Long-term and spatial memory effects of selective ß1-antagonists after transient focal ischaemia in rats.

BACKGROUND: Although various reports have shown that ß-antagonists provide neuroprotective effects after cerebral ischaemia, their effect on spatial memory after transient focal ischaemia is not known. We investigated the treatment of ß1-antagonists on neurological outcome spatial memory for 1 month after focal cerebral ischaemia in rats. METHODS: Male rats randomly received an i.v. infusion of saline 0.5 ml h(-1), esmolol 200 µg kg(-1) min(-1), or landiolol 50 µg kg(-1) min(-1). Infusion was initiated 30 min before middle cerebral artery occlusion and continued for 24 h. The infarct areas in the hippocampus and striatum were measured after the final retention trial and neurological examinations. RESULTS: Neurological deficit scores in the landiolol- and esmolol-treated rats were significantly lower than in the control rats at 1, 4, 7, and 11 days after ischaemia (P<0.05). Using the Morris water maze to assess spatial memory, we found that escape latency and swimming path length to the platform were significantly shorter in the landiolol-treated rats, compared with the saline-treated rats at 4 and 11 days after ischaemia (P<0.05). The mean (SD) infarct area was 19.1 (8.0)% in the striatum and 18.6 (10.0)% in the hippocampus of the landiolol-treated rats, and 16.8 (14.0)% and 16.8 (15.0)% in the striatum and hippocampus, respectively, of esmolol-treated rats. This was significantly less than in control rats [striatum 31.7 (14.0)% and hippocampus 29.8 (13.0)%, P<0.05]. CONCLUSIONS: The current study indicates that although esmolol and landiolol provided long-term neuroprotection in terms of histological outcome, they had no effect on neurological outcome and spatial memory retention.

The combined neuroprotective effects of lidocaine and dexmedetomidine after transient forebrain ischemia in rats.

BACKGROUND: We investigated whether coadministration of lidocaine and dexmedetomidine would reduce brain injury following transient forebrain ischemia in rats to a greater extent than either drug alone. METHODS: Adult male Sprague-Dawley rats were anesthetized with halothane to maintain normocapnia and normoxia. Rats received subcutaneous injection of saline 1 ml/kg, lidocaine 10 mg/kg, dexmedetomidine 3 microg/kg, or lidocaine 10 mg/kg plus dexmedetomidine 3 microg/kg. Thirty minutes after the drug injection, forebrain ischemia was induced by hemorrhagic hypotension and occlusion of the bilateral carotid arteries, and was confirmed by isoelectric EEG. At the end of 10-min ischemia, rats were reperfused. The same dose of drugs was administered 3, 24, and 48 h after ischemia. Neurological examination was done at 1, 2, and 7 days after ischemia. Seven days after ischemia, the brain was stained with hematoxylin and eosin. We counted ischemic cells in the CA1 hippocampal region, striatum, and cerebral cortex. We also measured extracellular glutamate and norepinephrine concentration in hippocampal CA1 in the four groups. RESULTS: As compared with saline-treated rats, rats receiving dexmedetomidine plus lidocaine showed less than neurological deficit scores at 2 and 7 days after ischemia, and had less ischemic cells in the CA1 region. However, administration of dexmedetomidine plus lidocaine did not alter the area under the glutamate concentration curve and norepinephrine concentration during ischemia in the CA1 region, compared with saline-treated rats. CONCLUSIONS: Our results suggest coadministration of lidocaine and dexmedetomidine improves the neurological outcome without alteration of glutamate and norepinephrine concentrations during forebrain ischemia in rats.

Gender differences in baroreflex response and heart rate variability in anaesthetized humans.

BACKGROUND: In conscious humans, men have a greater cardiovagal baroreflex gain than women. We studied gender-related differences in baroreflex function during general anaesthesia. METHODS: Sixty healthy patients (30 male and 30 female) were anaesthetized with sevoflurane 2% end-tidal in air and oxygen, and their lungs were mechanically ventilated. We recorded the ECG and invasive arterial pressure. Baroreflex gain was measured as the linear relationship of R-R interval with systolic arterial pressure changes caused by doses of phenylephrine i.v., and also the spontaneous changes in R-R interval and arterial pressure. In addition, consecutive R-R intervals were analysed using a fast Fourier transformation. RESULTS: Baroreflex gains (mean (sd)) assessed by the pharmacological method in men (7.98 (5.12) ms x mm x Hg(-1)) was significantly greater than that in women (4.89 (3.87) ms x mm x Hg(-1)). Similarly, spontaneous baroreflex gains were significantly greater in men than in women, and correlated well with high-frequency power, but not with low-frequency power or low/high ratio, of heart rate variability in both genders. CONCLUSIONS: Our results extend findings in conscious humans to sevoflurane anaesthesia. Men have greater cardiovagal reflex gains than women, which may reflect differences in parasympathetic action on heart rate.

Fentanyl decreases propofol requirement for laryngeal mask airway insertion.

BACKGROUND: Since fentanyl is a potent depressant of the upper airway reflex, preadministration of fentanyl may facilitate insertion of the laryngeal mask airway (LMA) using propofol. Accordingly, we tested the hypothesis that fentanyl pretreatment would reduce the dose of propofol required for the LMA insertion. METHODS: Forty-one healthy patients without sedative premedication were randomly assigned to either fentanyl group, receiving fentanyl 2 microg kg-1 intravenously, or control group, receiving equal volumes of normal saline. Then, 3 ml of 2% lidocaine was given intravenously to alleviate pain associated with propofol administration. Thirty s after the fentanyl or saline injection, a predetermined dose of 1% propofol was given at a rate of 100 mg min-1. Insertion of the LMA was attempted 90 s after the completion of the propofol injection. The dose of propofol given to a particular patient was determined by the response of the preceding patient in that group to a higher or lower dose, using the up-and-down method. The first patient in each group received 2.5 mg kg-1 of propofol, while the step-size was 0.25 mg kg-1. Patients responses were assessed by a blinded observer. RESULTS: ED50 and ED95 of propofol requirements were significantly less in the fentanyl group (0.82, 1.17 mg kg-1, respectively) than those in the control group (2.39, 2.62 mg kg-1, P < 0.001). CONCLUSION: Our results indicate that preadministration of fentanyl 2 microg kg-1 decreases the propofol requirement for the LMA insertion.

Neuroprotective effect of sigma(1)-receptor ligand 4-phenyl-1-(4-phenylbutyl) piperidine (PPBP) is linked to reduced neuronal nitric oxide production.

BACKGROUND AND PURPOSE: The potent final sigma(1)-receptor ligand 4-phenyl-1-(4-phenylbutyl) piperidine (PPBP) provides neuroprotection in experimental stroke. We tested the hypothesis that PPBP attenuates striatal tissue damage after middle cerebral artery occlusion (MCAO) by a mechanism involving reduction of ischemia-evoked nitric oxide (NO) production. Furthermore, we determined whether the agent fails to protect ischemic brain when neuronal nitric oxide synthase (nNOS) is genetically deleted or pharmacologically inhibited (selective nNOS inhibitor, 7-nitroindazole [7-NI]). METHODS: Halothane-anesthetized adult male Wistar rats were subjected to 2 hours of MCAO by the intraluminal filament occlusion technique. All physiological variables were controlled during the ischemic insult. In vivo striatal NO production was estimated via microdialysis by quantification of local, labeled citrulline recovery after labeled arginine infusion. In a second series of experiments, nNOS null mutants (nNOSKOs) and the genetically matched wild-type (WT) strain were treated with 90 minutes of MCAO. Brains were harvested at 22 hours of reperfusion for measurement of infarction volume by triphenyltetrazolium chloride histology. RESULTS: PPBP attenuated infarction volume at 22 hours of reperfusion in cerebral cortex and striatum and markedly attenuated NO production in ischemic and nonischemic striatum during occlusion and early reperfusion. Treatment with 7-NI mimicked the effects of PPBP. In WT mice, infarction volume was robustly decreased by both PPBP and 7-NI, but the efficacy of PPBP was not altered by pharmacological nNOS inhibition in combined therapy. In contrast, PPBP did not decrease infarction volume in nNOSKO mice. CONCLUSIONS: These data suggest that the mechanism of neuroprotection of PPBP in vivo is through attenuation of nNOS activity and ischemia-evoked NO production. Neuroprotective effects of PPBP are lost when nNOS is not present or is inhibited; therefore, PPBP likely acts upstream from NO generation and its subsequent neurotoxicity.

The efficacy of hemodynamic and T wave criteria for detecting intravascular injection of epinephrine test doses in anesthetized adults: a dose-response study.

UNLABELLED: Recent studies have shown that an epidural test dose containing 15 microg of epinephrine has a sensitivity and specificity of 100% for detecting intravascular injection based on the systolic blood pressure (SBP) (positive if > or =15-mm Hg increase) and the T wave criteria (positive if > or =0.1 mV and 25% decrease in amplitude), whereas the modified heart rate (HR) criterion (positive if > or =10-bpm increase) produced uncertain results in sevoflurane-anesthetized adults. Because a fractional dose of the test dose may be injected intravascularly in actual clinical situations, we designed this study to determine, in a dose-related manner, the efficacy and minimum effective dose of epinephrine based on those hemodynamic and the T wave criteria. Eighty healthy adult patients were randomly assigned to one of four groups according to a simulated IV test dose under 2% end-tidal sevoflurane and nitrous oxide anesthesia after endotracheal intubation (n = 20 each). The saline group received 3 mL of normal saline IV; the epinephrine-15 group received 3 mL of 1.5% lidocaine containing 15 microg of epinephrine (1); and the epinephrine-10 and -5 groups received 2 and 1 mL of the test dose of the identical components, respectively. HR, SBP, and lead II of the electrocardiograph were recorded continuously for 5 min after the IV injection of the study drug. Sensitivities and specificities of 100% were obtained based on the HR and the SBP criteria only if 15 microg of epinephrine was injected IV, whereas sensitivities and specificities of 100% were obtained based on both T wave criteria after 15 and 10 microg of epinephrine was injected IV. Two blinded observers were able to detect all T wave changes in patients who received 15, 10, and 5 microg of epinephrine IV, resulting in 100% efficacy (P: < 0.05 versus HR and SBP criteria). We conclude that minimum effective epinephrine doses for detecting accidental intravascular injection are 15 microg on the HR and the SBP criteria, and 10 microg on both T wave criteria, and that observing T wave changes may detect even smaller (5 microg) doses of epinephrine injected IV in adult patients anesthetized with sevoflurane and nitrous oxide. IMPLICATIONS: To determine whether an epidural catheter is in a blood vessel, an epidural test dose containing 15 microg of epinephrine is used. We found that a decrease in T wave amplitude appears to be more sensitive than heart rate and systolic blood pressure change for detecting accidental intravascular injection of a small dose of epinephrine-containing test dose in sevoflurane-anesthetized patients.

Evaluating hemodynamic and T wave criteria of simulated intravascular test doses using bupivacaine or isoproterenol in anesthetized children.

UNLABELLED: An increase in T wave amplitude > or =25% is a reliable indicator for detecting intravascular injection of lidocaine-epinephrine test dose in anesthetized children. We examined whether a simulated IV test dose containing bupivacaine instead of lidocaine, and isoproterenol instead of epinephrine, produces reliable changes in heart rate (HR) and T wave morphology. One hundred healthy infants and children (6-72 mo) were randomized to one of five groups (n = 20 each) during 1.0 minimum alveolar anesthetic concentration sevoflurane and 67% nitrous oxide in oxygen: atropine pretreatment (0.01 mg/kg IV) followed by 0.25% bupivacaine containing epinephrine 0.5 microg/kg IV, atropine followed by normal saline, atropine followed by 1% lidocaine containing isoproterenol 0.1 microg/kg, saline pretreatment followed by the lidocaine-isoproterenol test dose, and saline followed by saline. HR was recorded every 20 s and T wave amplitude of lead II was continuously recorded. All patients receiving the bupivacaine-epinephrine test dose and none receiving saline met the HR (positive if > or =10 bpm increase) and T wave criteria (positive if > or =25% increase in amplitude). The isoproterenol-containing test dose produced positive responses based only on the HR criterion with or without atropine pretreatment. Our results indicate that HR and T wave changes are useful if a bupivacaine-epinephrine test dose is used and that HR is the only useful indicator if an isoproterenol-containing test dose is used in sevoflurane-anesthetized children. IMPLICATIONS: To determine if an epidurally administered local anesthetic has been unintentionally injected into a blood vessel, a small dose of epinephrine or isoproterenol may be added to a local anesthetic. We found that an increase in heart rate > or =10 bpm and an increase in T wave amplitude of lead II >or =25% are useful indicators for detecting accidental intravascular injection of an epinephrine-containing test dose in sevoflurane-anesthetized children, whereas only a heart rate change is a reliable diagnostic tool if an isoproterenol-containing test dose is used.

Oral clonidine premedication reduces propofol requirement for laryngeal mask airway insertion.

PURPOSE: To determine the effect of oral clonidine premedication on propofol requirement (ED(50)) for the insertion of the laryngeal mask airway (LMA) in healthy patients undergoing abdominal hysterectomy. METHODS: After ethics committee approval and informed consent, 41 patients were randomly assigned to receive 5 microg x kg(-1) clonidine po premedication 90 min before entering the operating room (n = 22), or no clonidine (n = 19). To alleviate pain associated with iv propofol, 3 ml lidocaine 2%iv were administered. General anesthesia was induced, 30 sec later, with propofol at a rate of 100 mg x min(-1) (600 ml x hr(-1)) iv. The dose of propofol at which insertion of the LMA was attempted was predetermined by modification of Dixon's up-and-down method with an initial dose of 2.5 mg x kg(-1) and 0.25 mg x kg(-1) as the step size. An LMA was inserted, without muscle relaxants or other adjuvants 90 sec after completion of the propofol injection, by an anesthesiologist blinded to the treatment of the patient. RESULTS: The ED(50) of propofol for LMA insertion in clonidine-treated patients (2.0 +/- 0.2 mg x kg(-1), 1.8-2.3 mg x kg(-1) [95% confidence interval]), was less than that in patients without clonidine (2.5 +/- 0.1 mg x kg(-1), 2.4-2.6 mg x kg(-1), P < 0.01). CONCLUSION: Oral clonidine premedication reduces propofol requirement for LMA insertion.

Oral clonidine premedication enhances postoperative analgesia by epidural morphine.

UNLABELLED: This study was designed to evaluate the effects of oral clonidine premedication on postoperative analgesia by epidural morphine in a prospective, randomized, double-blinded design. Sixty consenting patients, scheduled for total abdominal hysterectomy, were randomly assigned to one of three groups (n = 20 each); the clonidine-morphine group received oral clonidine 5 microg/kg 90 min before arriving in the operating room and epidural morphine 2 mg before induction of general anesthesia, the clonidine-placebo group received oral clonidine 5 microg/kg and no epidural morphine, and the placebo-morphine group received no clonidine and epidural morphine 2 mg. An epidural catheter was placed at the L1-2 or L2-3 interspace, and 1.5% lidocaine was used for surgical anesthesia in all patients. General anesthesia was then induced with propofol, and maintained with a continuous infusion of propofol and 67% nitrous oxide in oxygen during surgery. Four patients were subsequently withdrawn from the study. After surgery, patient-controlled analgesia using IV morphine was used to assess analgesic requirement. Morphine consumptions determined every 6 h after surgery in the clonidine-morphine and placebo-morphine groups were significantly less than the clonidine-placebo group until 12 h after surgery, whereas those of the clonidine-morphine group were significantly less than the placebo-morphine group from 13 to 42 h after surgery. Visual analog (pain) scale (VAS) scores in the clonidine-morphine group were significantly lower than the placebo-morphine group at 48 h at rest, and at 1, 24, 36, and 48 h with movement. Similarly, VAS scores in the clonidine-morphine group were significantly lower than the clonidine-placebo group at 1 and 6 h both at rest and with movement, whereas VAS scores in the clonidine-placebo group were significantly lower than the placebo-morphine group at 24, 36, and 48 h at rest and with movement. The incidence of nausea and pruritus was similar between groups. We conclude that the combination of oral clonidine and epidural morphine produces more potent and longer lasting postoperative analgesia than either drug alone without increasing the incidence of adverse effects after major gynecologic surgeries. IMPLICATIONS: A small dose of epidural morphine is often used for postoperative analgesia. We found that oral clonidine premedication 5 microg/kg improves the analgesic efficacy of epidural morphine without increasing the incidence of adverse side effects.

Oral clonidine premedication reduces induction dose and prolongs awakening time from propofol-nitrous oxide anesthesia.

PURPOSE: To evaluate whether oral clonidine premedication affects the induction dose of propofol and awakening time from epidural and propofol anesthesia. METHODS: Thirty-nine female patients (ASA I or II) were randomly allocated to receive 5 microg x kg(-1) clonidine p.o. or no clonidine 90 min before induction of anesthesia. After epidural anesthesia was achieved with lidocaine, general anesthesia was induced with continuous i.v. infusion of propofol at a rate of 50 mg x min(-1) until loss of eyelash reflex and responses to verbal commands, which were judged by a blinded observer. After a laryngeal mask airway was inserted, anesthesia was maintained with N2O 67%, O2 33% and propofol adjusted to maintain hemodynamic stability. After completion of surgery, a blinded observer recorded the time from discontinuance of propofol and N2O until the patient was awake and responsive (awakening time), and then, the laryngeal mask airway was removed. RESULTS: The induction dose of propofol in the clonidine group (1.4 +/- 0.3 mg) was less than that in the control group (1.9 +/- 0.4 mg, P < 0.05), while the awakening time of the clonidine group (470 +/- 145 sec) was longer than that of the control group (329 +/- 123 sec, P < 0.05). CONCLUSION: Premedication with 5 microg x kg(-1) clonidine p.o. reduced the induction dose of propofol, but delayed emergence from propofol anesthesia.

Oral clonidine premedication enhances the pressor response to ephedrine during spinal anesthesia.

UNLABELLED: Clonidine premedication enhances the pressor effects of ephedrine in awake and anesthetized patients. To test the hypothesis that clonidine augments the pressor response to ephedrine during spinal anesthesia, 48 ASA physical status I or II patients were randomly assigned to either the clonidine group (n = 23), receiving oral clonidine approximately 5 microg/kg 90 min before spinal anesthesia, or the control group (n = 25), receiving no clonidine. Spinal anesthesia was performed at either the L2-3 or the L3-4 interspace using 0.5% hyperbaric tetracaine solution 1.4-3.0 mL. Blood pressure (BP), heart rate, and the upper dermatomal level of analgesia were determined at 1-min intervals with the patient in the supine position after tetracaine injections. When systolic BP decreased to <80% of the prespinal value or <100 mm Hg, IV ephedrine 0.2 mg/kg was administered as a bolus. There were no differences in the duration until the first dose of ephedrine after tetracaine injections, and the upper level of analgesia between groups (control group 8.5+/-3.7 min, T5; clonidine group 7.7+/-2.7 min, T6). Although prespinal and preephedrine BP values were higher in the control group, the magnitude of increases in mean BP after ephedrine was significantly greater in the clonidine group (P < 0.05). We conclude that oral clonidine premedication augments the pressor response to IV ephedrine during spinal anesthesia. IMPLICATIONS: The pressor effect of ephedrine is enhanced in patients given oral clonidine premedication during spinal anesthesia.

Oral clonidine premedication reduces the awakening concentration of isoflurane.

UNLABELLED: Because clonidine has analgesic and sedative properties, it may influence the awakening concentration or dose of an anesthetic. To investigate the effects of oral clonidine premedication on emergence from isoflurane anesthesia, we studied 61 ASA physical status I or II patients undergoing superficial operations. They were randomly allocated to one of three groups according to the dose of clonidine they received: the clonidine-2.5 group (n = 21), clonidine-5 group (n = 20), and control group (n = 20) received approximately 2.5, 5, or 0 microg/kg oral clonidine, respectively, in addition to 20 mg of famotidine 90 min before general anesthesia induction. Anesthesia was induced by thiamylal 5 mg/kg, and tracheal intubation was facilitated with succinylcholine 1.5 mg/kg I.V. Anesthesia was maintained with a 1.1% end-tidal isoflurane concentration and 67% N2O in oxygen, while ventilation was controlled to maintain end-tidal CO2 tension between 33 and 38 mm Hg. After surgery, N2O was discontinued while the end-tidal isoflurane concentration was maintained at 1.1%. After confirming the end-tidal N2O concentration of 0%, isoflurane was discontinued. The end-tidal isoflurane concentration at the time when patients responded to a standardized verbal command to open their eyes was recorded as MAC-Awake. The MAC-Awake values in the clonidine-5 group (0.22% +/- 0.09% [mean +/- SD]) was significantly less than those in the clonidine-2.5 and control groups (0.28% +/- 0.07% and 0.30% +/- 0.07%, respectively, P < 0.05). The wake-up time, from discontinuance of isoflurane until arousal, was longer in the clonidine-2.5 and clonidine-5 groups than in the control group (17.3 +/- 8.0, 16.9 +/- 7.0, and 10.6 +/- 5.3 min, respectively; P < 0.05). In conclusion, oral clonidine premedication 5 microg/kg decreases the awakening concentration of isoflurane, and arousal from isoflurane anesthesia is prolonged with oral clonidine in a dose of 2.5-5 microg/kg. IMPLICATIONS: Preanesthetic medication with oral clonidine, 2.5-5 microg/kg, is associated with prolonged recovery from isoflurane anesthesia in adults.

Oral clonidine premedication enhances the quality of postoperative analgesia by intrathecal morphine.

Since clonidine potentiates the analgesia by morphine, the current study was performed to investigate whether oral clonidine premedication would enhance the postoperative analgesia by intrathecal morphine. Twenty-six patients, aged 37-60 yr, schedule for abdominal total hysterectomy under spinal anesthesia, were studied. Patients were randomly allocated to one of two groups; the clonidine group (n = 13) received oral clonidine approximately 5 micrograms/kg, and the control group (n = 13) received no clonidine. All patients received hyperbaric tetracaine 12 mg dissolved in 10% dextrose and morphine 0.2 mg for spinal anesthesia. We measured duration of analgesia (time to the first request for supplemental analgesics) and motor block. We also recorded the total number of injections of supplemental analgesics, and intensity of postoperative visual analog pain scores, nausea, and pruritus for 48 h after intrathecal administration. Duration of analgesia in the clonidine group was longer than the control group (2017 +/- 263 vs 1190 +/- 199 min, mean +/- SEM; P < 0.05). Although there was no difference in the total number of injections of supplemental analgesics (1.1 +/- 0.4 and 2.2 +/- 0.3 in the clonidine and control groups, respectively), the number of patients not requiring supplemental analgesics during the entire study period was larger in the clonidine group than the control group (six patients versus one patient; P < 0.05). There were no differences at any observation point between groups in visual analog pain scores, or the incidence of nausea and pruritus. Oral clonidine preanesthetic medication enhances the postoperative analgesia of intrathecal morphine plus tetracaine without increasing the intensity of side effects from morphine.

The addition of epinephrine enhances postoperative analgesia by intrathecal morphine.

To investigate whether the addition of epinephrine would enhance postoperative pain relief by intrathecal morphine, we studied 36 patients scheduled to have spinal anesthesia for gynecologic surgery. Patients were randomly allocated to one of three groups: the first received epinephrine 0.12 mg, morphine 0.2 mg, and hyperbaric tetracaine 12 mg intrathecally (EMT group, n = 11); the second received morphine 0.2 mg and hyperbaric tetracaine 12 mg intrathecally (MT group, n = 13); and the third received epinephrine 0.12 mg and hyperbaric tetracaine 12 mg intrathecally (ET group, n = 12). The time to the first request for supplemental analgesics was longest (2182 +/- 251 min, mean +/- SEM) and the injection number of supplemental analgesics was least in the EMT group (P < 0.05). The percentage of patients who received supplemental analgesics in the EMT group (45.5%) was less than the other two groups (P < 0.05). Six patients in the EMT group and one in the MT group needed no additional analgesics during 48 h (P < 0.05 versus the MT and ET groups). The visual analog scale (VAS) pain score was larger in the ET group than the EMT group (P < 0.05), but was similar in the EMT and MT groups. There were no differences among groups in the incidence of nausea and pruritus. Our data show that the addition of epinephrine enhances postoperative analgesia by intrathecal morphine without increasing the incidence of adverse effects as compared with intrathecal morphine alone.

[Comparison of airway complications on tracheal extubation in deeply sevoflurane anesthetized versus awake children].

We investigated the incidence of respiratory complications and oxygen saturation level during emergence from sevoflurane anesthesia in children whose tracheas were extubated while they were anesthetized or after they became awake. Thirty children, aged 1-10 years, were studied. Anesthesia was induced with sevoflurane or thiopental and maintained with nitrous oxide, oxygen and sevoflurane. After nitrous oxide was discontinued at the end of surgery, the patients were randomly assigned to two groups: deeply anesthetized extubation group (anesthetized group) and awake extubation group (awake group). In anesthetized group, the patients were extubated while they were administered 1.5% or higher sevoflurane in 100% oxygen. In awake group, extubation was performed while the patients were awake. The incidence of respiratory complications such as apnea, laryngospasm, bronchospasm and arrythmias was not significantly different between the two groups. There was a significantly higher incidence of the airway obstruction but less incidence of cough and breath-holding in anesthetized group. Oxygen saturation level before and after tracheal extubation was not different between the two groups. In conclusion, with proper attention to airway obstruction, it may be possible to extubate while children are deeply anesthetized with sevoflurane.

[Influence of epidural anesthesia on the halothane MAC-intubation in emergence in infants and children].

The alveolar anesthetic concentration level at which the patient first shows movement when emerging from anesthesia is defined as MAC-intubation in emergence in infants and children. Twenty one patients of ASA physical status 1, were studied to determine the halothane MAC-intubation in emergence. The patients were divided into two groups; a general anesthesia alone group and a general anesthesia plus epidural anesthesia group. After endotracheal intubation without muscle relaxant, bupivacaine (0.25% with 200,000 epinephrine, 0.75 ml.kg-1) was injected into the lumbar epidural space in the epidural anesthesia group (n = 11). Each group was maintained at 1.0% end-tidal halothane concentration with oxygen under spontaneous respiration in the perioperative period. After the end of surgery, end-tidal halothane concentration, respiratory rate (RR), and ETCO2 were measured at the time halothane was discontinued and at the time of patient's first movement. The time from the discontinuation of halothane to the first body movement was recorded. The halothane MAC-intubation in emergence without epidural anesthesia was 0.26 +/- 0.03% (mean +/- SE) and that of the epidural anesthesia was 0.18 +/- 0.02% (P < 0.05). The time from the discontinuation of halothane to the first body movement tended to be longer without epidural anesthesia. RR and ETCO2 did not differ between the two groups of patients. The halothane MAC-intubation in emergence in the general anesthesia alone group was 0.26%, and adding epidural anesthesia decreased this concentration to 0.18%.

[Culture of the irrigating fluid of the epidural space obtained during chronic epidural catheterization].

The most serious complication during long-term epidural catheterization is epidural infection. Bacterial culture of the irrigating fluid of epidural space was carried out periodically in 39 patients in whom epidural catheters were inserted for a long period of time. Eight (17%) of 47 samples of epidural irrigating fluid were contaminated by the normal skin flora. All of these cases were accompanied with epidural contamination by the same organisms. No significant correlation was found between clinical signs of infection (low grade fever, leucocytosis and localized infective signs at the puncture site) and the contamination of the epidural irrigating fluid or that of the epidural catheter. When epidural irrigating fluid was contaminated, the epidural catheter was removed immediately and the patient was treated by antibiotics. None of the patients had epidural abscess or neurological deficit. In conclusion, bacterial culture of epidural irrigating fluid is valuable for the early diagnosis of epidural infection during long-term epidural catheterization.

Plasma lidocaine concentrations during epidural blockade with isoflurane or halothane anesthesia.

Because isoflurane maintains hepatic blood flow at higher flows than halothane, we proposed that the elimination of lidocaine would be different between these two volatile anesthetics. The plasma lidocaine concentrations were determined in 14 female patients undergoing epidural blockade plus isoflurane anesthesia and compared with those obtained during halothane anesthesia for lower abdominal surgery. General anesthesia was maintained with isoflurane (0.46% +/- 0.04% [mean +/- SE] inspired, n = 7) or halothane (0.48% +/- 0.05% inspired, n = 7) and 67% nitrous oxide in oxygen. All patients received 2% lidocaine solution, 10 mL as a bolus dose and continuous administration at a rate of 10 mL/h, through the epidural catheter. The plasma lidocaine concentrations over 180 min after the epidural injection in patients receiving isoflurane were similar to those in patients receiving halothane. The results suggest that low inspired concentrations of isoflurane do not reduce plasma lidocaine concentrations in patients during epidural blockade, compared with halothane.

[The effects of preanesthetic oral clonidine upon heart rate response to intravenous atropine in patients during general anesthesia].

In awake subjects the positive chronotropic effect of intravenously administered atropine 10 micrograms.kg-1 has been demonstrated to be blunted by preanesthetic medication of oral clonidine 5 micrograms.kg-1. The aim of the present study is to investigate whether general anesthesia could alter the clonidine-induced attenuation of positive chronotropic effect by atropine. Thirty-two patients were randomly assigned to one of the two groups; patients of the clonidine group received oral clonidine 5 micrograms.kg-1 (n = 12), whereas those of the control group received no clonidine. General anesthesia was induced with intravenous thiamylal 4-5 mg.kg-1, and was maintained with enflurane and nitrous oxide in oxygen after endotracheal intubation. Following the stable circulatory period of 10 min, hemodynamic measurements were made at 1 min intervals for 10 min after atropine 10 micrograms.kg-1 was administered intravenously as a bolus in both groups. A significant attenuation in heart rate response to intravenous atropine 10 micrograms.kg-1 was observed in patients receiving clonidine 5 micrograms.kg-1, as compared with that in the control group (P less than 0.01); maximal increases in heart rate were 15 +/- 8 and 22 +/- 6 beats.min-1 (mean +/- SD) in the clonidine and control groups, respectively. It is concluded that clonidine 5 micrograms.kg-1 blunts the heart rate response to intravenous atropine 10 micrograms.kg-1 in patients anesthetized with enflurane and nitrous oxide in oxygen.