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Patients with Parkinson's disease frequently suffer from impaired autonomic nervous function. To elucidate the effects of the induction of anesthesia with propofol on cardiovascular hemodynamics has become important, since the number of patients with Parkinson's disease undergoing deep brain stimulation under general anesthesia has increased recently.Effects of induction with propofol in patients with Parkinson's disease on cardiovascular hemodynamics and autonomic nervous activity were compared with those of the control patients. Moreover, possible different effect on hemodynamics between the propofol alone and the combination of propofol and fentanyl for the induction were examined in patients with Parkinson's disease.Although heart rate or blood pressure was not different between patients with Parkinson's disease and the control patients before the induction, sympathetic vasomotor activity was lower in patients with Parkinson's disease than the control patients. The induction of anesthesia significantly decreased blood pressure in patients with Parkinson's disease. However the decreasing systolic blood pressure after the induction of anesthesia was more marked in patients with Parkinson's disease than the control patients. We did not find differences in the changes of blood pressure between the propofol alone and the combination of propofol and fentanyl in patients with Parkinson's disease.No abnormal responses to the induction of anesthesia with propofol were found in the patients with Parkinson's disease.

The α(2)-adrenergic receptor agonist dexmedetomidine reportedly weakens heart rate (HR) responses to 'rapid' (during a few seconds) reduction in arterial pressure, but does not affect HR responses to 'gradual' (during 60 s) reduction in arterial pressure. As the speed of neurotransmission along the parasympathetic nerve is relatively rapid, alteration of parasympathetic-mediated arterial-cardiac baroreflex function plays a more important role in HR responses to 'rapid' changes in arterial pressure. We therefore hypothesized that dexmedetomidine attenuates parasympathetic-mediated arterial-cardiac baroreflex function.Twelve healthy men received placebo, low-dose (loading, 3 μg/kg/h for 10 min; maintenance, 0.2 μg/kg/h for 60 min) (low-DEX), or moderate-dose (loading, 6 μg/kg/h for 10 min; maintenance, 0.4 μg/kg/h for 60 min) (moderate-DEX) dexmedetomidine infusions in a randomized, double-blind, crossover study. Before and after 70 min of infusion, arterial-cardiac baroreflex function was assessed by spectral and transfer function analysis between arterial pressure variability and HR variability.The high-frequency power of systolic arterial pressure (SAP) variability increased significantly with low-DEX and moderate-DEX infusions (significant interaction effects, P = 0.005), whereas the high-frequency power of R-wave-R-wave interval (RRI) variability (as an index of cardiac parasympathetic activity) did not change significantly at any dose infusions. Then, transfer function gain in the high-frequency range (as an index of parasympathetic arterial-cardiac baroreflex) decreased significantly with low-DEX and moderate-DEX infusions (significant interaction effects, P = 0.007).The present results suggest that dexmedetomidine attenuates parasympathetic-mediated arterial-cardiac baroreflex function, implying weakened HR response to 'rapid' reduction in arterial pressure.

Triazolam reportedly has greater amnesic potential than other benzodiazepines. The present study was designed to investigate whether this amnesic potential can be applied to surgical patients as premedication, thus relieving them from postoperatively remembering preoperative fears of anesthesia and surgery.We prospectively evaluated the effect on amnesia of triazolam administered during the preoperative period in 80 patients between 20-64 years of age (mean, 43.1 +/- 14.3 years) who underwent surgeries for non-malignant diseases under general anesthesia maintained with sevoflurane and nitrous oxide in oxygen throughout the operation, or general anesthesia maintained with the same anesthetics combined with epidural or spinal anesthesia. Patients with diseases or factors influencing the effect of triazolam, such as a history of mental diseases, recent sedative or antihistamine usage, or current sleep disturbances, were excluded from this study. Triazolam was administered to the 80 patients orally at a dose of 0.375 mg 60 minutes prior to entering the operating room. During structured interviews on postoperative day 1, the patients were asked to state what they remembered of the preoperative period. Amnesia was classified based on the patients' last memory before the anesthetic induction as follows: loss of memory from immediately after taking triazolam, loss of memory at departure from the ward, loss of memory at the entrance to the operating room, loss of memory at the operating table and some recall of events at the operating table.Interviews revealed that 26.3% of the patients experienced loss of memory immediately after taking triazolam, this number increasing to 28.8% of the patients at departure from the ward, 35.0% at the entrance to the operating room and 67.5% on the operating table. The remaining patients (32.5%) had some memory of the operating room and table. Triazolam caused no respiratory depression at the operating table, although 2 of the patients experienced dizziness, 1 patient had nausea and 1 patient felt heavy-headed during the period between taking triazolam and the induction of anesthesia. Although 13 patients had delayed emergence from general anesthesia, these patients remaining anesthetized even 5 minutes after the concentration of sevoflurane in the expired gas decreased and remained below 0.1 percent, all these patients emerged immediately after intravenous administration of flumazenil.The use of triazolam as premedication produced a high incidence of amnesia for preoperative events without causing respiratory depression. Triazolam appears to be a useful premedicant for surgical patients who wish to have no memory at the operating room.

The main aim of this study was to compare the onset times of rocuronium evaluated subjectively and by acceleromyography at the masseter muscle (MM). Forty female patients were sequentially enrolled in this study. In the first 20 patients, neuromuscular block was evaluated subjectively. After induction of anesthesia with fentanyl and propofol, both the left masseter and ulnar nerves were stimulated in 2-Hz train-of-four (TOF) mode using peripheral nerve stimulators. Contractions of the MM were felt with an anesthesiologist’s left hand holding an anesthesia facemask; those of the adductor pollicis (APM) were visually observed. All the patients received a bolus of rocuronium, 0.6 mg/kg. Onset times after rocuronium were defined as the duration until the contractions became impalpable at the MM or invisible at the APM. At the time contraction of the MM had not been felt, intubating conditions were assessed. In the next 20 patients, contractions of the MM and the APM were concurrently quantified using acceleromyography after induction of anesthesia and laryngeal mask insertion. Following 0.6 mg/kg rocuronium, onset of the action was recorded. Onset of the action of rocuronium at the MM evaluated subjectively [mean (SD), 70.3 (17.7) s] was similar to that monitored acceleromyographically [73.3 (27.6) s, P > 0.05], and significantly shorter than that at the APM acceleromyographically [111.0 (34.8) s, P = 0.016]. Intubating conditions of 20 patients were graded either excellent or good. Subjective evaluation of contractions of the MM by an anesthesiologist’s hand may be reliable to determine faster timing for safe tracheal intubation.

Background Although midazolam and propofol reduce cerebral blood flow (CBF) similarly, they generate different effects on the autonomic nervous system and endothelium-induced relaxation. Midazolam induces sympathetic dominance, whereas propofol induces parasympathetic dominance. Midazolam has no effect on endothelium-dependent relaxation, whereas propofol suppresses endothelium-dependent relaxation. Moreover, midazolam apparently constricts cerebral arterioles. We therefore hypothesized that midazolam and propofol have different effects on dynamic cerebral autoregulation. Methods Ten healthy male subjects received midazolam, propofol, and placebo administrations in a randomized, single-blind, crossover study. The modified Observer's Assessment of Alertness/Sedation scale was used to assess sedation depth. After reaching a target depth of sedation (Observer's Assessment of Alertness/Sedation scale score 3, responds only after name is called loudly and/or repeatedly) or after 15 minutes of normal saline administration as placebo, dynamic cerebral autoregulation was evaluated by spectral and transfer function analyses between mean arterial blood pressure variability in the radial artery measured by tonometry, and CBF velocity variability in the middle cerebral artery measured by transcranial Doppler ultrasonography. Results Steady-state CBF velocity decreased significantly with midazolam and propofol administration (significant interaction effects, P = 0.024). However, transfer function gain in the low-frequency range decreased significantly only with midazolam administration (significant interaction effects, P = 0.015), suggesting a reduced magnitude of transfer from mean arterial blood pressure oscillations to CBF fluctuations during midazolam sedation. Conclusion Our results suggest that midazolam and propofol sedation have different effects on dynamic cerebral autoregulation despite causing equivalent decreases in steady-state CBF velocity. Only midazolam sedation is likely to improve dynamic cerebral autoregulation.

We examined the efficacy and safety of a new transdermal fentanyl citrate patch (HFT-290), which was applied once daily in patients with cancer pain who were receiving a stable dose of once-every-three-day application transdermal fentanyl patch [TDF (72 hr)]. After TDF (72 hr) was applied for three days at the same dose used before starting the study, treatment was switched to HFT-290 (once daily) for 9 days. The analgesic effect was judged with a 5-point scale based on each patient's assessment of pain on a 100-mm visual analog scale (VAS). Seventy-eight patients were enrolled. The efficacy rate (95% confidence interval) of the analgesic effect at the time of final removal of HFT-290 (the primary efficacy end-point) was high at 83.9% (71.7-92.4%; 47/56 patients). Furthermore, based on the shift of the VAS, good pain control was achieved after switching. All adverse drug reactions were either mild or moderate, and the main reactions were those commonly observed with opioid analgesics. No respiratory depression was observed. HFT-290 demonstrated good tolerability after switching from TDF (72 hr) and provided stable pain control.

The efficacy of pregabalin was demonstrated in a randomized double-blind placebo-controlled 13-week trial in 371 Japanese patients with postherpetic neuralgia (PHN). In this study, we evaluated the long-term efficacy and safety of pregabalin for relief of PHN.126 patients were enrolled from the preceding double-blind study into the 52-week open-label study. Patients were given pregabalin 150 to 600 mg x day(-1). Pain intensity was measured using the Short-Form McGill Pain Questionnaire (SF-MPQ: total score, visual analogue scale and present pain intensity).The efficacy parameter SF-MPQ showed a decrease over the treatment-term. The changes of visual analogue scale and present pain intensity at the endpoint were -28.3 mm and -1.1 score, respectively. The commonly reported adverse events were dizziness, somnolence, peripheral edema and weight gain, and most of them were mild to moderate in intensity. No new adverse events were observed due to long-term pregabalin administration.These results suggest that long-term treatment of pregabalin may be beneficial in patients with PHN.

The aim of this study was to examine optimum intubating dose of rocuronium in adult patients who had been scheduled for short duration surgery.Thirty patients were randomly assigned to receive rocuronium 0.4 mg x kg(-1), 0.5 mg x kg(-1) or 0.6 mg x kg(-1) during induction with propofol and fentanyl. Immediately after the adduction of thumb to the ulnar nerve stimulation could not be visually observed, the patients were intubated tracheally and the intubating conditions were evaluated. Thereafter, time to recover to train-of-four (TOF) counts of 4 was recorded during sevoflurane and nitrous oxide anesthesia.Intubating conditions after rocuronium 0.5 and 0.6 mg x kg(-1) were all graded either excellent or good. In contrast, inadequate conditions for safe and easy tracheal intubation were observed in 60% of the patients receiving 0.4 mg x kg(-1). Time to spontaneous recover to the TOF counts of 4 correlated with the intubating doses of rocuronium.For short duration surgeries, rocuronium 0.5 mg x kg(-1) was appropriate to perform safe tracheal intubation and minimize duration of action of rocuronium.

The main purpose of this study was to examine the effectiveness of the timing principle with 1 mg kg(-1) rocuronium for rapid sequence intubation. As secondary outcomes, propofol and lidocaine with or without remifentanil were examined to note their effects on the cardiovascular responses to laryngoscopy and intubation.Thirty patients were randomly allocated to one of two groups of 15 patients each: a lidocaine-treated group (L) and a lidocaine/remifentanil-treated group (LR). Thirty seconds after lidocaine 1 mg kg(-1) with or without infusion of remifentanil 1 microg kg(-1) min(-1), all patients received a bolus of rocuronium 1 mg kg(-1). Shortly afterwards, patients were given propofol 2-2.5 mg kg(-1). Intubating conditions and cardiovascular responses were observed 60 s after rocuronium. The time to spontaneous recovery of visible train-of-four (TOF) counts of 4 was observed at the thumb during 1.0-1.5% end-tidal sevoflurane and remifentanil anesthesia.All patients had excellent or good intubating conditions. Hypertension and tachycardia during laryngoscopy were well prevented in group LR, whereas they were significantly observed in group L. The times to reappearance of TOF counts of 4 were comparable in all groups [mean (SD); 63.6 (8.6) min in group L and 63.5 (11.6) min in group LR].Application of the timing principle with 1 mg kg(-1) rocuronium is beneficial for rapid tracheal intubation. Co-administered lidocaine, remifentanil and propofol can definitely suppress cardiovascular responses during laryngoscopy and intubation.

Introduction: During and immediately following a 2-wk spaceflight, dynamic cerebral autoregulation is improved, leading to stable cerebral blood flow velocity (CBFV). However, the factors inducing this improved cerebral autoregulation remain unclear. Although mild reduction of plasma volume (one of the key adaptations to spaceflight) may lead to improved cerebral autoregulation, there have been no reports estimating the alteration of dynamic cerebral autoregulation during mild dehydration. We, therefore, investigated the effect of mild intravascular dehydration on dynamic cerebral autoregulation. Methods: Furosemide, 0.2 mg · kg ―1 , was administered to 14 men. Dynamic cerebral autoregulation was estimated before and approximately 45 min after furosemide administration using spectral and transfer function analyses between mean blood pressure (MBP) variability and mean CBFV variability. We then assessed the degree of dehydration as plasma volume changes, and/or central venous pressure (CVP). Results: Furosemide administration caused an approximate 10% reduction in plasma volume, with CVP decreasing by 1.2 mmHg. Steady state MBP and mean CBFV did not change. However, transfer function gain in the low-frequency range significantly decreased, implying a decrease in the magnitude of transfer from MBP oscillations to mean CBFV fluctuations. Discussion: The present degree of dehydration was similar to the alteration observed after short-term spaceflight, and enhanced dynamic cerebral autoregulation in the low-frequency range with unchanged steady state mean CBFV. Consequently, these results on cerebral circulation were consistent with those of a previous spaceflight study. Thus, it is suggested that mild intravascular dehydration partly explains the improved dynamic cerebral autoregulation observed during and immediately after spaceflight.

Two patients with spinocerebellar ataxia received epidural analgesia with no exacerbation of their symptoms. The patients developed transient, but extremely severe, low back pain as a result of the epidural analgesia.

Fade of the muscle contraction evoked by indirect tetanic nerve stimulation shows residual neuromuscular block. Anticholinesterases can reverse the partial block; however, they may also inhibit normal neuromuscular transmission and can cause fading responses by misuse of these drugs. The aim of this study is to investigate how neostigmine acts on normal neuromuscular function.In cats, we observed a series of 8 consecutive muscular compound action potentials (mCAPs; M1-8) of the gastrocnemius muscle evoked by repetitive sciatic nerve stimulation at 100 Hz and calculated the M8/M1 amplitude ratio as an index of fading phenomenon. Neostigmine 0.05 mg x kg(-1) repetitively every 5 minutes before neuromuscular blocking agent had been administered, or after the complete recovery from vecuronium-induced block had been obtained.Neostigmine caused dose-dependent fade in the mCAPs. The mean doses (SD) of neostigmine for depressing M8/M1 ratio to 50% of baseline were 0.087 (0.029) mg x kg(-1) before use of neuromuscular blocking agent and 0.161 (0.070) mg x kg(-1) after the recovery from neuromuscular block. The fading responses induced by neostigmine were paradoxically reversed by small doses of vecuronium.Therapeutic doses of neostigmine administered during normal neuromuscular function cause fade of the repetitive muscle contractions. Neuromuscular monitoring should be used before the reversal with neostigmine.

Intractable chronic pain resists any therapy, and the mechanism of the pain varies from patient to patient even with the same disease. Therefore, patients with chronic pain tend to look for a doctor who would successfully attenuate their pain. Consequently, a patient may visit several doctors only to get similar treatments after wasting time and money. To avoid the situation, pharmacological classification (so called drug challenge test) to determine the mechanism of a patient's pain is conducted. Drugs tested are morphine, ketamine, lidocaine, thiopental, phentolamine, midazolam, ATP clomipramine, PGE1, and neurotropin. A test for each drug is conducted on a separate day. As each drug has a different pain-attenuating mechanism, mechanism of a patient's pain will be clarified when an effective drug is found. A drug is administered as a bolus several times or continuously intravenously. According to the results of our tests conducted in sixty-five patients with neuropathic pain due to peripheral nerve injuries, ketamine proves to be the most effective in alleviating pain followed by ATP, morphine and thiopental. Therapies based on the results were provided to the patients.

The aim of this study was to examine the effect of landiolol hydrochloride, an ultrashort-acting beta(1)-blocker, on suxamethonium-induced neuromuscular block.Thirty patients were randomly allocated to receive a loading dose of landiolol, 0.125 mg x kg(-1) x min(-1) for 1 min, followed by an infusion at 0.04 mg x kg(-1) x min(-1), or placebo. Twenty minutes after the infusion of landiolol or placebo, suxamethonium 1 mg x kg(-1) was administered during propofolfentanyl-nitrous oxide anesthesia. Neuromuscular block was monitored by train-of-four (TOF) responses of the adductor pollicis muscle, applying acceleromyographic stimuli to the ulnar nerve.The onset of neuromuscular block did not differ between the groups. The time from administration of suxamethonium to spontaneous recovery to the first twitch of TOF (T1) of control was significantly longer in the landiolol group (mean [SD]; 12.2 [2.5] min), when compared with the control group (9.8 [2.6] min). However, the TOF ratios measured when the T1 had spontaneously recovered to 10%, 25%, 50%, 75%, 90%, and 100% of control was comparable between the groups.Landiolol delayed recovery from suxamethonium-induced paralysis. However, the interaction between the drugs seemed to be small in the clinical setting.

Frequent changes in the perioperative central blood volume could affect cerebral autoregulation through alterations in sympathetic nerve activity, cardiac output, blood viscosity, and cerebral vasomotor tone. However, the effect of dynamic cerebral autoregulation has not been studied during acute wide-ranging changes in central blood volume, especially with respect to central hypervolemia with hemodilution.We evaluated dynamic cerebral autoregulation during central hypovolemia and central hypervolemia with hemodilution using spectral and transfer function analysis between mean arterial blood pressure (MBP) and cerebral blood flow (CBF) velocity variability in 12 individuals. Rapid changes in central blood volume were achieved using two levels of lower body negative pressure (-15 and -30 mm Hg) and two discrete infusions of normal saline (15 mL/kg and total 30 mL/kg). We then estimated changes in central blood volume as central venous pressure (CVP) and/or cardiac output using impedance cardiography.Steady-state CBF velocity and cardiac output decreased at -30 mm Hg lower body negative pressure (changes of CVP approximately -4 mm Hg) or were increased by each saline infusion (changes of CVP 4-6 mm Hg), without a significant change in MBP. However, transfer function gain (magnitude of transfer) between MBP and CBF velocity variability significantly increased only after saline infusion, suggesting an increased magnitude of transfer from MBP oscillations to CBF fluctuations during central hypervolemia with hemodilution.Our results suggest that, although steady-state CBF velocity changes under both central hypervolemia and hypovolemia, only hypervolemic hemodilution impairs dynamic cerebral autoregulation.

BACKGROUND: Although intrathecal midazolam has been reported to produce antinociceptive effects mediated by -aminobutyric acid type A-benzodiazepine receptor complexes in the spinal cord, the effects of systemic midazolam on nociception remain unclear. We performed this study to examine the effects of IV-administered midazolam on somatosympathetic A and C reflex discharges in brain-intact cats and decerebrate cats (with transection at midbrain level). METHODS: Somatosympathetic A and C reflexes were elicited in the inferior cardiac sympathetic nerve by electrical stimulation of myelinated (A) and unmyelinated (C) afferent fibers of the superficial peroneal nerve in 28 mature cats. After control somatosympathetic reflex responses were obtained, midazolam was administered IV to four groups of randomly allocated cats as follows: brain-intact cats at a dose of 0.03 mg/kg, brain-intact cats at a dose of 0.1 mg/kg, brain-intact cats at a dose of 0.5 mg/kg, and decerebrate cats at a dose of 0.1 mg/kg. RESULTS: C reflex discharges were significantly augmented at the dose of 0.03 mg/kg and significantly depressed at the dose of 0.1 and 0.5 mg/kg in brain-intact cats. C reflex discharges were also significantly depressed at the dose of 0.1 mg/kg in decerebrate cats. CONCLUSIONS: We have demonstrated that IV midazolam produces dose-related effects on somatosympathetic reflex discharges. The clinical implication of these findings is that the effect of midazolam on nociception depends on its dosage. It also appears that the infra-midbrain region plays a major role in mediating the depressive effects of midazolam on somatosympathetic C reflex discharges. (Anesth Analg 2007;105:832‐7)

A 79-year-old man was scheduled to undergo transurethral resection of the hypertrophied prostate during general anesthesia. Anesthesia was maintained with sevoflurane 0.5-1.0% and nitrous oxide 50% in oxygen mixture. Immediately after using an evacuator to remove small resected pieces of the prostate, end-tidal carbon dioxide pressure (EtCO2) decreased suddenly from 31 mmHg to 18 mmHg. Concurrently, decreases in systolic blood pressure from 110 mmHg to 60 mmHg and oxygen saturation from 100% to 95%, and an increase in arterial-alveolar carbon dioxide tension difference (a-ADCO2) were observed. We initially suspected the onset of pulmonary thrombosis as the cause of these events, ventilated the patient's lungs with 100% oxygen and administered 5,000 units of heparine and vasopressors intravenously. However, transesophageal echocardiography done subsequently revealed the presence of strongly echogenic images compatible with the air in the left cardiac atrium and the contribution of the air to those events. The EtCO2, blood pressure, and oxygen saturation improved in about 20 minutes after the initial decrease of the EtCO2 had been detected. Thereafter, surgical procedure was done uneventfully. In routine anesthetic management of transurethral surgery, it should be considered that the sudden deterioration in vital signs may have been caused by evacuator used.

A surgical patient with ventricular septal rupture after acute myocardial infarction is presented. The primary concern of general anesthesia was in the maintenance of systemic arterial pressure and reduction of afterload. General anesthesia was induced with a combination of fentanyl, ketamine, and propofol, which successfully suppressed fluctuations of hemodynamic variables associated with induction of anesthesia and tracheal intubation. Intravenous milrinone was used for inotropic support and reduction of systemic vascular resistance. The ventricular septal rupture was successfully repaired.

Sevoflurane reduces autonomic neural control, which plays a significant role in cerebral autoregulation. Therefore, we hypothesized that sevoflurane influences cerebral autoregulation. We investigated the effects of sevoflurane on dynamic cerebral blood flow (CBF) autoregulation by using spectral and transfer function analysis between blood pressure variability and CBF velocity variability. Eleven healthy male subjects received 0.5%, 1.0%, and 1.5% sevoflurane via facemask. Dynamic cerebral autoregulation was evaluated by transfer function gain, phase, and coherence between CBF velocity in the middle cerebral artery measured by transcranial Doppler, and blood pressure in the radial artery. Coherence in the very low-frequency range (0.02-0.07 Hz) increased above 0.5 during administration of 0.5% and 1.0% sevoflurane. Transfer function gain in this frequency range (0.02-0.07 Hz), as an index of dynamic cerebral autoregulation, increased significantly with 0.5% and 1.0% sevoflurane. Transfer function gain and coherence in the low- and high-frequency ranges, however, remained unchanged during administration of sevoflurane. These results suggest that sevoflurane impairs dynamic cerebral autoregulation in the very-low-frequency range even with small concentrations, whereas dynamic cerebral autoregulation in the low- and high-frequency ranges remained unchanged.

Humans encounter increased partial pressures of inspired oxygen in some kinds of diving as well as during use of hyperoxic mixtures to shorten decompression times and hyperbaric oxygen therapy for decompression sickness or other clinical conditions. Although it is known that hyperoxia may affect cardiovascular regulation, such effects are generally obscured by stress and the diving reflex. In this study, we evaluated cardiovascular neuroregulation for various levels of hyperoxia in a laboratory setting.There were 10 healthy adults who were exposed to 21, 40, 70, and 100% oxygen administered via mask as a series of stepwise increases. Subjects breathed at a fixed respiratory rate of 15 breaths x min(-1) while their heart rate (HR) and blood pressure (BP) were measured continuously over 5-min intervals.HR decreased with increasing fraction of inspired oxygen (FIO2) (21%: 65 +/- 9, 40%: 63 +/- 9, 70%: 61 +/- 8, 100%: 60 +/- 8 bpm) and the high-frequency power of HR variability (an index of cardiac parasympathetic activity) increased as FIO2 rose (21%: 773 +/- 565, 40%: 880 +/- 590, 70%: 966 +/- 681, 100%: 1114 +/- 715 ms2); both changes were significant at the 70% and 100% oxygen levels. The low-frequency power of systolic BP variability (an index of vasomotor sympathetic activity) did not change. Low- and high-frequency transfer function gains (indices of arterial-cardiac baroreflex function) increased with FIO2.Parasympathetic activity and arterial-cardiac baroreflex function increased with hyperoxia in a dose-dependent manner. This increase may help reduce the likelihood of arrhythmias during diving.

IT is well known that phantom limb pain can reappear or be exacerbated transiently during spinal anesthesia in amputees. 1 However, to the best of our knowledge, the reappearance of phantom limb pain immediately after nonamputation surgery in an amputee has not been reported. We herein present a patient with chief complaint of reactivation of phantom limb pain the day immediately after cervical myelopathy surgery.

We report a case of recurrent ST-segment elevations totaling 7 times over 3 hours during subtotal gastrectomy and the early postoperative period in a patient with no history of coronary artery disease. Possible contributing factors include cold stimulus, epidural anesthesia, and inadequate depth of anesthesia. The first episode almost resulted in cardiac arrest and was treated with intravenous epinephrine. The second episode was associated with ventricular fibrillation, which was treated with defibrillation and intravenous verapamil. The third to the seventh episodes were successfully treated with intravenous nitrate. The electrocardiographic changes and postoperative coronary angiography were consistent with a clinical diagnosis of coronary artery spasm. This case suggests that coronary artery spasm is capable of occurring repeatedly in a cyclic pattern during perioperative periods.

The purpose of this study was to clarify the relationship between skin temperature over the thenar muscles and the duration of action of vecuronium measured acceleromyographically at the thumb in anesthetized patients.In 15 patients undergoing elective open abdominal surgery under propofol, fentanyl, and nitrous oxide anesthesia, train-of-four (TOF) stimuli were delivered over the ulnar nerve at 2 Hz every 15 s, and the degree of neuromuscular block was measured acceleromyographically at the thumb. Each patient received an intubating dose of vecuronium 0.1 mg x kg(-1), followed by maintenance doses of 0.02 mg x kg(-1) administered repeatedly whenever the first twitch of TOF responses had recovered to 25% of control. The interval between maintenance doses was defined as the clinical duration (DUR25). The median values of skin temperature (ST) over the ipsilateral thenar muscles and esophageal temperature (ET) were recorded during the action of the first and all subsequent maintenance doses. The relationships between change in temperature and change in DUR25 were analyzed.Whereas ET showed only minor changes (median, -0.3 degrees C), ST fluctuated markedly between +0.9 degrees and -6.3 degrees C (median, -1.4 degrees C). Increase and decrease were also seen in a series of DUR25s, as expected from the changes in ST. The median values of DUR25 produced by the first and last maintenance vecuronium doses were 21.5 and 32.3 min, respectively. A negative linear correlation was found between the change in DUR25 and that in ST, demonstrating that DUR25 increased by 20% of baseline with each 1 degrees C decrease in ST.Our results show that peripheral ST decreases considerably during open abdominal surgery without reduction in core temperature, and the decrease contributes to the potentiation of neuromuscular block in the periphery during propofol, fentanyl, and nitrous oxide anesthesia.

Dynamic cerebral blood flow autoregulation during sevoflurane anesthesia and total intravenous anesthesia (TIVA) is unclear. We examined the cerebral circulation autoregulation during anesthesia by sevoflurane or TIVA.We measured mean blood pressure (MBP) and blood flow velocity of the middle cerebral artery by a transcranial Doppler ultrasonography before and during anesthesia using sevoflurane (volatile induction and maintenance of anesthesia (VIMA) group) and using propofol and fentanyl (TIVA group), and the relationship between changes in MBP and cerebral blood flow velocity was evaluated using the method of transfer function analysis. We calculated transfer gain and coherence by cross-spectrum from autospectra of MBP and cerebral blood flow velocity.Transfer gain during anesthesia by TIVA in the low frequency range and high frequency range was near 1 cm.sec-1.mmHg-1. It was about equal to the value of transfer gain before anesthesia. But transfer gain during anesthesia by VIMA was above 2 cm.sec-1.mmHg-1.These results suggest that TIVA by propofol and fentanyl maintains the dynamic autoregulation of cerebral blood flow, but sevoflurane impairs the autoregulation.

Antinociceptive effect of intrathecal neostigmine has been investigated using withdrawal responses in laboratory experiments. However, neostigmine administered in this route can induce muscle weakness or sedation. As a result, these effect can modify withdrawal responses. In this study we investigated the antinociceptive effect of intrathecally administered neostigmine bromide (NB) in cats objectively and quantitatively using somato-sympathetic reflex potentials.Anesthetized cats were inserted with a spinal catheter via atlanto-occipital membrane and 10 micrograms (n = 5), 50 micrograms (n = 5), 250 micrograms (n = 8) or 2 mg (n = 5) of NB was administered through this route. Somato-sympathetic reflex potentials (A and C reflex) derived from lumbar sympathetic ganglion by stimulation of the femoral nerve and mean arterial blood pressure (MAP) and heart rate (HR) in each dose were monitored and recorded.Reflex potential was reduced in a dose dependent fashion by NB but these changes were not significant. On the other hand, 250 micrograms and 2 mg of NB maximally reduced C reflex potential to 55.2% and 24.0% of control values respectively 20 minutes after the administration (P0.01), and this reduction was reversed by 250 to 2 mg of intrathecal administration of atropine sulfate to 89.4%, 68.6% of control values respectively. MAP and HR decreased in dose dependent fashion by NB to 57.6%, 65.2% of control values after the administration of 2 mg of NB and these cardiovascular changes recovered by intrathecally administered atropine sulfate.These results objectively indicate that intrathecally administered neostigmine bromide shows antinociceptive effect and this inhibition is partially mediated by cholinergic mechanism.

To the Editor: During ultrasound-guided nerve blocks, physicians generally hold the ultrasound transducer in one hand while inserting the nerve block needle with the other. However, since it is sometimes difficult for the anesthesiologist to single-handedly manipulate the ultrasonographic transducer for simultaneous visualization of the nerve and the tip of the needle, anesthesiologists who perform ultrasound-guided nerve blocks usually require an assistant for local anesthetic injection and catheter insertion. A guideline for ultrasound-guided nerve blocks, jointly published by the American Society of Regional Anesthesia (ASRA) and European Society of Regional Anesthesia (ESRA) in 2009 [1], points out that for safety purposes, continuous visualization of the needle tip during advancement is important. On the other hand, Site et al. [2] reported that visualization of the needle tip is not easy. Several ultrasound transducer stabilization devices are already available to overcome the previously mentioned issues in clinical practice. These stabilizers are secured to the skin surface as desired by the physician. However, they lack portability. For example, the weight of one of the available stabilizers, ultraStand (Wellan Medical, Inc., NH, USA), is 7 kg. In addition, to the best of our knowledge, although the structures and characteristics of these devices have been described in brochures, they have not been described in any independent research papers. Hence, to improve the portability of the stabilizer, we developed a portable, lightweight (1.45 kg) ultrasound transducer stabilization device that can freely move in any direction and allow easier adherence of the transducer to the skin surface of the patient, as desired by the physician. Our unique patented device (patent number 2008-317507 in Japan) is more compact and portable than the devices currently available (Fig. 1). It was designed to accompany the infusion stands available in every operation room and outpatient pain clinic in Japan, unlike transducer stabilization devices, which require their own special stands. The device consists of both transducer and infusion stand holders (Fig. 2) and attaches to either linearor convextype transducers. Figure 3 demonstrates the use of the stabilization device to attach the linear-type transducer to the left neck for interscalene nerve block. Figure 4 demonstrates how it also enables continuous and unassisted catheter insertion for right interscalene nerve block in a patient with complex regional pain syndrome. In conclusion, our new portable ultrasound transducer stabilization device might facilitate unassisted local anesthetic injection and catheter insertion during ultrasoundguided nerve blocks.

We investigated the antinociceptive effect of intrathecally administered S(-)-baclofen and R (+)-baclofen in cats using somato-sympathetic reflex potentials derived from lumbar sympathetic ganglion by stimulation of the femoral nerve. S(-)-baclofen 10 mg maximally reduced both A reflex potential and C reflex potential to 65.3% and 83.7% of control values, respectively, 1 minute after the administration, but these changes were not significant. The inhibition of A reflex potential at this dosage was greater than that of blood pressure and heart rate induced by the same dosage of S(-)-baclofen. While, R(+)-baclofen 1 mg maximally inhibited A reflex potential to 48.6% of control value 20 minutes after the administration, and this change was significant (P0.05). The inhibition of A reflex potential was greater than that of blood pressure and heart rate induced by the same dosage of R(+)-baclofen. This dosage of baclofen reduced C reflex potential to 66.4% of control value 10 minutes after the administration. The degree of reduction of A and C reflex potentials induced by 1 mg of R(+)-baclofen was higher in comparison with that induced by 10 mg of S(-)-baclofen. These reduction of A and C reflex potentials were reversed by 1 to 1.5 mg of intrathecally administered saclofen. These results indicate that R(+)-baclofen has higher potency than S(-)-baclofen and suggest that S(-)-baclofen and R(+)-baclofen show antinociceptive effect by intrathecal administration. On the other hand, it is possible that these two drugs exert antinociceptive effect via A delta fiber.

UNLABELLED Superoxide is generated by reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase that exists in the cell membrane of neutrophils and contains p47 phox in the enzyme complex. Superoxide is closely related to various diseases, including infection, myocardial infarction, and aspiration pneumonia. Therefore we performed this study to establish how lidocaine acts on NADPH oxidase. We examined the effects of lidocaine on superoxide production in neutrophils using the method of 2-methyl-6-phenyl-3,7-dihydro [1,2-a] pyrazin-3-one (CLA phenyl)-dependent chemiluminescence activated by opsonized zymosan (OZ). Treatment with lidocaine 15 microM suppressed OZ-activated CLA phenyl-dependent chemiluminescence by approximately 40% compared with that of OZ only-activated neutrophils. It was further demonstrated that the suppressive effect of lidocaine on superoxide production was dependent on the concentration of lidocaine. Translocation of p47 phox from the cytosol to the cell membrane was studied using immunoblot analysis with a polyclonal anti-p47 phox antibody. Lidocaine suppressed OZ-induced p47 phox translocation in a dose-dependent manner. Our results suggest that suppression of superoxide production by a therapeutic dose of lidocaine correlates strongly with suppression of p47 phox translocation. IMPLICATIONS We report on the effects of lidocaine on superoxide production in opsonized zymosan-activated neutrophils. Lidocaine suppresses superoxide production in a dose-dependent manner. This suppression correlates strongly with the suppression of translocation of p47 phox, a new subunit of NADPH-oxidase.

A patient with severe right chest pain and mechanical allodynia induced by an intercostal drainage tube to his chest is presented. It was not relieved by treatment with diclofenac sodium and was worsened by movement and touch to the right chest wall. Mechanical allodynia was also present. The patient's wrenching pain disappeared immediately after stitch removal, but the dull pain and mechanical allodynia persisted, gradually decreasing to zero in 7 days.

A randomized, double-blind, controlled study was designed to evaluate the effect of presurgical local infiltration of bupivacaine in the surgical field on postsurgical wound pain relief and analgesic requirements in 28 healthy patients scheduled for laparoscopic gynecologic examinations.After induction of general anesthesia by routine methods, the patients were randomly divided into two groups. In the bupivacaine (B) group (n = 15), patients were injected with 5 ml of 0.25% bupivacaine at each incisional area (four sites, total of 20 ml) approximately 15 minutes before skin incision. In the control (C) group (n = 13), the surgical field was injected with an equal volume of physiologic saline solution (four sites, total of 20 ml).Postsurgical wound pain at rest was evaluated by a 10-cm visual analog pain scale at 1, 10, 24, and 72 hours and 1 month after surgery. The patients were interviewed via telephone 1 month after hospital discharge for re-evaluation of resting pain.The results indicated that the incidence of postsurgical wound pain for up to 10 hours after surgery in group B was significantly lower (p0.05) than in group C. Pain intensity ranged from mild to moderate (2-5 cm). In addition, the mean visual analog pain scale pain intensity was significantly less for group B (0.31 +/- 0.85 cm) than for group C (2.62 +/- 2.06 cm) for up to 10 hours after surgery (p0.05). The number of patients who requested analgesics and complained of sleep disturbances was significantly higher in group C (p0.05). The mean cumulative dose of diclofenac sodium at 24 hours was significantly (p0.05) lower in group B (6.67 +/- 17.6 mg) than in group C (30.8 +/- 25.3 mg). Prolonged postsurgical wound pain persisting 1 month after surgery was observed in one patient in group C.It is concluded that presurgical infiltration of 0.25% bupivacaine in the surgical field is a useful method for decreasing postsurgical wound pain for up to 10 hours and analgesic consumption for up to 24 hours after laparoscopic gynecologic examination.

Two techniques for evaluating human baroreflex sensitivity (BRS), i.e. the sequence technique and the cross-spectral technique, were compared during the following four different body positions; 6 degrees head-down tilt (HDT), supine (Sup), 60 degrees head-up tilt (HUT) and upright (Upr). The sequence technique is based on the slope of linear regression between beat-to-beat RR intervals and systolic blood pressures. The cross-spectral technique is based on the cross-spectral analysis of RR interval and systolic blood pressure variabilities, and the estimates of BRS were computed separately for the low-frequency region (0.04-0.15 Hz) and the high-frequency region (0.15-0.5 Hz). The BRS obtained by the sequence technique had a significant correlation to that obtained by the cross-spectral technique for the low-frequency region in HDT, Sup and HUT, but not in Upr. There was a significant correlation between the BRS obtained by the sequence technique and that obtained by the cross-spectral technique for the high-frequency region in every body position. It became clear that the sequence technique is mutually related to the cross-spectral technique for the high-frequency region, but not necessarily identical to the cross-spectral technique for the low-frequency region. Moreover, a comparison was also made between the baroreceptor activating sequence and the deactivating sequence in the sequence technique during the four different body positions. Although the estimates of BRS of the activating sequence and the deactivating sequence were similar in every body position, the numbers of their sequences were progressively separated in the order of HDT, Sup, HUT and Upr. The numbers of the activating sequence and the deactivating sequence in the sequence technique were found to be separated in a sympathetically dominant condition.

Recently, heart rate spectral analysis has become recognized as a powerful tool for quantitatively evaluating autonomic nervous system activity. The purpose of this study was to analyze parasympathetic nervous activity by heart rate spectral analysis after administration of atropine and neostigmine for reversal of residual neuromuscular blockade. For our study, 36 female patients (26–37 years of age), ASA physical status (PS) I, who were scheduled for laparoscopic examination, were randomly allocated to one of the following four groups: In group A (1∶1), 9 patients received 1.0mg atropine followed 4 min later by 1.0 mg neostigmine. In group B (1∶2), 9 patients received 0.5 mg atropine followed 4 min later by 1.0 mg neostigmine. In group C (1∶2.5), 9 patients received 1.0 mg atropine followed 4 min later by 2.5 mg neostigmine. In group D (1∶2 mix), 9 patients received a mixed solution of atropine 0.5 mg and neostigmine 1.0mg. After finishing the laparoscopic examination, additional anesthesia was maintained with 70% nitrous oxide, 30% oxygen, and 0.5% isoflurane. The control data were obtained 10 min after finishing the laparoscopic examination. After that, the data on atropine were obtained between 2 and 4min after administration of atropine, and the data on neostigmine were obtained between 5 and 7 min after administration of neostigmine. We selected power spectral density of the high-frequency component (HF-p) in heart rate spectral analysis as an index to assess parasympathetic activity. In groups A, B, and C, the HF-p decreased after administration of atropine. In groups B and C, the HF-p increased after administration of neostigmine as compared to the control. In group A, the HF-p increased after neostigmine but did not differ from the control. The difference between groups D and B was not statistically significant. From the results of this study, we concluded that the muscarinic effect of neostigmine could not be sufficiently blocked by atropine at 1/2 dosages of neostigmine, but could be sufficiently blocked by atropine at equivalent dosages of neostigmine, under light isoflurane anesthesia.

The effects of nitrous oxide on the late reflex potential, a medullary component of somato-sympathetic reflex potentials, induced from the lumbar sympathetic trunk by electrical stimulation of the femoral nerve was investigated in brain intact cats and midbrain decerebrated cats under adequate anaesthesia with intravenous urethane and α-chloralose. The late reflex potential was depressed by inhalation of 75% nitrous oxide in oxygen in brain intact cats. Midbrain decerebration itself caused marked potentiation of the late reflex potential, although subsequent inhalation of 75% nitrous oxide did not cause any depressive effect on the potentiated late reflex potential. No significant changes in arterial pressure and heart rate were seen during the experiments. From these results, we concluded that anaesthetic concentrations of nitrous oxide might activate the descending inhibitory system from higher areas in the central nervous system.

Dear Editor, A 14-year-old girl reported severe pain of the left first toe after a sprain of the left ankle joint when she was 9 years old. She complained of continuous pain in her chest, back, abdomen, and left first toe. The pain at all the sites was of a burning type with intensity of 6 on the numerical rating pain scale. She was unable to walk due to pain. Mechanical allodynia was present. Redness and swelling were recognized over the left first toe. …

We evaluated vecuronium-induced neuromuscular block in both arms of a patient with cerebral palsy and hemiplegia. A remarkable resistance to vecuronium was observed in the hemiplegia side compared with cerebral palsy side. Complete recovery from neuromuscular block should be assessed in the cerebral palsy side that shows a delayed recovery.

Somato-sympathetic reflex discharges (SSRDs) which were induced from the lumbar sympathetic truck elicited by train pulse stimulation of femoral nerves in anesthetized cats were examined during and after intravenous infusion of 1 mg.kg(-1).min(-1) of procaine. The infusion demonstrated that amplitudes were suppressed with prolonged latencies and/or their tendencies in A- and C-reflex potentials of SSRDs. Heart rate and blood pressure decreased slightly, and the decreases correlated with time courses of suppressed SSRDs. These results suggest that the systemic procaine infusion may be a reliable method to alleviate somato-sympathetic reflexes under such conditions as extreme stimulation of somatic afferent nerves observed in surgical procedures.

We have frequently obtained good results with difficult pain using an improved acupuncture anesthesia method, cutaneous meridian stimulation, in which the patients himself can administer stimulation. However we have had a great variety of experience using these methods. There have even been cases in which therapy had no effect whatsoever. It has long been known that the effects of stimulation produced analgesia, (SPA) one form of acupuncture anesthesia, vary remarkably from person to person.In one hand it has been indicated that the pain-killing effects are related with the endogenous morphine-like substances however recently Takeshige and colleagues, believing that the individual differences in effect are based on the activity of the individual's amino peptidase, administered the peptidase interferrent, D-phenylalanine (DPA) and proved experimentally that so doing causing a change from ineffective to effective in SPA results.We studied the effects produced by DPA on the cutaneous pain threshold using transcutaneous nerve stimulation, by administering DPA in cases in which the pain threshold did not rise due to transcutaneous electric nerve stimulation alone. The subjects of the study were 9 healthy volunteers between the ages of 24-30 with no neurological diseases and 8 stubborn pain patients. The stimulation points were 2, right LI-4 and right LI-10. Stimulation was administered using a spike-type conductor rubber external electrode.Results1. Looking at changes in the pain threshold due to transcutaneous electric nerve stimulation only, it was observed that in 11 of 17 cases there was almost no change or slight fluctuation around the pain threshold.2. Upon administering 4g. DPA to the 6 cases in which the pain threshold did not change and administering transcutaneous electric nerve stimulation in the same manner as before, the threshold rose in 1 case.3. The serum concentration of phenylalanine increased 5 times that of pre-medication levels.

A hundred and twenty-four patients of herpes zoster who were treated by nerve blocks within one month after beginning of the disease were analyzed with the questionnaire and from their clinical charts.The results showed that (1). Slight to moderate pain remained in 21% of the 124 patients. (2). Pain recured in 16 cases who relieved their pain completely. (3). it is emphasized that nerve blocks have to be started quiclky as soon as possible after finding the disease, and the block should be continued till two weeks later than their pain relief. Some problems related the prognosis such as affected areas, character of pain and age of the patients were also discussed.

Fourteen patients whose post-herpetic neuralgia could not be alleviated by conventional methods were treated with cryocautery using a stick of solid carbon dioxide (dry ice) applied directly to the hyperesthetic skin areas of the cutaneous scars. Follow-up evaluation revealed that 5 of 14 subjects maintained excellent pain relief and another 5 subjects showed good relief. Ten subjects discontinued further therapeutic procedures after cryocautery even though some low grade pain persisted. We believe that cryocautery of localized skin areas is a valuable method for treating patients with post-herpetic neuralgia who have not been improved by conventional methods. Disadvantages of this procedure are discussed.