynamic variables with skin incision was greater with isoflurane than with halothane at the same minimum alveolar anesthetic concentration level.

Adult↗
PubMed1997

The effects of epidural fentanyl on hemodynamic responses during emergence from isoflurane anesthesia and tracheal extubation: a comparison with intravenous fentanyl.

To investigate the effects of epidural fentanyl infusion on hemodynamic responses to recovery of consciousness and tracheal extubation, we studied 50 unpremedicated patients scheduled for abdominal hysterectomy. All patients underwent epidural catheterization and blind infusion of placebo and study drug. Patients were assigned randomly to three groups: Group I received epidural and intravenous (i.v.) bolus injections and infusion of saline at the rate of 0.2 mL x kg(-1) x h(-1); Group II received an i.v. injection of fentanyl 2 microg/kg for 30 s followed by 25 ng x kg(-1) x min(-1), and Group III received epidural injection and infusion using the same administration regimen as Group II. Anesthesia was induced with and maintained by isoflurane alone in an air-oxygen mixture. The study drug was administered at the start of retroperitoneal suturing. Hemodynamic variables, including systolic and diastolic arterial pressures (SAP and DAP, respectively) and heart rate (HR), were recorded every minute between the start of administration of the study and 5 min after tracheal extubation. During emergence from anesthesia and tracheal extubation, the increases in SAP, DAP, and HR in Groups II and III were significantly diminished (P < 0.05) compared with those in Group I. Arterial pressures, but not HR, were attenuated more significantly in Group III than in Group II during and after tracheal extubation, although the plasma fentanyl concentration was significantly lower (P < 0.01) in Group III (0.64 +/- 0.03 ng/ mL, [mean +/- SD]) than in Group II (1.15 +/- 0.09 ng/mL). The incidence of coughing during and after extubation was also lower with Group III. Suppression of respiratory rate prior to tracheal extubation was similar in the two groups receiving fentanyl. These findings suggest that the significant reduction in arterial pressures responses to tracheal extubation due to epidural fentanyl infusion may arise from more suppression of cough reflex than i.v. fentanyl infusion, which could be provided by the spinal action of epidural fentanyl as well as the supraspinal action.

Adjuvants, Anesthesia↗
PubMed1997

A comparative study of the antinociceptive action of xenon and nitrous oxide in rats.

UNLABELLED: We attempted to clarify the mechanism of antinociceptive action induced by xenon and nitrous oxide. Eighty percent of nitrous oxide or 80% xenon was applied to rats inside enclosed clear plastic glass cylinders with their tails protruding for assessment of the tail-flick response to radiant heat. With repeated testing, there was a rapid reduction to nitrous oxide antinociception within 90 min, which was interpreted as development of tolerance, but not to xenon antinociception. Nitrous oxide antinociception was blocked by the intraperitoneal administration of 0.1 or 1.0 mg/kg yohimbine, but not by 1.0 or 5.0 mg/kg L659-066 or by 5.0 or 10 mg/kg naloxone. Xenon antinociception was not affected by any of these drugs. Yohimbine and L659-066 are characterized as alpha 2-adrenoceptor antagonists. Although yohimbine penetrates the blood-brain barrier after systemic administration, L659-066 does not penetrate it and act peripherally. Therefore, the results indicate that alpha 2-adrenoceptors, but not opioid receptors, may play a key role in antinociception induced by nitrous oxide in the central nervous system. Furthermore, the mechanism of xenon antinociception differs from that of nitrous oxide because it does not involve either alpha 2 or opioid receptors. IMPLICATIONS: The precise mechanism of antinociceptive action of nitrous oxide and xenon remains unknown. It is still controversial whether an opioid system plays a role in antinociception induced by nitrous oxide. The results of the study showed that antagonism of central alpha 2-adrenoceptors, but not opioid receptors, reverses the antinociception induced by nitrous oxide but not by xenon, which indicates that alpha 2-adrenoceptors may play a key role in nitrous oxide antinociception.

Analgesics, Non-Narcotic↗
PubMed1997

The effect of imidazoline receptors and alpha2-adrenoceptors on the anesthetic requirement (MAC) for halothane in rats.

BACKGROUND: Recent evidences have documented that several pharmacologic actions of alpha2-adrenoceptor agonists are mediated via activation of not only alpha2-adrenoceptors, but also by imidazoline receptors, which are nonadrenergic receptors in the central nervous system. However, the effect of imidazoline receptors on the anesthesia is not well known, and it is important to clarify the effects of both receptors on anesthesia. METHODS: Seventy-two rats were anesthetized with halothane, and the anesthetic requirement for halothane was evaluated as minimum alveolar concentration (MAC). The MAC for halothane was determined in the presence of dexmedetomidine (0, 10, 20, and 30 microg/kg, intraperitoneally [IP]), a selective alpha2-adrenoceptor agonist with weak affinity for imidazoline receptors. Then, the authors evaluated the inhibitory effect of rauwolscine (20 mg/kg, IP), an alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 microg/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 microg/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated. RESULTS: Dexmedetomidine decreased the MAC for halothane dose-dependently, and this MAC-reducing action of dexmedetomidine was completely blocked by rauwolscine. Rilmenidine alone did not change the MAC for halothane. CONCLUSIONS: The present data indicate that the anesthetic sparing action of dexmedetomidine is most likely mediated through alpha2- adrenoceptors, and the stimulation of imidazoline receptors exerts little effect on the anesthetic requirement for halothane.

Adrenergic alpha-Agonists↗
PubMed1997

Tension pneumopericardium following tracheoplasty for congenital tracheal stenosis.

Tension pneumopericardium is a rare complication of mechanical ventilation following tracheoplasty for congenital tracheal stenosis. This case report describes fatal tension pneumopericardium in a three-month-old male infant some 24 hours following tracheoplasty for this condition. Because of persisting stenosis of the left main bronchus, ventilation pressures of PIP 23 cm H2O and PEEP 5 cm, progressing to PIP 28 cm and PEEP 7 cm were needed to maintain adequate respiratory exchange. Partial relief of the pneumopericardium was achieved by vigorous cardiac massage, but three days later the infant died of massive airway haemorrhage.

Acidosis, Respiratory↗