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Fumio Goto

Publications and source records attributed to Fumio Goto.

At least 73 records · Page 4Linked to original sources
PubMed2004

The effect of diabetes on the interrelationship between jugular venous oxygen saturation responsiveness to phenylephrine infusion and cerebrovascular carbon dioxide reactivity.

In this study, we examined whether cerebrovascular carbon dioxide (CO(2)) reactivity was related to the response of jugular venous oxygen saturation (SjvO(2)) to phenylephrine infusion in diabetic patients during cardiopulmonary bypass. Forty diabetic patients scheduled for coronary artery bypass graft surgery were studied, and 40 age-matched nondiabetic cardiopulmonary bypass patients served as controls. Cerebrovascular CO(2) reactivity was measured continuously using transcranial Doppler. Mean arterial blood pressure (MAP) was increased by repeated phenylephrine infusion until reaching 100% of baseline values. There was a significant difference in absolute CO(2) reactivity between the diabetic and control groups (controls, 2.8 +/- 0.7 cm. s(-1). mm Hg(-1); diabetics, 2.2 +/- 1.1 cm. s(-1). mm Hg(-1); P = 0.02). Among the diabetics, absolute CO(2) reactivity in insulin-dependent patients was less than that in noninsulin-dependent patients (diet therapy group, 3.2 +/- 0.7; glibenclamide group, 2.6 +/- 0.7; insulin-dependent group, 1.0 +/- 0.7; P < 0.01). There was a correlation between absolute CO(2) reactivity and the mean slope of SjvO(2) versus MAP for increasing MAP (r = 0.54; P < 0.0001). In conclusion, we found that the interrelationship between SjvO(2) responsiveness to phenylephrine infusion and cerebrovascular CO(2) reactivity, as well as impaired cerebrovascular autoregulation, were associated with previous hyperglycemia.

Aged↗
PubMed2004

[Molecular mechanism of morphine tolerance and biological approaches to resolve tolerance].

One of the major problems associated with the chronic use of morphine is tolerance. Repeated uses of morphine to relieve pain often cause patients to develop increasing resistance to the effects of the drugs, so that progressively higher doses are required to achieve the same analgesic effects. Acquired tolerance is thought to be different from dependence or addiction, but molecular mechanism underlying the development of tolerance is still unclear. Tolerance has been explained by desensitization of opioid receptor signaling and loss of functional receptors in the cell surface. The classical hypothesis was that phosphorylation and arrestin binding resulted in uncoupling of the receptor from G proteins, and reduced agonist efficacy. The receptor internalization would then result in fewer functional receptors at the cell surface. These events would cause so-called signaling desensitization. However, recent molecular biological studies have led researchers to revise the classical view of tolerance from observations that morphine does not always promote efficient receptor internalization. Among several key processes, the sequestration and subsequent internalization of the opioid receptor may play an important role for morphine tolerance. In fact, recent studies have suggested that receptor internalization can reduce tolerance. In addition, activation of the NMDA subtype of the glutamate receptor has been suggested as an anti-opioid system in the development of morphine tolerance. In this review, we focus on recent research progress on the morphine tolerance, and molecular biological and clinical approaches to resolve morphine tolerance.

Animals↗
PubMed2004

[Postoperative laryngeal edema presumably due to hypoalbuminemia causing acute airway obstruction after extubation in a patient after nephrectomy].

We report here a case of upper airway obstruction occurring after extubation in a 55-yr-old 60 kg man after elective nephrectomy. Anesthesia was maintained with O2 (33%), N2O, sevoflurane (1.5-2%), and propofol infusion (2 mg x kg(-1) x hr(-1)). Blood loss was 1,965 ml, part of which was substituted by blood transfusion and albumin infusion. After surgery, the patient recovered uneventfully and could be extubated shortly. Twenty minutes after extubation, he developed dyspnea progressively with stridor and became cyanotic despite the use of oxygen mask and assisted ventilation. Oxygen saturation decreased gradually, and bradycardia (<30 beats x min(-1)) and severe hypotension were also observed. Cardiopulmonary resuscitation using epinephrine was immediately started. Re-intubation of the trachea was difficult due to severe edema, but eventually performed using a tube of a smaller size (internal diameter 7.0 mm). Subsequent investigations using a fiberscope confirmed extensive soft tissue swelling, maximal at the level of the vocal cord and extending up- and down-wards to the trachea, indicating that the obstruction is caused by severe laryngeal edema. We believe that edema may have been caused by hypoalbuminemia (1.3 g x dl(-1)) at the end of operation. Therefore, it should be noted that hypoalbuminemia may cause laryngeal edema leading to acute airway obstruction.

Acute Disease↗
PubMed2004

[Ventricular tachycardia induced by the change of position for epidural catheter insertion in a patient with hypertrophic obstructive cardiomyopathy].

We report here a case of ventricular tachycardia (VT) induced by the change of position for insertion of an epidural catheter before the induction of general anesthesia. A 79-yr-old woman was scheduled for elective right lung surgery. Past history included hypertension and hypertrophic obstructive cardiomyopathy (HOCM), which were treated with a calcium channel blocker and an anti-arrhythmic drug. Preoperative echocardiogram (ECG) showed first degree arterio-ventricular block and left ventricular hypertrophy. Before the induction of general anesthesia, the patient was turned into the left lateral position for the insertion of an epidural catheter. Shortly after the change of position, ECG showed transient VT, which lasted for approximately 40 sec, and she was forced to be turned to the supine position and required recovery for a time. VT was successfully treated and terminated by changing to the supine position and intravenous injection of 2% lidocaine (2 ml). The left radial artery was cannulated for monitoring arterial blood pressure and sampling. Since no abnormality was observed in ECG for the next twenty minutes, the patient was turned to the left lateral position again and epidural catheterization was performed through T 7-8 interspace. Considering some risk factors such as intraoperative change of position, the surgery was cancelled on that day. Postoperatively amiodarone was used and an implantable cardioverter defibrillator (ICD) was planted for risk reduction of sudden cardiac death due to ventricular arrhythmia. The cause of VT in our case is not certain; we believe that VT might be closely related to the left lateral position, especially keeping of the forward-bending position, which might cause compression to the heart and produce stenosis of the left ventricular outflow tract. It should be noted that severe tachyarrhythmia might occur after turning patients with HOCM.

Aged↗
PubMed2004

[Comparison of the effects of colloid and crystalloid solution for volume preloading on maternal hemodynamics and neonatal outcome in spinal anesthesia for cesarean section].

BACKGROUND: The role of crystalloid or colloid preloading to prevent hypotension associated with spinal anesthesia in parturients during cesarean section has recently been questioned. The aim of the current study was to investigate the effects of volume preload with either crystalloid or colloid, or with no preload on changes of maternal hemodynamics and neonatal outcomes. METHODS: After written informed consent had been obtained from each patient, thirty-two healthy parturients undergoing cesarean section were randomized to receive either acetated Ringer's solution (1,000 ml, n=8, AR group), 6% hydroxyethylstarch (1,000 ml, n=9, HES group), or no preload (n=10) before spinal anesthesia. In addition, emergency cases (n=5) such as prolonged labor without any maternal complication were also included for analysis. The incidence of hypotension, systolic blood pressure <80% of baseline or <100 mmHg, and the amount of ephedrine used to treat hypotension were compared. Neonatal outcome was also assessed measuring pH and lactate concentration in umbilical arterial blood samples. Apgar score was also measured at 1 and 5 min after delivery. RESULTS: There was no difference in demographic characteristics among the four groups. Minimal systolic arterial pressure (SAP) after spinal anesthesia did not differ among AR, HES, and no preload groups. However, a significant decline in SAP was observed in emergency group (82.2 +/- 14.3 mmHg, P<0.05). Although there was no difference in umbilical arterial blood pH, lactate concentration was significantly higher in emergency group (3.7 +/- 1.0 mmol x l(-1), P<0.01) than those of other groups. Apgar score at 1 min after delivery was significantly lower in emergency group. CONCLUSION: In healthy patients with full-term pregnancy, volume preloading has little effect on maternal hemodynamics and neonatal outcomes, suggesting that stable perioperative management is possible with or without volume preload before spinal anesthesia. However, preloading may be needed for prevention of hypotension in emergency cases.

Adult↗
PubMed2003

Diabetic patients have an impaired cerebral vasodilatory response to hypercapnia under propofol anesthesia.

BACKGROUND AND PURPOSE: The purpose of this study was to examine the effects of diabetes mellitus and its severity on the cerebral vasodilatory response to hypercapnia. METHODS: Thirty diabetic patients consecutively scheduled for elective major surgery were studied. After induction of anesthesia, a 2.5-MHz pulsed transcranial Doppler probe was attached to the patient's head at the right temporal window, and mean blood flow velocity of the middle cerebral artery (Vmca) was measured continuously. After the baseline Vmca, arterial blood gases, and cardiovascular hemodynamic values were measured, end-tidal CO2 was increased by reducing ventilatory frequency by 2 to 5 breaths per minute. Measurements were repeated when end-tidal CO2 increased and remained stable for 5 to 10 minutes. RESULTS: Significant differences were observed in absolute and relative CO2 reactivity between the diabetes and control groups (absolute CO2 reactivity: control, 2.8+/-0.7; diabetes mellitus, 2.1+/-1.3; P<0.01; relative CO2 reactivity: control, 6.3+/-1.4; diabetes mellitus, 4.5+/-2.7; P<0.01, Mann-Whitney U test). Significant differences were also found between diabetic patients with retinopathy and those without retinopathy in absolute (P=0.002) and relative (P=0.002) CO2 reactivity, glycosylated hemoglobin (P=0.0034), and fasting blood sugar (P=0.01) (Scheffé's test, Mann-Whitney U test). There was an inverse correlation between absolute CO2 reactivity and glycosylated hemoglobin (r=0.69, P<0.001). CONCLUSIONS: Insulin-dependent diabetic patients have an impaired vasodilatory response to hypercapnia compared with that of the control group, and the present findings suggest that their degree of impairment is related to the severity of diabetes mellitus.

Anesthesia↗
PubMed2003

Fluvoxamine modulates pain sensation and affective processing of pain in human brain.

To better understand the antinociceptive effect of fluvoxamine, we measured regional cerebral blood flow during laser-evoked pain and hot sensations using H(2)15O positron emission tomography and also subjective pain and hot sensations before and after fluvoxamine or placebo administration for 7 days to 12 healthy volunteers. The subjectively rated pain score was significantly reduced by fluvoxamine administration. Painful stimuli activated multiple brain regions. After fluvoxamine administration the ipsilateral anterior cingulate cortex (ACC), contralateral insular cortex (IC), and contralateral secondary somatosensory cortex (SII) activations were reduced. The bilateral IC activation was also reduced in the placebo group. These results suggest that fluvoxamine specifically reduced activation of the ACC and SII, which are areas concerned with the affective and integrative components of pain.

Adult↗
PubMed2003

Interactions of 5-HT2 receptor agonists with acetylcholine in spinal analgesic mechanisms in rats with neuropathic pain.

Serotonin type 2 (5-HT(2)) receptors reportedly inhibit neuropathic pain in the spinal cord, but little is known about how spinal 5-HT(2) receptors might act against such abnormal sensitivity. We examined whether the cholinergic and tachykinin systems were involved in the antiallodynic effect of intrathecally administered 5-HT(2) receptor agonists in rats with nerve injury. Allodynia was produced by tight ligation of the left L5 and L6 spinal nerves, and determined by applying von Frey hairs to the left hindpaw. Effects of intrathecal pretreatment with 5-HT(2) receptor antagonists (ketanserin and RS-102221), muscarinic receptor antagonists (atropine and scopolamine), a choline uptake blocker (hemicholium-3), and an NK(1) receptor antagonist (L-706336) were assessed in rats subsequently given a 100- micro g intrathecal dose of a 5-HT(2) receptor agonist either alpha-methyl-5-HT or iododimethoxy aminopropane (DOI). Antiallodynic effects of 5-HT(2) receptor agonists were attenuated by the 5-HT(2A) receptor antagonist ketanserin (30 micro g), but not by the 5-HT(2C) receptor antagonist RS-102221 (40 micro g). Muscarinic receptor antagonists (30 micro g each), the choline uptake blocker (10 micro g), and the NK(1) receptor antagonist (30 micro g) also inhibited the antiallodynic effects of 5-HT(2) receptor agonists. Antiallodynic effects of intrathecally administered 5-HT(2) receptor agonists may be mediated by spinal release of acetylcholine induced via 5-HT(2A) and NK(1) receptors.

Acetylcholine↗
PubMed2003

Transfer of NMDAR2 cDNAs increases endogenous NMDAR1 protein and induces expression of functional NMDA receptors in PC12 cells.

The pheochromocytoma cell line (PC12) has been used as a model system for the study of regulation of expression of NMDA receptors. PC12 cells express a substantial amount of NMDAR1 subunit (NR1) mRNA, whereas they express only a small amount of NR1 protein. The level of functional NMDA receptor expression is almost negligible. To test the possibility that NMDAR2 subunits (NR2) control expression of functional NMDA receptors as well as NR1 protein, we transferred NR2A-D cDNAs into PC12 cells using adenovirus vectors. Prominent NMDA receptor-mediated currents were recorded in PC12 cells to which NR2A or NR2B cDNA was delivered without NR1 cDNA. The amplitudes of these responses were similar to those in PC12 cells to which NR1 cDNA was delivered together with NR2A or NR2B cDNA. In cells to which either NR2C or NR2D cDNA alone was delivered, NMDA receptor-mediated currents were also detected, although to a much lesser extent. These results showed that NR2 proteins produced by gene transfer are co-assembled with the endogenous NR1 protein to form functional heteromeric receptors. The delivery of NR2A-D cDNAs also increased the amount of NR1 protein but not that of NR1 mRNA, suggesting that this protein increase is due to post-transcriptional mechanisms. The effects of NR2A-B gene transfer on expression of NR1 protein were much more efficient than those of NR2C-D gene transfer.

Adenoviridae↗
PubMed2003

Epidural abscess in a patient with dorsal hyperhidrosis.

PURPOSE: To report the management of a patient who developed a lumbar epidural abscess when an epidural catheter was placed three years after a thoracic sympathectomy. The possible contribution of hyperhidrosis is discussed. CLINICAL FEATURES: A 62-yr-old male had compensatory hyperhidrosis in his back after thoracic sympathectomy. The patient, who suffered from thromboangeitis obliterans, underwent lumbar (L2-3) epidural catheterization in order to improve arterial circulation and ameliorate resting pain in his left leg. On the third day after catheterization, the patient complained of a dull pain in his back. Emergency magnetic resonance imaging revealed a 12-mm abscess in the epidural space. On the tenth day after catheterization, laminotomy at the 3-4 lumbar vertebrae and local drainage were performed. A 14-mm abscess was removed from the epidural space. The patient was discharged on day 21 after catheterization without any disability. CONCLUSION: Special precautions against infection may be necessary in patients with hyperhidrosis in the area where continuous epidural catheterization is attempted.

Anesthesia, Epidural↗
PubMed2003

Comparative effects of propofol versus fentanyl on cerebral oxygenation state during normothermic cardiopulmonary bypass and postoperative cognitive dysfunction.

BACKGROUND: The purpose of this study was to examine the comparative effects of propofol and fentanyl on cerebral oxygenation during normothermic cardiopulmonary bypass and postoperative cognitive dysfunction. METHODS: One hundred eighty patients scheduled for elective coronary artery bypass grafting were randomly divided into two groups: propofol group (n = 90) and fentanyl group (n = 90). After induction of anesthesia, a fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor jugular venous oxygen hemoglobin saturation continuously. Hemodynamic measurements and arterial and jugular venous blood gases were measured at seven time points. All patients underwent a battery of neurologic and neuropsychological tests on the day before the operation and at 6 months after the operation. RESULTS: Cerebral desaturation (defined as a jugular venous oxygen hemoglobin saturation value less than 50%) during cardiopulmonary bypass was more frequent in the fentanyl group than in the propofol group. Cerebral desaturation time (duration when jugular venous oxygen hemoglobin saturation was less than 50%) and the ratio of cerebral desaturation time to total cardiopulmonary bypass time in the fentanyl group differed significantly from those in the propofol group (fentanyl group: 27 +/- 14 minutes, 20% +/- 9%; propofol group: 18 +/- 11 minutes, 14% +/- 7%, respectively, p < 0.05). There was no significant difference in postoperative cognitive dysfunction at 6 months after operation between the two groups (propofol group: 5 of 77, 6%; fentanyl group: 5 of 75, 7%). CONCLUSIONS: Propofol preserved cerebral oxygenation state estimated by jugular venous oxygenation during cardiopulmonary bypass compared with the fentanyl group. However, propofol did not affect postoperative cognitive dysfunction.

Aged↗
PubMed2003

The effects of volatile anesthetics on nonadrenergic, noncholinergic depressor responses in rats.

UNLABELLED: The effects of volatile anesthetics on nonadrenergic, noncholinergic (NANC) transmission mediated by calcitonin gene-related peptide (CGRP) are unclear. We studied the effects of isoflurane, halothane, and sevoflurane on NANC depressor responses to electrical spinal cord stimulation in pithed rats whose mean arterial blood pressure was maintained near 120 mm Hg by continuous infusion of methoxamine. Autonomic outflow was blocked by hexamethonium. After 30 min of inhalation of different concentrations of anesthetics, spinal cord stimulation at the lower thoracic level (10 V at 4 Hz; duration, 1 ms) was applied for 30 s to induce a NANC depressor response. Isoflurane at 2% and halothane at 1.5% attenuated NANC depressor responses significantly, whereas isoflurane at 1%, halothane at 0.75%, and sevoflurane at 2% or 4% did not. Volatile anesthetics did not attenuate the release of CGRP after spinal cord stimulation, whereas isoflurane at 2% and halothane at 1.5% significantly inhibited depressor responses to exogenously administered CGRP. Sevoflurane at 4% did not significantly affect CGRP-induced depressor responses. Thus, isoflurane and halothane at large concentrations attenuate NANC depressor responses by attenuating the depressor action of CGRP, not CGRP release. IMPLICATIONS: The anesthetics isoflurane and halothane attenuate nonadrenergic, noncholinergic depressor responses mediated by calcitonin gene-related peptide in the rat without affecting the release of the peptide.

Anesthetics, Inhalation↗
PubMed2003

Anesthetic management for clipping a giant basilar artery aneurysm with moderate hypothermia, extracorporeal circulation assistance, and propofol infusion.

A 65-year-old female patient underwent surgery to clip a giant basilar artery aneurysm with closed-chest extracorporeal circulation using femorofemoral bypass. Moderate hypothermia (27 degrees C-30 degrees C), retention of spontaneous circulation, and propofol infusion (3-5 mg. kg(-1). h(-1)) were used under general anesthesia. Blood outflow via femoral vein was sufficient to maintain cardiopulmonary bypass and to induce hypothermia. Hemodynamics were controlled with dopamine and noradrenaline. In this case, extracorporeal circulation under moderate hypothermia was used to assist rather than substitute for spontaneous circulation, and spontaneous circulation was maintained at all times. We think that this method had advantages over deep hypothermic circulatory arrest with regard to intraoperative risks and postoperative complications.

Aged↗
PubMed2003

End-tidal carbon dioxide monitoring stabilized hemodynamic changes during ECT.

Accumulation of carbon dioxide (CO2) can disturb systemic and cerebral hemodynamics in patients receiving electroconvulsive therapy (ECT). The purpose of this study was to identify the effects of end-tidal CO2 monitoring on hemodynamic changes in patients who received ECT under propofol anesthesia. ECT was prescribed to 40 patients under propofol anesthesia. Ventilation was assisted using a face mask and 100% oxygen, with or without end-tidal CO2 monitoring. Heart rate was significantly increased in patients without end-tidal CO2 monitoring at 1 to 5 minutes after electrical stimulation (p < 0.01). Mean arterial blood pressure and middle cerebral artery blood flow velocity in the group without end-tidal CO2 monitoring were significantly larger than the values in the group with the monitor at 1 to 5 minutes after electrical stimulation. Arterial CO2 tension in the group without end-tidal CO2 monitoring was larger than the value in the group with the monitoring at 1 minute (45+/-5 mm Hg with the monitor and 56+/-8 without the monitor) and 5 minutes (37+/-4 mm Hg with the monitor and 51+/-8 without the monitor) after electrical stimulation (p < 0.01). Application of end-tidal CO2 monitoring is considered beneficial for safe and effective anesthesia management of patients undergoing ECT, especially patients with an intracranial disorder or ischemic heart disease.

Adult↗
PubMed2003

Antinociception with intrathecal alpha-methyl-5-hydroxytryptamine, a 5-hydroxytryptamine 2A/2C receptor agonist, in two rat models of sustained pain.

UNLABELLED: Type 2 serotonin (5-hydroxytryptamine [5-HT](2)) receptors in the spinal cord have been reported to mediate antinociception using pain threshold tests, but little is known about the actions of spinal 5-HT(2) receptors in sustained pain. In rats, we examined antinociceptive effects of the intrathecal administration of a 5-HT(2A/2C) receptor agonist, alpha-methyl-5-HT maleate (alpha-m-5-HT), using the formalin test and the chronic constriction injury (CCI) model. An intrathecal catheter was implanted for injection of drugs. In the formalin test, flinches were counted from Minute 1 to 2 and Minute 5 to 6 (Phase 1) and then for 1-min periods at 5-min intervals from 10 to 60 min (Phase 2). In rats with CCI, hind paw withdrawal latency after thermal stimulation was measured. In the formalin test, intrathecal administration of alpha-m-5-HT (1 to 100 microg) dose-dependently suppressed the number of flinches in both Phases 1 and 2. In the CCI model, intrathecally administered alpha-m-5-HT (10 to 100 microg) attenuated thermal hyperalgesia in a dose-dependent manner. These effects were reversed by intrathecal pretreatment with a 5-HT(2A/2C) antagonist, ketanserin (30 microg), or a muscarinic receptor antagonist, atropine (30 microg). These findings suggest that spinal 5-HT(2A/2C) receptors mediate antinociception in inflammatory pain and neuropathic pain, and the muscarinic receptors contribute to this action. IMPLICATIONS: Activation of spinal 5-hydroxytryptamine(2A/2C) receptors mediate antinociception in rat-sustained pain models such as inflammatory pain and neuropathic pain, and spinal muscarinic receptors are involved in this action.

Animals↗
PubMed2003

Neurotrophic factors can partially reverse morphological changes induced by mepivacaine and bupivacaine in developing sensory neurons.

UNLABELLED: Both bupivacaine and mepivacaine induce morphological changes in growing neurons. We designed this study to investigate the role of some neurotrophic factors (NTFs) in supporting developing neurons exposed to the deleterious effects of these drugs. Dorsal root ganglia were isolated from chick embryos and exposed to either bupivacaine or mepivacaine. After 60 min of exposure, the culture media were replaced with fresh culture media free from local anesthetics. NTFs-brain-derived NTF, glial-derived NTF, or neurotrophin-3-were added to the replacement media, and the cells were examined up to 48 h after the washout. The growth cone collapse assay was applied by a quantitative method of assessment. When the replacement media were not supported by any NTF, the growth cone collapse values were significantly larger than the control values at 20 h after the washout of mepivacaine and 48 h after the washout of either bupivacaine or mepivacaine (P < 0.05). However, when any of the NTFs were used, the collapsing activity was significantly attenuated, and growth cone collapse values showed no statistically significant differences in comparison with the control values at these time points (P > 0.05). We conclude that several NTFs support the recovery of neurons after exposure to local anesthetics. The supporting effects of NTFs on the reversibility of mepivacaine-induced collapse tended to be more obvious than those seen after the bupivacaine washout. IMPLICATIONS: Three neurotrophic factors (NTFs) can partially support the reversibility of mepivacaine- and bupivacaine-induced growth cone collapse in growing primary cultured sensory neurons. The effect of NTFs is more apparent after mepivacaine than after bupivacaine washout.

Anesthetics, Local↗