Biomedical subjects

Mayumi Takasaki

Publications and source records attributed to Mayumi Takasaki.

At least 19 recordsLinked to original sources

PubMed2006

Alteration of regional cerebral blood flow in patients with chronic pain--evaluation before and after epidural spinal cord stimulation.

BACKGROUND: Chronic pain is defined as intractable pain caused by abnormal pain transmission or impairment of the pain control system per se. Alteration of regional cerebral blood flow (rCBF) is known to occur under the presence of pain stimulation. Epidural spinal cord stimulation (SCS) is occasionally effective in relieving the symptom. OBJECTIVE: The aim of the current study is to investigate the alteration of rCBF in baseline condition and to find the association between the rCBF change and the efficacy of SCS in chronic pain. METHODS: A total of 18 patients underwent Tc-99m-HMPAO SPECT before and after SCS. Analysis with three-dimensional stereo-tactic surface projections (3D-SSP) with stereo-tactic extraction estimation (SEE) software was adopted to evaluate the rCBF. We assessed the extent score of the abnormal region in each segment (rate of the coordinates with a Z-value that exceeds three kinds of threshold value 2.0, 2.5 and 3.0 in all coordinates within a segment). According to the therapeutic response defined by visual analogue scale, we categorized patients into two groups, the good responder (GR) group (n=12) and poor responder (PR) group (n=6). In the analysis, we compared the extent score in the following two conditions. (1) Comparison between the PR group and normal control group under both baseline condition and after SCS. (2) Comparison between the GR group and normal control group under both baseline condition and after SCS. RESULTS: (1) In the PR group, increased rCBF was observed in left thalamus, bilateral precuneus and bilateral cerebellum under the baseline condition. After SCS, the range of these increased rCBF areas localized but remained. Decrease of rCBF was noted in bilateral subcallosal gyrus, superior temporal gyrus (STG) and bilateral anterior cingulate gyrus (ACG). They localized after SCS, but remained. (2) In the GR group, increased rCBF areas were noted in bilateral precuneus and bilateral cerebellum under the baseline condition. After SCS, they localized in bilateral precuneus but those of bilateral cerebellum remained. Decreased rCBF area was noted in bilateral subcallosal gyrus, STG and bilateral ACG under the baseline. After SCS, they localized in bilateral subcallosal gyrus and bilateral STG. In contrast, they enlarged in bilateral ACG. CONCLUSION: Chronic pain patients demonstrated abnormal rCBF distribution on both baseline and post SCS conditions. Increased rCBF of thalamus and precuneus under both conditions in the PR group and decreased rCBF of ACG under post SCS conditions in the GR group were characteristic patterns. Tc-99m-HMPAO SPECT with 3D-SSP and SEE analysis is likely objective and effective in monitoring and evaluating therapeutic outcome by SCS in chronic pain. In addition, it provides information that is useful in the selection of SCS candidates.

Brain↗

PubMed2006

Increase in intracellular Ca2+ concentration is not the only cause of lidocaine-induced cell damage in the cultured neurons of Lymnaea stagnalis.

PURPOSE: To determine whether the increase in intracellular Ca2+ concentration induced by lidocaine produces neurotoxicity, we compared morphological changes and Ca2+ concentrations, using fura-2 imaging, in the cultured neurons of Lymnaea stagnalis. METHODS: We used BAPTA-AM, a Ca2+ chelator, to prevent the increase in the intracellular Ca2+ concentration, and Calcimycin A23187, a Ca2+ ionophore, to identify the relationship between increased intracellular Ca(2+) concentrations and neuronal damage without lidocaine. Morphological changes were confirmed using trypan blue to stain the cells. RESULTS: Increasing the dose of lidocaine increased the intracellular Ca2+ concentration; however, there was no morphological damage to the cells in lidocaine at 3 x 10(-3) M. Lidocaine at 3 x 10(-2) M increased the intracellular Ca2+ concentration in both saline (from 238 +/- 63 to 1038 +/- 156 nM) and Ca2+-free medium (from 211 +/- 97 to 1046 +/- 169 nM) and produced morphological damage and shrinkage, with the formation of a rugged surface. With the addition of BAPTA-AM, lidocaine at 3 x 10(-2) M moderately increased the intracellular Ca2+ concentration (from 150 +/- 97 to 428 +/- 246 nM) and produced morphological damage. These morphologically changed cells were stained dark blue with trypan blue dye. The Ca2+ ionophore increased the intracellular Ca2+ concentration (from 277 +/- 191 to 1323 +/- 67 nM) and decreased it to 186 +/- 109 nM at 60 min. Morphological damage was not observed during the 60 min, but became apparent a few hours later. CONCLUSION: These results indicated that the increase in intracellular Ca2+ concentration is not the only cause of lidocaine-induced cell damage.

Anesthetics, Local↗

PubMed2006

A comparison of intracellular lidocaine and bupivacaine concentrations producing nerve conduction block in the giant axon of crayfish in vitro.

Clinically, lidocaine requires a larger concentration than bupivacaine to block nerves. Bupivacaine has a higher lipid solubility, tissue permeability, and affinity for sodium channels than lidocaine, resulting in greater anesthetic potency. Local anesthetics require access to the sodium channel from the intracellular milieu. In this study, we sought to determine the intracellular concentration of lidocaine and bupivacaine when a nerve was blocked in the giant axon of a crayfish. A solution of lidocaine or bupivacaine was perfused, and a nerve block was determined as the absence of an evoked action potential after tonic or phasic electrical stimulation. The intracellular lidocaine or bupivacaine concentration was measured using a lidocaine- or bupivacaine-sensitive glass micro-electrode. A phasic block was more effectively and rapidly achieved with a smaller concentration of bupivacaine than with lidocaine. The intracellular concentration and intra- to extracellular ratios were significantly larger with lidocaine than with bupivacaine when nerve conduction was blocked. These findings suggest that bupivacaine has a higher potency than lidocaine, at least in the giant axon of a crayfish in vitro. The implications of the present results are that bupivacaine is a more potent nerve block and produces a use-dependent (phasic) block at smaller concentrations than lidocaine.

Action Potentials↗

PubMed2006

[Epidural infusion of low dose bupivacaine after combined spinal-epidural anesthesia using needle through needle method provided no analgesic effect on postoperative pain after caesarian section].

BACKGROUND: In order to evaluate the analgesic efficacy of low dose epidural bupivacaine infusion with and without morphine after caesarean section we performed combined spinal-epidural anesthesia (CSEA) using needle through needle method. Three different epidural analgesic regimens were compared retrospectively. METHODS: The number of analgesic use during 24 hours after operation was compared. Patients were categorized into three groups; group N : intraoperative bolus epidural morphine (2.5 mg) alone, group L : bolus morphine (2.5 mg) plus epidural bupivacaine infusion (32 ml of 0.2% bupivacaine) at a rate of 2.1 ml x hr(-1), group M : bolus morphine (2.4 mg) plus epidural bupivacaine-morphine (33 ml of 0.2% bupivacaine containing morphine 2.3 mg) infusion at a rate of 2.1 ml x hr(-1). Used analgesics included pentazocine 15 mg i.m., diclofenac 25 mg suppo. and loxoprofen 60 mg p.o.. RESULTS: The mean number of analgesic use during the first 24 hours in group M (0.29 +/- 0.46) was significantly smaller than those of group N (0.97 +/- 0.91) and group L (0.84 +/- 0.95). Percentage of patients requiring no analgesic during the first 24 hours was significantly less in group M (70.8%) than in group N (33.4%) and group L (42.1%). CONCLUSIONS: A 2.1 ml x hr(-1) infusion of epidural bupivacaine has no analgesic effect after caesarean section under CSEA using NTN method.

Anesthesia, Epidural↗

PubMed2006

[Plasma levobupivacaine concentrations following epidural administration of levobupivacaine conjugated with or without maltosyl-beta-cyclodextrin].

BACKGROUND: To investigate the pharmacokinetics of complexation of levobupivacaine with maltosyl-beta-cyclodextrin, the plasma concentrations of levobupivacaine were measured following epidural administration of levobupivacaine conjugated with maltosyl-beta-cyclodextrin or levobupivacaine alone in a rabbit model. METHODS: Rabbits were randomly divided into two groups, levobupivacaine (1%) group (n = 6) and levobupivacaine (1%) conjugated with maltosyl-beta-cyclodextrin (100 mM) group (n = 6). One ml of each solution was randomly injected through an epidural catheter placed at L5-6. The plasma levobupivacaine concentrations were measured before and 5, 10, 15, 30, 60, 120, 240, 360, and 480 min after injection. RESULTS: The plasma levobupivacaine concentrations were significantly higher in the levobupivacaine conjugated with maltosyl-beta-cyclodextrin group than in levobupivacaine group at 5 min (1,465 +/- 311, 1,033 +/- 347 ng x ml(-1)), 10 min (1,068 +/- 237, 731 +/- 191), and 15 min (958 +/- 311, 605 +/- 118). There were no differences in area under the curve (1,551 +/- 387, 1,176 +/- 154 ng x hr x ml(-1)) and elimination half life (100 +/- 54, 78 +/- 37 min) between the two groups. CONCLUSIONS: The results of this study indicated that the absorption of levobupivacaine conjugated with maltosyl-beta-cyclodextrin from the epidural space and the elimination from the blood were similar to plain levobupivacaine.

Anesthesia, Epidural↗

PubMed2005

Long-term exposure to local but not inhalation anesthetics affects neurite regeneration and synapse formation between identified lymnaea neurons.

BACKGROUND: General and local anesthetics are used in various combinations during surgical procedures to repair damaged tissues and organs, which in almost all instances involve nervous system functions. Because synaptic transmission recovers rapidly from various inhalation anesthetics, it is generally assumed that their effects on nerve regeneration and synapse formation that precede injury or surgery may not be as detrimental as that of their local counterparts. However, a direct comparison of most commonly used inhalation (sevoflurane, isoflurane) and local anesthetics (lidocaine, bupivacaine), vis-a-vis their effects on synapse transmission, neurite regeneration, and synapse formation has not yet been performed. METHODS: In this study, using cell culture, electrophysiologic and imaging techniques on unequivocally identified presynaptic and postsynaptic neurons from the mollusc Lymnaea, the authors provided a comparative account of the effects of both general and local anesthetics on synaptic transmission, nerve regeneration, and synapse formation between cultured neurons. RESULTS: The data show that clinically used concentrations of both inhalation and local anesthetics affect synaptic transmission in a concentration-dependent and reversal manner. The authors provided the first direct evidence that long-term overnight treatment of cultured neurons with sevoflurane and isoflurane does not affect neurite regeneration, whereas both lidocaine and bupivacaine suppress neurite outgrowth completely. The soma-soma synapse model was then used to compare the effects of both types of agents on synapse formation. The authors found that local but not inhalation anesthetics drastically reduced the incidence of synapse formation. The local anesthetic-induced prevention of synapse formation most likely involved the failure of presynaptic machinery, which otherwise developed normally in the presence of both sevoflurane and isoflurane. CONCLUSION: This study thus provides the first comparative, albeit preclinical, account of the effects of both general and local anesthetics on synaptic transmission, nerve regeneration, and synapse formation and demonstrates that clinically used lidocaine and bupivacaine have drastic long-term effects on neurite regeneration and synapse formation as compared with sevoflurane and isoflurane.

Action Potentials↗

PubMed2005

Sevoflurane blocks cholinergic synaptic transmission postsynaptically but does not affect short-term potentiation.

BACKGROUND: As compared with their effects on both inhibitory and excitatory synapses, little is known about the mechanisms by which general anesthetics affect synaptic plasticity that forms the basis for learning and memory at the cellular level. To test whether clinically relevant concentrations of sevoflurane affect short-term potentiation involving cholinergic synaptic transmission, the soma-soma synapses between identified, postsynaptic neurons were used. METHODS: Uniquely identifiable neurons visceral dorsal 4 (presynaptic) and left pedal dorsal 1 (postsynaptic) of the mollusk Lymnaea stagnalis were isolated from the intact ganglion and paired overnight in a soma-soma configuration. Simultaneous intracellular recordings coupled with fluorescent imaging of the FM1-43 dye were made in either the absence or the presence of sevoflurane. RESULTS: Cholinergic synapses, similar to those observed in vivo, developed between the neurons, and the synaptic transmission exhibited classic short-term, posttetanic potentiation. Action potential-induced (visceral dorsal 4), 1:1 excitatory postsynaptic potentials were reversibly and significantly suppressed by sevoflurane in a concentration-dependent manner. Fluorescent imaging with the dye FM1-43 revealed that sevoflurane did not affect presynaptic exocytosis or endocytosis; instead, postsynaptic nicotinic acetylcholine receptors were blocked in a concentration-dependent manner. To test the hypothesis that sevoflurane affects short-term potentiation, a posttetanic potentiation paradigm was used, and synaptic transmission was examined in either the presence or the absence of sevoflurane. Although 1.5% sevoflurane significantly reduced synaptic transmission between the paired cells, it did not affect the formation or retention of posttetanic potentiation at this synapse. CONCLUSIONS: This study demonstrates that sevoflurane blocks cholinergic synaptic transmission postsynaptically but does not affect short-term synaptic plasticity at the visceral dorsal 4-left pedal dorsal 1 synapse.

Anesthetics, Inhalation↗

PubMed2005

Lidocaine excites both pre- and postsynaptic neurons of reconstructed respiratory pattern generator in Lymnaea stagnalis.

Lidocaine causes both inhibition and excitation in the central nervous system, including the respiratory pattern. The excitation induced by an excessive dose of local anesthetic is thought to be the result of an initial blockade of an inhibitory pathway in the cerebral cortex. To clarify the effect of lidocaine on the pre- and postsynaptic neurons of an inhibitory synapse, a cultured soma-soma respiratory pattern generator model consisting of two neurons from the snail Lymnaea stagnalis were reconstructed in vitro. First we investigated the effects of lidocaine on single presynaptic (RPeD1) or postsynaptic (VD4) neurons. While RPeD1 and VD4 were simultaneously recorded, the number of action potentials, the membrane potential, and the wavelength of the action potential were compared before and after lidocaine (0.01, 0.1, and 1 mM) administration. Lidocaine increased the number of action potentials and the wavelength of a single action potential, and it depolarized the resting membrane potential in both RPeD1 and VD4 neurons in a dose-dependent manner. Furthermore, lidocaine decreased outward potassium currents. In soma-soma pairs, RPeD1 excitation and VD4 suppression occurred in 0.01 mM lidocaine, whereas both RPeD1 and VD4 neurons were excited by 0.1 and 1 mM lidocaine. In conclusion, lidocaine causes a reduction in synaptic transmission and general neuronal excitation in both presynaptic and postsynaptic neurons.

Action Potentials↗

PubMed2005

[Reevaluation of protective effects of alprostadil on hepatic function in patients undergoing hepatectomy].

BACKGROUND: The protective effect of alprostadil (PGE1), used during hepatectomy, on hepatic function has not been clearly proven. We reevaluated this effect by measuring serum alpha-glutathione S-transferase (aGST), which detects liver injury sensitively. METHOD: Thirty hepatocellular carcinoma patients scheduled for hepatectomy were randomly assigned to control (n=12) and PGE1 (n=10) groups. In the latter group, PGE1 was administered intravenously at a rate of 0.05 microg x kg(-1) x min(-1) during surgery. For measuring alphaGST, arterial blood samples were obtained before anesthesia, following laparotomy, and immediately, 2, 4, and 6 hrs after liver resection. RESULTS: The alphaGST concentrations after liver resection were significantly higher, while mean arterial pressures were significantly lower in the PGE1 group. CONCLUSIONS: Our findings suggest that PGE1 medication during hepatectomy cannot protect hepatic function during and after liver resection.

Aged↗

PubMed2005

[Optimal dose of fentanyl for postoperative epidural analgesia after cesarean section].

BACKGROUND: The aim of this study was to investigate which dose of fentanyl in ropivacaine for epidural anesthesia will provide effective analgesia with minimal side effects after cesarean section (CS). METHODS: Fifty eight patients scheduled for CS were randomly allocated to two groups according to fentanyl dose in epidural analgesia: group F1 (11 microg x hr(-1); n=30) or group F 2 (21 microg x hr(-1); n= 28). Ropivacaine 0.2% 100 ml with fentanyl 400 or 800 microg was administered into the epidural space in the groups F1 and F 2, respectively. Pain scores (visual analogue scale: VAS) with cough or movement, Bromage score, incidence of diclofenac or pentazocine administration, satisfaction score (VAS) and side effects (nausea, vomiting and pruritus) were recorded after CS. RESULTS: Pain scores with cough or movement were significantly lower in the group F 2 than the group F 1 at twelve and twenty-four hours after CS. Bromage score at twelve hours was lower in the group F 2 than the group F 1. The incidences of side effects were similar between the two groups. Satisfaction score was significantly higher in the group F 2 than the group F 1. CONCLUSIONS: We conclude that continuous epidural administration of fentanyl 21 microg x hr(-1) with ropivacaine provides the optimum balance between pain relief and side effects compared with fentanyl 11 microg x hr(-1) with ropivacaine after CS.

Adult↗

PubMed2005

[A case of anaphylactic shock due to an antibiotic used preoperatively].

We report a case of an anaphylactic reaction due to a preoperatively administered antibiotic. A 72-year-old man scheduled to undergo cholecystectomy and choledocholithotomy received a cefoperazone infusion after being turned to a lateral position for insertion of an epidural catheter. Immediately after local injection of lidocaine, he, complained of inguinal itching. His systolic blood pressure then decreased to 60 mmHg and complained of discomfort and vomited. Soon, his systolic blood pressure decreased to 40 mmHg and he lost consciousness. Antibiotic infusion was stopped and he was returned to a prone, head-down position. His Spo2 decreased to 90%, and oxygen was administered. Following ephedrine 10 mg injection, his systolic blood pressure increased to 80 mmHg and he became conscious, but an erhythemic area appeared on his precordial region. Repeated epinephrine 0.05 mg injection restored his blood pressure to the preoperative level. Since a blood sample obtained 15 minutes after the event revealed high serum IgE levels, he was diagnosed as IgE-mediated anaphylactic reaction. Subsequent intradermal tests were tentatively positive to cefoperazone and negative to lidocaine. Surgery was successfully performed using cefotiam, which was also negative in a preoperative intradermal test.

Aged↗

PubMed2004

Cardiorespiratory effects of epidural administration of morphine and fentanyl in dogs anesthetized with sevoflurane.

OBJECTIVE: To determine the cardiorespiratory effects of epidural administration of morphine alone and in combination with fentanyl in dogs anesthetized with sevoflurane. DESIGN: Prospective study. ANIMALS: 6 dogs. PROCEDURE: Dogs were anesthetized with sevoflurane and allowed to breathe spontaneously. After a stable plane of anesthesia was achieved, morphine (0.1 mg/kg [0.045 mg/lb]) or a combination of morphine and fentanyl (10 microg/kg [4.5 microg/lb]) was administered through an epidural catheter, the tip of which was positioned at the level of L6 or L7. Cardiorespiratory variables were measured for 90 minutes. RESULTS: Epidural administration of morphine alone did not cause any significant changes in cardiorespiratory measurements. However, epidural administration of morphine and fentanyl induced significant decreases in diastolic and mean arterial blood pressures and total peripheral resistance. Stroke volume was unchanged, PaCO2 was significantly increased, and arterial pH and base excess were significantly decreased. Heart rate was significantly lower after epidural administration of morphine and fentanyl than after administration of morphine alone. None of the dogs had any evidence of urine retention, vomiting, or pruritus after recovery from anesthesia. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that epidural administration of morphine at a dose of 0.1 mg/kg in combination with fentanyl at a dose of 10 microg/kg can cause cardiorespiratory depression in dogs anesthetized with sevoflurane.

Analgesics, Opioid↗

PubMed2004

Lidocaine increases intracellular sodium concentration through voltage-dependent sodium channels in an identified lymnaea neuron.

BACKGROUND: The local anesthetic lidocaine affects neuronal excitability in the central nervous system; however, the mechanisms of such action remain unclear. The intracellular sodium concentration ([Na]i) and sodium currents (INa) are related to membrane potential and excitability. Using an identifiable respiratory pacemaker neuron from Lymnaea stagnalis, the authors sought to determine whether lidocaine changes [Na]i and membrane potential and whether INa is related to these changes. METHODS: Intracellular recording and sodium imaging were used simultaneously to measure membrane potentials and [Na]i, respectively. Measurements for [Na]i were made in normal, high-Na, and Na-free salines, with membrane hyperpolarization, and with tetrodotoxin pretreatment trials. Furthermore, changes of INa were measured by whole cell patch clamp configuration. RESULTS: Lidocaine increased [Na]i in a dose-dependent manner concurrent with a depolarization of the membrane potential. In the presence of high-Na saline, [Na]i increased and the membrane potential was depolarized; the addition of lidocaine further increased [Na]i, and the membrane potential was further depolarized. In Na-free saline or in the presence of tetrodotoxin, lidocaine did not change [Na]i. Similarly, hyperpolarization of the membrane by current injections also prevented the lidocaine-induced increase of [Na]i. In the patch clamp configuration, membrane depolarization by lidocaine led to an inward sodium influx. A persistent reduction in membrane potential, resulting from lidocaine, brings the cell within the window current of INa where sodium channel activation occurs. CONCLUSION: Lidocaine increases intracellular sodium concentration and promotes excitation through voltage-dependent sodium channels by altering membrane potential in the respiratory pacemaker neuron.

Anesthetics, Local↗

PubMed2004

The effects of propofol on hypothalamic paraventricular nucleus neurons in the rat.

UNLABELLED: The mechanism of hypotension induced by anesthetics is not completely understood. Because no electrophysiologic examination of the effects of propofol on the central nervous system has shown its involvement in the control of sympathetic and cardiovascular functions, we investigated the actions of propofol on rat hypothalamic paraventricular nucleus (PVN) neurons using the whole-cell mode of the patch-clamp technique in rat hypothalamic PVN slice preparations. Propofol induced Cl(-) currents at concentrations of 10(-5) and 10(-4) M, which were sensitive to picrotoxin and, to a lesser extent, to strychnine. Propofol (10(-6) M) enhanced gamma-aminobutyric acid(A) (GABA(A); 10(-6) M)-induced current synergistically. Moreover, propofol (10(-5) and 10(-4) M) significantly increased the decay time of evoked-inhibitory postsynaptic currents, which suggests a postsynaptic modulation of GABA(A) receptors. In addition, propofol (10(-5), 10(-4), and 2 x 10(-4) M) reversibly inhibited voltage-gated Ca(2+) currents. Taken together, these results suggest that propofol enhancement of GABA(A)-receptor mediated currents and inhibition of voltage-gated Ca(2+) currents at the central level, which is involved in the control of cardiovascular and sympathetic functions may be, at least in part, involved in general anesthetic-induced cardiovascular and sympathetic depression. IMPLICATIONS: We investigated the actions of propofol on the rat hypothalamic paraventricular nucleus neurons, which are involved in the control of cardiovascular and sympathetic functions. The results suggest that propofol enhancement of gamma-aminobutyric acid(A)-receptor mediated currents and inhibition of voltage-gated Ca(2+) currents at the central level may be, at least in part, involved in general anesthetic-induced cardiovascular and sympathetic depression.

Anesthetics, Intravenous↗

PubMed2004

[Evaluation of a lockable combined spinal-epidural device for use with needle-through-needle technique].

BACKGROUND: Recently, a new combined spinal-epidural (CSE) device has been introduced which allows the spinal needle to be extended a maximum of 15 mm beyond the Tuohy needle and locked onto the epidural needle after dural puncture. The aim of this study was to compare this lockable CSE device with the conventional CSE device, which allows the spinal needle to be extended 9 mm beyond the Tuohy needle, and to measure the length of the protrusion of the spinal needle beyond the Tuohy needle (top-to-top distance: TTD). METHODS: We studied sixty patients scheduled to undergo elective gynecological surgery and cesarean section. Patients were divided into three groups: patients in Group I (n = 20) using the conventional CSE device in gynecological surgery; patients in Group II (n = 20) using the lockable CSE device in gynecological surgery; and patients in Group III (n = 20) using the lockable CSE device in cesarean section. RESULTS: The success rate of spinal anesthesia with needle-through-needle technique was higher with the lockable CSE device (100%) than with the conventional CSE device (75%). The TTD was 7.9 +/- 1.8 (SD) cm in non-pregnant group (Group II) and 8.7 +/- 1.5 cm in pregnant group (Group III). This difference was not statistically significant. In the lockable CSE device groups (Group II and III), 10 patients (25%) had a TTD of 10 mm or more. CONCLUSIONS: The lockable CSE device improves the success rate of spinal anesthesia in needle-through-needle CSE anesthesia.

Adult↗

PubMed2004

[Combined spinal and epidural anesthesia for cesarean section: a retrospective study with 0.5% hyperbaric bupivacaine].

BACKGROUND: We investigated retrospectively the relationship between the intrathecal dose of 0.5% hyperbaric bupivacaine and the use of 2% mepivacaine through an epidural catheter. METHODS: Forty-nine patients undergoing cesarean section with combined spinal and epidural anesthesia (CSEA) were analyzed. They were divided into two groups; with (CSEA group) and without additional epidural injection group (spinal group). RESULTS: In the CSEA group (24 patients received 1.2 +/- 0.4 ml of 0.5% hyperbaric bupivacaine), 5-10 ml of 2% mepivacaine were required to achieve the adequate surgical anesthesia. In the spinal group (25 patients received 1.6 +/- 0.3 ml of 0.5% hyperbaric bupivacaine), cesarean section was performed without additional mepivacaine before delivery. The analgesic level and the amount of fluid infusion were similar in the two groups. However, 20% of patients in the spinal group showed hypotension (systolic blood pressure below 80 mmHg), although no patients in the CSEA group developed hypotension. The amount of ephedrine used before delivery was significantly larger in the spinal group (8.9 +/- 7.7 mg) than in the CSEA group (3.9 +/- 4.3 mg). CONCLUSIONS: Spinal anesthesia induced by 1.2 ml of 0.5% hyperbaric bupivacaine with sequential epidural block induced by 5-10 ml of 2% mepivacaine caused no hypotension during cesarean section.

Adult↗

PubMed2004

[Glucose attenuating local anesthetic-induced hemolysis].

BACKGROUND: The effect of glucose on local anesthetic-induced neural damage has not been fully studied. We examined the effect of glucose on hemolysis induced by local anesthetics. METHODS: The mean EC50 values (the local anesthetic level that causes destruction of half of the red blood cells in vitro) of lidocaine HCl, tetracaine HCl and dibucaine HCl were determined with 0% and 7.5% glucose contained in Krebs solution at pH 6.4. RESULTS: The mean EC50 values of lidocaine HCl, tetracaine HCl, and dibucaine HCl in 0%-glucose Krebs solution were 6.51%, 0.45%, 0.17%, respectively, which increased significantly to 7.05%, 0.64% and 0.23%, in 7.5% glucose Krebs solution at pH 6.4. CONCLUSIONS: Glucose may have a protective role in local anesthetic-induced neural damage.

Anesthetics, Local↗

PubMed2004

[Anesthetic management for removal of a giant ovarian tumor by monitoring transesophageal Doppler cardiac output].

Transesophageal Doppler cardiac output was monitored in two cases for removal of a giant ovarian tumor. In case 1, cardiac output (CO) increased following the drainage of the tumor, and CO decreased following blood loss. In case 2, CO increased following the removal of the tumor, and remained stable because of small blood loss. Cardiovascular parameters changed remarkably with the drainage of tumors and blood loss. Therefore, noninvasive Doppler cardiac output monitor was useful for rapid estimation of cardiovascular changes.

Adult↗