Comparison of anesthetic effects of epidural and intravenous administration of buprenorphine during operation

Thirty six patients were received epidural anesthesia with or without buprenorphine (BPN) during upper abdominal surgery. They were divided into three groups of 12 patients as follows; G-I received 20ml of 1% lidocaine epidurally, G-II received 20ml of 1% lidocaine epidurally and 0.6mg BPN intravenously, G-III received 20ml of 1% lidocaine with 0.6mg BPN epidurally. Additional 5ml of 1% lidocaine was given to any patient if systolic blood pressure or heart rate increased 10% compared to control value. Trachea was intubated following anesthetic induction with thiopental. The lungs were ventilated with a mixture of N₂O/O₂ (33%) and pancuronium was used for muscle relaxation. The total required doses of lidocaine in G-II and G-III were decreased 60% compared to control group (G-I) (P 0.05). The mean period of time until the first administration of pentazocine for postoperative pain was 13 ± 10hr (mean ± SD) in G-II and 19 ± 24hr in G-III compared to 5 ± 4hr in G-I (P 0.001). The dose of the administration of pentazocine that was required for pain relief during the first 48 postoperative hr in G-III was 54 ± 10mg (mean ± SD) compared to 150 ± 21mg in G-I (P 0.02) and 106 ± 28mg in G-II (P 0.05). Recovery from anesthesia in G-III was more rapid than that in G-I (P 0.05). The Pa_{CO 2} values in G-II and G-III increased 15% compared to control group at about 4hr and 8hr after administration of BPN, but any clinical treatment was not needed for them. Nonrespiratory side effects, e.g., nausea, vomiting, fatigue and headache, were comparably common in all groups. Mild hematuria associated with acute hypotension occurred in two patients in G-II (17%) immediately after the intravenous injection of 0.6mg of BPN. The results showed that 0.6mg of BPN given epidurally demonstrated better anesthetic and more potent postoperative analgesic effects and lesser side effects than 0.6mg of BPN given intravenously in patients undergoing upper abdominal surgery.(Yonemura E, Fukushima K.: Comparison of anesthetic effects of epidural and intravenous administration of buprenorphine during operation. J Anesth 4: 242–248, 1990)     

Comparative inotropic effects of local anesthetics in isolated cat papillary muscles

The direct inotropic action of seven local anesthetics: procaine, mapivacaine, lidocaine, tetracaine, chloroprocaine, bupivacaine and etidocaine were compared in isolated cat papillary muscles. All of the local anesthetics produced a dose-related depression of maximal velocity of shortening (Vmax), maximal developed force (Fm) and maximal dF/dt. The more potent local anesthetics such as bupivacaine and etidocaine depressed myocardial contractility at significantly lower concentrations than the less potent local anesthetics such as lidocaine and mepivacaine. Depression of Vmax by bupivacaine or etidocaine was three times greater than that by lidocaine and ten times greater than that by procaine. At the same concentration (10^–4M), direct myocardial depression was demonstrated in the following order of severity: etidocaine bupivacaine tetracaine chloroprocaine lidocaine mepivacaine procaine.(Kemmotsu O, Nakata F, Ueda M, et al.: Comparative inotropic effects of local anesthetics in isolated cat papillary muscles. J Anesth 4: 1–8, 1990)     

Enhancement of lidocaine-induced epidural anesthesia by deoxyaconitine in the rabbit

Purpose.Aconiti tuber has been used in traditional Oriental medicine to alleviate pain. The antinociceptive property of aconiti tuber is due to the action of its extracted alkaloids such as deoxyaconitine. The purpose of this study was to investigate the effect of epidural deoxyaconitine on epidural lidocaine anesthesia. Methods.Five adult rabbits were used. Three different combinations of drugs were injected into the epidural space, in the following order: first (combination A), 1.5ml of 2% lidocaine; second (combination B), 1.5ml of 2% lidocaine and 150µg deoxyaconitine; and third (combination C), 3mg nor-binaltorphimine followed by 1.5ml of 2% lidocaine and 150µg deoxyaconitine 30min later. The latency of onset and the duration of three end-points (sensory loss in the tail, loss of weight-bearing ability, and flaccid paresis of hind limb) were measured. Results.Onset times for the three end-points were not changed by deoxyaconitine or by nor-binaltorphimine. The duration of sensory loss was 27.0 ± 2.7min, the duration of loss of weight-bearing ability was 33.0 ± 2.7min, and the duration of flaccid paresis was 21.0 ± 4.2min in the combination A group. In the combination B group, deoxyaconitine extended the time of sensory loss by 80%, the time of loss of weight-bearing by 50%, and that of flaccid paresis by 60% compared with the combination A group. In the combination C group, this phenomenon was partially antagonized by pretreatment with nor-binaltorphimine, a -opioid antagonist. Conclusions.Based on our observations, deoxyaconitine enhanced epidural lidocaine anesthesia in the rabbit, and this effect seemed to be partly mediated by -opioid receptors.     

Propofol inhibits lidocaine metabolism in human and rat liver microsomes

Purpose.When two drugs are metabolized by similar P450 isoforms, one drug inhibits the metabolism of the other when both the present. The metabolism of lidocaine and propofol can be mediated by similar P450 isoforms. Therefore, we investigated the relationship in the metabolism between lidocaine and propofol in both rat and human liver microsomal P450 (CYP) systems in vitro. Methods.(1) Propofol, 4µg·ml^–1, as the substrate and lidocaine (between 0.5 and 8µg·ml^–1) and (2) lidocaine, 4.7µg·ml^–1, as the substrate and propofol (between 0.5 and 40µg·ml^–1) were reacted separately with human and rat microsomes. The concentrations of lidocaine, its major metabolite (monoethylglycinexylidide, MEGX) and propofol were measured using high-pressure liquid chromatography. The metabolism of lidocaine was presented as a reaction activity (MEGX/lidocaine). Results.The dose-dependent inhibitory effects of propofol on lidocaine metabolism were observed in both the human and rat groups. The IC50 (the concentration producing 50% maximal inhibition) of propofol was 5.0µg·ml^–1 and 0.70µg·ml^–1 in the human and the rat groups, respectively. The propofol concentration of 5.0µg·ml^–1 is within the range of clinical doses for humans. On the other hand, lidocaine did not change propofol metabolism. Conclusion.Propofol possesses a dose-dependent inhibitory effect on the metabolism of lidocaine in both human and rat CYP systems in vitro.     

Percutaneous and Open Renal Revascularizations Have Equivalent Long-Term Functional Outcomes

Atherosclerotic renal artery stenosis is a significant cause of poorly controlled hypertension and progressive renal dysfunction leading to ischemic nephropathy and other end-organ damage. The optimal treatment of renovascular disease contributing to hypertension and renal dysfunction is not known. This study compares the anatomic and functional outcomes of both open and endovascular therapy for chronic, symptomatic atherosclerotic renal artery disease. We performed a retrospective analysis of records from patients who underwent renal arterial interventions, endovascular or open bypass, between January 1984 and January 2004. Principal indications for intervention were hypertension (51%), chronic renal insufficiency (13%), and hypertension and elevated creatinine (36%). A total of 247 patients (109 males; mean age 69±10, range 44–89 years) underwent 314 interventions (109 open procedures; 205 angioplasties, 71% with stent placement). There was a significant difference in 30-day mortality (4% vs. <1%; p < 0.005) between the open and endoluminal groups, but not at 1, 3, or 5 years. Patients in the open group had a higher primary patency rate at 5 years (83±5% vs. 76±6%; p=0.03), but patients in the endoluminal group had a higher assisted primary patency rate at 5 years (92±5% vs. 84±5; p=0.03). There was no significant difference between both treatment groups in cumulative freedom from presenting symptom or in freedom from dialysis and renal-related death. Patients who presented with hypertension were more likely to have shown improvement in their blood pressure with endoluminal intervention at 1, 3, and 5 (59±6% endoluminal vs. 83±5% open; p=0.01) years. From these results we conclude that open repair and endoluminal repair of atherosclerotic renal artery stenosis have similar immediate and long-term functional and anatomic outcomes. Patients who present with hypertension may have greater benefit with an endoluminal repair.Presented at the Twenty-ninth Annual Meeting of the Peripheral Vascular Surgery Society, Anaheim, CA, June 4-5, 2004.     

Preadministration of low-dose ketamine reduces tourniquet pain in healthy volunteers

We evaluated whether preadministration of low-dose ketamine could attenuate tourniquet pain and arterial pressure increase using high tourniquet pressure in ten healthy awake volunteers. Ketamine, 0.1mg·kg^–1, or normal saline was given intravenously in a double-blind fashion before tourniquet inflation with a pressure of 400mmHg at the thigh. Visual analog scale (VAS) scores and systolic blood pressure (SBP) were measured at 5-min intervals. Ketamine significantly reduced VAS scores compared to saline just after tourniquet inflation [90 (64–100) mm, median (range), with saline versus 66 (50–81) mm with ketamine, P < 0.01] and at 30min [92 (61–100) mm with saline versus 70 (50–100) mm with ketamine, P < 0.03), and significantly prolonged tourniquet time (28 ± 6min with saline, mean ± SD, versus 37 ± 7min with ketamine, P < 0.01). SBP (120 ± 9mmHg) significantly increased before tourniquet deflation (133 ± 16mmHg) in the saline trial, but not in the ketamine trial. The results show that preadministration of low-dose ketamine attenuates tourniquet pain and arterial pressure increase during high-pressure tourniquet application and prolongs tourniquet time in healthy volunteers.     

The effects of sevoflurane on lidocaine-induced convulsions

The influence of sevoflurane on lidocaine-induced convulsions was studied in cats. The convulsive threshold (mean ± SD) was 41.4 ± 6.5mg·l ^–1 with lidocaine infusion (6mg·kg^–1·min^–1), increasing significantly to 66.6 ± 10.9mg·l ^–1 when the end-tidal concentration of sevoflurane was 0.8%. However, the threshold (61.6 ± 8.7mg·l ^–1) during 1.6% sevoflurane was not significant from that during 0.8% sevoflurane, indicating a celling effect. There was no significant difference in the convulsive threshold between sevoflurane and enflurane. The rise in blood pressure became less marked when higher concentrations of sevoflurane or enflurane were administered and the blood pressure at convulsions decreased significantly in 1.6% sevoflurane, and in 0.8% and 1.6% enflurane. However, there was no significant difference in the lidocaine concentrations measured when the systolic blood pressure became 70mmHg. Apamin, a selective blocker of calcium-dependent potassium channels, was administered intracerebroventricularly in rats anesthetized with 0.8% sevoflurane to investigate the mechanism of the anticonvulsive effects. Apamin (10ng) had a tendency to decrease the convulsive threshold (21.6 ± 2.2 to 19.9 ± 2.5mg·l ^–1) but this was not statistically significant. It is suggested that sevoflurane reduces the convulsive effect of lidocaine toxicity but carries some risk due to circulatory depression.(Karasawa F: The effects of sevoflurane on lidocaine-induced convulsions. J Anesth 5: 60–67, 1991)     

Inhaled Nitric Oxide Therapy After Fontan-Type Operations

Purpose Inhaled nitric oxide (NO) therapy is a newly developed strategy designed to reduce pulmonary vascular resistance after the Fontan-type operation. We reviewed our experience to evaluate its efficacy and true indications.Methods We retrospectively examined 47 children who received inhaled NO therapy after the Fontan-type operation between August 1996 and December 2002. The maximal dose of NO ranged from 5 to 30ppm (median 10ppm), and the duration of inhaled NO therapy ranged from 5h to 52 days (median 2 days).Results Inhaled NO significantly decreased the central venous pressure (CVP), from 16.2 ± 2.2 to 14.6 ± 2.2mmHg (P < 0.0001), and the transpulmonary pressure gradient between the CVP and left atrial pressure, from 9.9 ± 2.9 to 8.4 ± 2.7mmHg (P < 0.0001). It also increased the systolic systemic arterial pressure from 71.9 ± 15.2 to 76.8 ± 14.5mmHg (P < 0.05). In 26 patients with additional fenestration, inhaled NO led to a significant improvement in SaO₂ from 90.1% ± 9.6% to 93.3% ± 7.9% (P < 0.01). However, patients with a CVP <15mmHg or a transpulmonary pressure gradient <8mmHg, or both, after the Fontan-type operation, showed no significant changes in hemodynamics during inhaled NO therapy.Conclusions We propose that a CVP 15mmHg or a transpulmonary pressure gradient 8mmHg, or both, after Fontan-type operations are appropriate indications for inhaled NO therapy.     

Cyclic alteration in the anticonvulsant effect of nitrous oxide in rats

The anticonvulsant action of nitrous oxide and its time course were studied in rats. Bicuculline, a GABA-receptor antagonist, was administered intravenously at a rate of 0.2mg·kg^–1·min^–1 during exposure to air (n = 60) or 75% nitrous oxide in oxygen (n = 80). The convulsant dose of bicuculline was determined. The rats were divided into subgroups according to the duration of exposure to air or nitrous oxide, from 0 to 120min at 15min intervals. Although the convulsant dose of bicuculline was consistent in the air group (1.03 ± 0.06mg·kg^–1, mean ± SEM), it showed two peaks at 30- and 90min exposures to nitrous oxide. The threshold dose in the nitrous oxide group was significantly higher than in the air group at only 15- and 30min exposures (1.50 ± 0.16, 2.15 ± 0.25mg·kg^–1, respectively, P 0.05). We conclude that nitrous oxide has an anticonvulsant action against bicuculline-induced seizure, and that a cyclic nature exists in its action.(Shingu K, Osawa M, Mori K: Cyclic alteration in the anticonvulsant effect of nitrous oxide in rats. J Anesth 4: 309–312, 1990)     

Changes of local brain tissue oxygen pressure after vasopressin during spontaneous circulation

Summary. Background. Brain tissue oxygen pressure (PbtO₂) correlates to cerebral blood flow (CBF) during spontaneous circulation, with one important regulator being nitric oxide (NO). Although it is established that arginine vasopressin (AVP) improves CBF and global cerebral oxygenation during cardiopulmonary resuscitation, it is unknown whether similar beneficial effects are present during spontaneous circulation. The purpose of this study was to investigate the effects of AVP with and without pre-treatment with the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) on local brain tissue oxygenation in a beating heart model.Methods. Following approval of the Animal Investigational Committee, nine healthy piglets underwent general anaesthesia, and were instrumented with a probe in the cerebral cortex to measure PbtO₂. Each animal was assigned to receive AVP (0.4U·kg^–1), and after a wash-out period, L-NAME (25mg·kg^–1 over 20min) followed by AVP (0.4U·kg^–1). After each AVP administration, nitroglycerine (25µg·kg^–1 over 1min) as a NO donor was infused to test the vascular reactivity independently from NOS inhibition.Findings. Three minutes after administration of AVP, PbtO₂ increased significantly (P<.05; mean±SEM, 31±11 versus 43±14mmHg, +39%), compared with baseline. After pre-treatment with L-NAME, the changes of PbtO₂ after AVP were not significant (32±11 versus 28±10, –13%) when compared with the baseline.Conclusion. In this beating heart porcine model, local brain tissue oxygenation was improved after AVP alone, but not after inhibition of NO synthesis with L-NAME.     

Efficacy of landiolol in attenuating hemodynamic responses to local epinephrine infiltration in patients undergoing vaginal total hysterectomy

Purpose Local epinephrine infiltration often causes ₁-adrenoceptor-mediated tachycardia, hypertension, and arrhythmia. Landiolol, a short acting ₁-adrenoceptor blocker, may represent the most ideal agent to attenuate these adverse effects. In this study, we examined the effects of landiolol on the hemodynamic changes resulting from local infiltration of epinephrine.Methods Thirty-six patients undergoing vaginal total hysterectomy under general anesthesia were randomly assigned to one of three groups: control group (n = 12), L5 group (n = 12), and L10 group (n = 12). In the control, L5, and L10 groups, the patients were given saline, landiolol 5mg, and 10mg, respectively, just before infiltration of epinephrine(1:300000; total dose, about 100µg) into the surgical field. Blood pressure and heart rate was assessed before and 5, 10, 15, 20, 25, 30min after the initiation of epinephrine infiltration. If systolic blood pressure and heart rate exceeded 160mmHg and 120 beats·min^–1, respectively, Ca blockers of either diltiazem 5mg or nicardipine 1mg and/or 2% sevoflurane were given.Results Epinephrine infiltration significantly increased systolic blood pressure from 122 ± 15 to 170 ± 29mmHg and heart rate from 63 ± 8 to 106 ± 10 beats·min^–1. In both the L5 and L10 groups, the increase in heart rate (from 69 ± 16 to 87 ± 16 beats·min^–1, P < 0.01, and from 70 ± 18 to 76 ± 9 beats·min^–1, P < 0.01, respectively) was significantly smaller compared to the control group, but the increase in systolic blood pressure was significantly attenuated in the L10 group (from 116 ± 18 to 140 ± 27mmHg, P < 0.01). The number of patients given either Ca blockers or sevoflurane in the control group was significantly higher than that in the landiolol groups (P < 0.01).Conclusion The present study suggests that landiolol 10mg may be a more suitable dose than landiolol 5mg to antagonize hyperdynamic states induced by local administration of epinephrine.     

Neuromuscular effects of pipecuronium during sevoflurane anesthesia compared with isoflurane and enflurane anesthesia

We evaluated the neuromuscular effects of pipecuronium during anesthesia with equipotent concentrations of either sevoflurane, isoflurane or enflurane.Twenty-seven patients scheduled for minor elective otolaryngeal or plastic surgery were studied and randomly assigned to 3 groups, one group per anesthetic agent. Anesthesia was induced with thiamylal 5mg·kg^–1 and the trachea was intubated with succinylcholine 1mg·kg^–1, then anesthesia was maintained with 60% nitrous oxide in oxygen and sevolfurane, isoflurane or enflurane, depending on the group. Neuromuscular blocking effects were monitored by recording the electromyographic activity of the adductor pollicis muscle from supramaximal stimulation of the ulnar nerve at 10-s intervals. Pipecuronium 40µg·kg^–1 was administered when electromyographic activity had reached a stable state, 30min after succinylcholine administration. The maximum effect (% block of control) and clinical duration (time to 25% recovery) of pipecuronium were 99.1 ± 1.4% and 63.7 ± 14.7min (mean ± S.D.) for sevoflurane, 99.0 ± 2.0% and 60.9 ± 20.5min for isoflurane, and 98.0 ± 2.5% and 62.8 ± 28.7min for enflurane, respectively. There were no significant differences in these values between the anesthetics. Cardiovascular stimulant effects were not observed in any of the groups.We conclude that the effect of pipecuronium under seveflurane anesthesia is similar to that under isoflurane and enflurane anesthesia.(Nakao Y, Ohno M, Imai M, et al.: Neuromuscular effects of pipecuronium during sevoflurane anesthesia compared with isoflurane and enflurane anesthesia. J Anesth 7: 405--410, 1993)     

Elevation of the extracellular glutamate concentration in the hippocampus after total cerebral ischemia related to the deterioration of the recovery in EEG and evoked potentials in dogs

The concentrations of extracellular glutamate (Glu), aspartate (Asp) and glycine (Gly) were measured by microdialysis method in the cortex and hippocampus before, during and after 15min of total cerebral ischemia in dogs. The correlations between the concentrations of amino acids and the changes in EEG and evoked potentials (EP) after ischemia were evaluated. Total cerebral ischemia was achieved by occluding the ascending aorta and the caval veins. The concentrations of Glu in the hippocampus significantly increased from 1.73 ± 0.59 (mean ± SEM) nmol·ml^–1 at pre-ischemia to 5.46 ± 1.34 (P 0.05) during ischemia and 14.37 ± 3.70 (P 0.01) 0–15min after ischemia, and returned to the pre-ischemic level 30min after ischemia. The concentration of hippocampal Glu 0–15min after ischemia had significant negative correlations with the EEG-EP scores (0 = serious deterioration of electrical function and 6 = normal electrical function) 30min, 3hr and 5hr after ischemia (r = –0.69, P 0.05:r = –0.67, P 0.05:r = –0.70, P 0.05, respectively). The increase of the extracellular Glu concentration in the hippocampus immediately after ischemia may aggravate the neurological outcome after total cerebral ischemia.(Ono K, Iwatsuki N, Tajima T, et al.: Elevation of the extracellular glutamate concentration in the hippocampus after total cerebral ischemia related to the deterioration of the recovery in EEG and evoked potentials in dogs. J Anesth 7: 334–340, 1993)     

Plasma concentration for optimal sedation and total body clearance of propofol in patients after esophagectomy

The present study investigated plasma propofol concentration for optimal sedation and total body clearance in patients who required sedation for mechanical ventilation after esophagectomy. Seven patients after esophagectomy were enrolled in this study. Plasma propofol concentrations were measured with high performance liquid chromatography. Total body clearance was calculated from the steady-state concentration. The infusion rate of propofol for achieving the sedation score of level 3 (drowsy, responds to verbal stimulation) was 1.74 ± 0.82mgkg^–1h^–1 (mean ± SD, n = 7) when the plasma propofol concentration and the total body clearance were 0.85 ± 0.24µgml^–1 and 1.83 ± 0.54lmin^–1 (mean ± SD, n =7), respectively.     

The effects of calcium antagonists on EEG,evoked potentials and neurologic recovery after complete global brain ischemia for 15 minutes in dogs

The effects of three calcium antagonists on the recovery from neurologic damages after complete global brain ischemia were examined by evaluating the change of a electroencephalogram (EEG), evoked potentials (EP) and a neurologic recovery score (NRS) in dogs. Fifteen minutes global brain ischemia was achieved by occluding the ascending aorta and the caval veins. Nicardipine (NC), flunarizine (FL) and diltiazem (DL) were administered with continuous infusions for three days after the ischemia. The EEG-EP scores (0:no response – 6:normal) 3hr after the ischemia were 1.4 ± 0.4 (mean ± SE) in the control, 2.2 ± 0.3 in the NC, 2.2 ± 0.4 in the FL and 2.1 ± 0.2 in the DL. There were no significant differences between the 4 groups. The survival rates on the 7th day after the ischemia were 67% (6/9) in the control, 78% (7/9) in the NC, 56% (5/9) in the FL and 89% (8/9) in the DL. No significant differences were presented between the 4 groups. The NRSs (0:death – 100:normal) on the 7th day were 40.3 ± 7.3 in the control, 59.0 ± 8.5 in the NC, 63.2 ± 9.7 in the FL and 55.7 ± 3.3 in the DL. Each treated group showed a tendency to have a higher NRS than that in the untreated control group. The NRS in all dogs treated by the Ca⁺⁺ antagonists on the 7th day was 58.7 ± 4.1, which was significantly higher than that in the control group (P < 0.05). We conclude that the continuous administration of calcium antagonists for three days after the global brain ischemia would be beneficial for the neurologic recovery.(Ono K, Iwatsuki N, Takahashi M, et al.: The effect of calcium antagonists on EEG, evoked potentials and neurologic recovery after complete global brain ischemia for 15 minutes in dogs. J Anesth 5: 114–122, 1991)     

Seasonal changes of serum 25-hydroxyvitamin D and intact parathyroid hormone levels in a normal Japanese population

We conducted an observational study in order to assess the prevalence of hypovitaminosis D and its seasonal changes, in the Tokai area (N35.3 E137.0), in 197 normal subjects in Japan. The mean serum 25-hydroxyvitamin D (25-OHD) level measured by direct radioimmunoassay (RIA) was lowest at the end of winter, and highest at the end of summer (15.1 ± 7.1ng/ml in March; 21.5 ± 5.5ng/ml in June; 31.6 ± 5.6ng/ml in September; 23.1 ± 5.3ng/ml in December; mean ± SD). The prevalence of hypovitaminosis D (<20ng/ml) was 86.7%, 33.4%, 1.0%, and 26.0% in March, June, September, and December, respectively. Mean plasma intact parathyroid hormone (iPTH) concentration was lowest at the end of summer and highest at the end of winter (28.2 ± 9.3pg/ml in March; 21.7 ± 7.0pg/ml in June; 19.8 ± 6.9pg/ml in September; and 25.7 ± 9.2pg/ml in December; mean ± SD). Serum 25-OHD was inversely associated with iPTH (coefficient, –0.223; r = 0.251; P < 0.001). Serum 25-OHD levels were higher in men than in women. The serum 25-OHD level was positively associated with age, body weight, and body mass index, but not with body fat content. These results suggest a high prevalence of hypovitaminosis D associated with elevation of iPTH in Japan, in winter, even in a sunny area.     

Single sodium channels from human skeletal muscle in planar lipid bilayers: characterization and response to pentobarbital

Purpose To investigate the response to general anesthetics of different sodium-channel subtypes, we examined the effects of pentobarbital, a close thiopental analogue, on single sodium channels from human skeletal muscle and compared them to existing data from human brain and human ventricular muscle channels.Methods Sodium channels from a preparation of human skeletal muscle were incorporated into planar lipid bilayers, and the steady-state behavior of single sodium channels and their response to pentobarbital was examined in the presence of batrachotoxin, a sodium-channel activator. Single-channel currents were recorded before and after the addition of pentobarbital (0.34–1.34mM).Results In symmetrical 500mM NaCl, human skeletal muscle sodium channels had an averaged single-channel conductance of 21.0 ± 0.6pS, and the channel fractional open time was 0.96 ± 0.04. The activation midpoint potential was –96.2 ± 1.6mV. Extracellular tetrodotoxin blocked the channel with a half-maximal concentration (k_1/2) of 60nM at 0mV. Pentobarbital reduced the time-averaged conductance of single skeletal muscle sodium channels in a concentration-dependent manner (inhibitory concentration 50% [IC₅₀] = 0.66mM). The steady-state activation was shifted to more hyperpolarized potentials (–16.7mV at 0.67mM pentobarbital).Conclusion In the planar lipid bilayer system, skeletal muscle sodium channels have some electrophysiological properties that are significantly different compared with those of sodium channels from cardiac or from central nervous tissue. In contrast to the control data, these different human sodium channel subtypes showed the same qualitative and quantitative response to the general anesthetic pentobarbital. The implication of these effects for overall anesthesia will depend on the role the individual channels play within their neuronal networks, but suppression of both central nervous system and peripheral sodium channels may add to general anesthetic effects.     

Effects of intravenous or endotracheal lidocaine on circulatory changes during Recovery from general anesthesia

Intravenous lidocaine (1.5mg·kg^–1) was not effective in attenuating the circulatory changes and the cough reflex induced by airway stimulation during recovery from general anesthesia, whereas endotracheal 4% lidocaine (3ml) was effective. The arterial concentration of the intravenously administered-lidocaine peaked at a level of 9.52 ± 0.81µg·ml^–1 0.5min later. The arterial concentration of the endotracheally administered-lidocaine peaked at 1.44 ± 0.13µg·ml^–1 15min later. These findings indicate that the endotracheal administration of lidocaine may be superior to the intravenous administration for attenuating the circulatory changes and the cough reflex during recovery from general anesthesia, and that the arterial concentration of lidocaine did not correlate with the clinical efficacy for this purpose.(Okuda M, Furuhashi K, Konishi K et al.: Effects of intravenous or endotracheal lidocaine on circulatory changes during recovery from general anesthesia. J Anesth 4: 331–336, 1990)     

Bench test assessment of the new Raumedic Neurovent-P ICP sensor: a technical report by the BrainIT group

Summary. Background. In clinical practice, fiberberoptic and piezo-electric ICP probes are often used for measuring intracranial pressure (ICP). A number of similar technologies, although performing well in bench test studies, have been shown to exhibit unacceptable zero drift, fragility or both during trials conducted under clinical conditions. Recently, a new technology has become available, the Neurovent-P (Raumedic AG+CO, Raumedic, Germany). As a pre-requisite for a clinical trial, we have conducted and report on bench test studies to confirm the manufacturers long term zero-drift performance for this technology.Method. In a test rig static tests (recording of 20mmHg pressure) and dynamic tests, ranging from 5 to 50mmHg have been performed.Findings. 10 ICP probes have been tested for a total of 60 days. All the catheters, after the connection with the ICU monitor displayed a static pressure of 0±1mmHg and did not required pre-insertion alteration. At five days, mean zero drift was 0.6±0.9mmHg. Overall, zero drift ranged from 0 to 2mmHg. At a fixed static pressure of 20mmHg, the mean recorded value was 20.6±0.8mmHg, ranging from 19 to 23mmHg. A regression analysis of the relationship between the applied pressure and the recorded pressure during the dynamic tests of the 10 catheters yielded a correlation coefficient R² of 0.997. Applying the Altman and Bland method to assess the bias and confidence limits for the Raumedic catheter responses during the dynamic tests against the applied gold-standard hydrostatic column pressures, the average bias of –0.66±0.85mmHg, with 95% CLs of –2mmHg and 1mmHg.Conclusions. Mean zero drift, after five days, was very small and long-term continuous recording of a stable pressure was very precise. The response at dynamic tests, i.e. the changes of pressure in a wide range, was excellent. The average bias of the Raumedic catheter compared with the hydrostatic column is very small. After this bench test, the next and most critical step will be to conduct a trial of this promising technology under more demanding clinical environment.     

Timing of injection and plasma concentration of lidocaine before endotracheal intubation

The optimal time of intravenous lidocaine for attenuation of pressor responses to laryngoscopy and endotracheal intubation was evaluated in fifty adult patients and the correlation between plasma lidocaine level and its clinical effects were also studied.The plasma lidocaine levels were highest 0.5min after administration of lidocaine 1.5mg·kg^–1 intravenously. However, endotracheal intubation 0.5min after lidocaine administration caused significant increase in mean arterial pressure (MAP) and heart rate (HR). Mean arterial pressure and HR increased with endotracheal intubation following 1, 2 and 3min after lidocaine administration, but the magnitude of increase was not statistically significant. There were no significant differences in MAP changes among these three groups. It was concluded that the plasma lidocaine levels did not correlate with its suppressive effect on circulatory responses due to laryngoscopy and endotracheal intubation. Laryngoscopy and endotracheal intubation should be carried out at least 1min after intravenous lidocaine administration.(Okuda M, Ohi Y, Kurata M et al.: Timing of injection and plasma concentration of lidocaine before endotracheal intubation. J Anesth 4: 150–154, 1990)