Retraction notice to "Recoveries of post-tetanic twitch and train-of-four responses after administration of vecuronium with different inhalation anaesthetics and neuroleptanaesthesia" [Br J Anaesth 1993; 70: 402-404].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief of British Journal of Anaesthesia. The study is retracted for the following reasons: Statistical analysis suggests that the data may be fabricated. Y Saitoh provided a statement in a personal communication to a member of the editorial board of British Journal of Anaesthesia that the study was not approved by the Institutional Review Board and that no evidence exists to support the study findings. Additionally, the Japanese Society of Anesthesiologists has recommended retraction of this article: http://www.anesth.or.jp/english/pdf/news20170925.pdf.

Retraction notice to "Relationship between post-tetanic twitch and single twitch response after administration of vecuronium" [Br J Anaesth 1993; 71: 443-444].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief of British Journal of Anaesthesia. The study is retracted for the following reasons: Y Saitoh provided a statement in a personal communication to a member of the editorial board of British Journal of Anaesthesia that the study was not approved by the Institutional Review Board and that no evidence exists to support the study findings.

Retraction notice to "Post-tetanic count and single twitch height at the onset of reflex movement after administration of vecuronium under different types of anaesthesia" [Br J Anaesth 1994; 72: 688-690].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief of British Journal of Anaesthesia. The study is retracted for the following reasons: Y Saitoh provided a statement in a personal communication to a member of the editorial board of British Journal of Anaesthesia that the study was not approved by the Institutional Review Board and that no evidence exists to support the study findings.

Retraction notice to "Effect of tetanic stimulation on subsequent train-of-four responses at various levels of vecuronium-induced neuromuscular block" [Br J Anaesth 1994; 73: 416-417].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief of British Journal of Anaesthesia. The study is retracted for the following reasons: Y Saitoh provided a statement in a personal communication to a member of the editorial board of British Journal of Anaesthesia that the study was not approved by the Institutional Review Board and that no evidence exists to support the study findings.

Retraction notice to "Post-tetanic burst: a new monitoring method for intense neuromuscular block" [Br J Anaesth 1995; 74: 293-295].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief of British Journal of Anaesthesia. The study is retracted for the following reasons: Statistical analysis suggests that the data may be fabricated. Y Saitoh provided a statement in a personal communication to a member of the editorial board of British Journal of Anaesthesia that the study was not approved by the Institutional Review Board and that no evidence exists to support the study findings.

Changes in respiratory physiological dead space and compliance during non-abdominal, upper abdominal and lower abdominal surgery under general anaesthesia.

BACKGROUND AND OBJECTIVE: To evaluate the temporal changes in respiratory physiological dead space and dynamic compliance of the respiratory system during non-abdominal, upper abdominal and lower abdominal surgery under general anaesthesia with intermittent positive pressure ventilation. METHODS: Thirty-four adult patients were studied (non-abdominal surgery, n = 8; upper abdominal surgery, n = 13 and lower abdominal surgery in lithotomy position, n = 13). Physiological dead space was measured using the single breath carbon dioxide test. The physiological dead space to tidal volume ratio (VD/VT), dynamic compliance of respiratory system, expiratory tidal volume and respiratory rate were measured 10 min after tracheal intubation, and 30, 60 and 120 min later. RESULTS: In lower abdominal surgery group, VD/VT was significantly increased at 120 min compared with 0 min (P = 0.005) and 30 min (P = 0.009). There were no significant differences in VD/VT between the three groups at any time point. Compliance decreased significantly in patients with upper abdominal (120 min) and lower abdominal surgery (60 and 120 min), but there were no significant changes during non-abdominal surgery. CONCLUSIONS: We found that the VD/VT increased in patients undergoing lower abdominal surgery in lithotomy and head down tilt, and compliance decreased in those undergoing upper abdominal and lower abdominal surgery over time.

Comparative effects of xenon and nitrous oxide on diaphragmatic contractility in dogs.

BACKGROUND: Xenon at two different concentrations (30%, 60%) has no effect on diaphragmatic contractility. This study was undertaken to compare the effects of xenon and nitrous oxide (N2O), a commonly used and well-established gas anesthetic, on diaphragmatic contractility in dogs. METHODS: Twenty-one pentobarbitone-anesthetized dogs were randomly divided into three groups of seven each: group 1 received xenon 30% (0.25 MAC) in oxygen; group 2 received N2O 47% (0.25 MAC) in oxygen; and group 3 received N2O 60% (0.32 MAC) in oxygen. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at low- (20-Hz) and high-frequency (100-Hz) stimulation, after maintaining 60 min of stable condition. The integrated electrical activity of diaphragm (Edi) to each stimulus was measured. RESULTS: With an inhalation of xenon 30%, N2O 47%, or N2O 60%, Pdi and Edi at both stimuli did not change. No difference in Pdi or Edi was observed among the groups. CONCLUSION: When used at clinical concentration, xenon or N2O does not affect contractility and electrical activity of the diaphragm in dogs.

Inhaled olprinone improves contractility of fatigued canine diaphragm.

BACKGROUND: Diaphragmatic fatigue is implicated as a cause of respiratory failure. This study was undertaken to evaluate the effects of inhaled olprinone, a newly developed phosphodiesterase III inhibitor, on the contractility of fatigued diaphragm in dogs. METHODS: Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz stimulation applied for 30 min. When fatigue was established, group I (n=8) received inhaled vehicle; group II (n=8) received inhaled olprinone 1 mg; group III (n=8) received inhaled olprinone 2 mg. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi, cm H2O). RESULTS: In the presence of fatigue, in each group, Pdi at low-frequency (20 Hz) stimulation decreased from baseline values (P<0.05), whereas Pdi at high-frequency (100 Hz) stimulation did not change. In groups II and III, during olprinone administration, Pdi at both stimuli increased from fatigued values (20 Hz stimulation: group II (mean (SD)) 10.8 (1.0) to 12.5 (1.3), group III 10.9 (1.7) to 15.0 (3.0); 100 Hz stimulation: group II 20.1 (1.9) to 22.6 (1.3), group III 20.6 (2.0) to 24.5 (2.0), P<0.05). The increase in Pdi was larger in group III than in group II (P<0.05). CONCLUSIONS: Inhaled olprinone produces a dose-dependent improvement in contractility of fatigued canine diaphragm.

Chromatographic determination of free lidocaine and its active metabolites in plasma from patients under epidural anesthesia.

OBJECTIVE: We developed a simple and selective assay method for simultaneous determination of free lidocaine (LDC) and its active metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX) in plasma, by using high-performance liquid chromatography (HPLC). The method was applied to the plasma concentration monitoring in continuous epidural anesthesia with LDC. MATERIALS AND METHODS: Free fraction was separated from plasma by using an ultrafiltration technique. Free and total LDC, MEGX and GX in plasma were analyzed by HPLC equipped with ordinary octadecylsilyl silica (ODS) column and ultraviolet (UV) detector. PATIENTS: Five male patients with cancer who received epidural injection of 1.5% LDC for 5 hours in elective thoracic surgery, were enrolled to determine the plasma levels of total and free LDC, MEGX and GX. RESULTS AND DISCUSSION: The calibration curve for free LDC, MEGX and GX were linear at the concentration of 25 to 1,000 ng ml(-1) (r = 0.9998 - 0.9999). The recoveries for LDC, MEGX and GX from plasma water were ranged 73.2-89.1%. The coefficient variations for intra- and inter-day assay for LDC, MEGX and GX were less than 4.1%. The detection limit ofeach drug was 20 ng ml(-1). Plasma-free MEGX after 180 min epidural injection was higher than free LDC, even though the total concentration of MEGX was 4 times lower than that of LDC. The percentages of free fraction for LDC, MEGX and GX were 11.7, 48.5 and 78.3% after 5-hour epidural administration of LDC. Since the free fraction of MEGX and GX increases and exceeds the concentration of free LDC during continuous epidural anesthesia, accumulation of these toxic metabolites should be carefully monitored as well as LDC. CONCLUSION: The present method is a reliable technique and can be applied to monitoring free LDC, MEGX and GX, which provide us beneficial information as to the LDC metabolism and toxicity.

Effect of intravenous prostaglandin E1 on pial vessel diameters and intracranial pressure in rabbits.

BACKGROUND: The main advantages of prostaglandin E1 (PGE1) for induced hypotension during neurosurgery include a rapid onset of action, a quick recovery from hypotension, lack of toxicity, maintenance of adequate perfusion to vital organs, and maintenance of cerebral blood flow reactivity to carbon dioxide during hypotension. However, there is no report that shows the effect of PGE1 on cerebral microvessel diameter and only a few data are available that show the effect of PGE1 on intracranial pressure. The aim of this study was to measure cerebral arteriole and venule diameters and intracranial pressure (ICP) during PGE1-induced hypotension to evaluate whether PGE1 is suitable for neuroanesthesia. METHODS: We measured the effects of 0.1, 0.3, 1.0, 3.0, and 10.0 microg x kg(-1) x min(-1) of intravenous PGE1 on mean arterial pressure (MAP), cerebral arteriole and venule diameters and ICP in anesthetized rabbits. RESULTS: MAP decreased statistically significantly from baseline at the infusion rates of 1.0, 3.0, and 10.0 microg x kg(-1) x ml(-1). Arteriole diameter increased significantly from the baseline at the infusion rate of 10.0 microg x kg(-1) x ml(-1) (18% from control). Venule diameter did not change from baseline value at any infusion rate. ICP did not change from baseline value at any infusion rate. CONCLUSION: We conclude that PGE1 might be a suitable drug for induced hypotension in neurosurgery from the viewpoint of its small effect on the cerebral microvessels and ICP.

Plasma lidocaine concentrations during continuous thoracic epidural anesthesia after clonidine premedication in children.

UNLABELLED: There is no report concerning oral clonidine's effects on epidural lidocaine in children. Therefore, we performed a study to assess the concentrations of plasma lidocaine and its major metabolite (monoethylglycinexylidide [MEGX]) in children receiving continuous thoracic epidural anesthesia after oral clonidine premedication. Ten pediatric patients, aged 1-9 yr, were randomly allocated to the Control or Clonidine 4 microg/kg group (n = 5 each). Anesthesia was induced and maintained with sevoflurane in oxygen and air (FIO2 40%). Epidural puncture and tubing were carefully performed at the Th11-12 intervertebral space. An initial dose of 1% lidocaine (5 mg/kg) was injected through a catheter into the epidural space, followed by 2.5 mg x kg(-1) x h(-1). Plasma concentrations of lidocaine and MEGX were measured at 15 min, 30 min, and every 60 min for 4 h after the initiation of continuous epidural injection. The concentrations of lidocaine and MEGX were measured using high-pressure liquid chromatography with ultraviolet detection. Hemodynamic variables were similar between members of the Control and Clonidine groups during anesthesia. The Clonidine group showed significantly smaller lidocaine concentrations (p < 0.05) and the concentration of MEGX tended to be smaller in the plasma of the Clonidine group for the initial 4 h after the initiation of epidural infusion. In conclusion, oral clonidine preanesthetic medication at a dose of 4 microg/kg decreases plasma lidocaine concentration in children. IMPLICATIONS: Oral clonidine decreases the plasma lidocaine concentration in children. Our finding may have clinical implications in patients receiving continuous epidural anesthesia. Additionally, perhaps an additional margin of safety regarding lidocaine toxicity is gained through the use of oral clonidine in children who will receive epidural lidocaine.

The dose-range effects of propofol on the contractility of fatigued diaphragm in dogs.

UNLABELLED: Diaphragmatic fatigue may contribute to the development of respiratory failure. We studied the dose-range effects of propofol on the contractility of fatigued diaphragm in dogs. Animals were divided into three groups of eight each. In each group, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz stimulation for 30 min. Immediately after the end of a fatigue-producing period, Group 1 received no study drug; Group 2 was infused with small-dose propofol (0.1 mg/kg initial dose plus 1.5 mg x kg(-1) x h(-1) maintenance dose); Group 3 was infused with large-dose propofol (0.1 mg/kg initial dose plus 6.0 mg x kg(-1) x h(-1) maintenance dose). We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). After the fatigue-producing period, in each group, Pdi at low-frequency (20-Hz) stimulation decreased from baseline values (P < 0.05), whereas there was no change in Pdi at high-frequency (100-Hz) stimulation. In Groups 2 and 3, with an infusion of propofol, Pdi at 20-Hz stimulation decreased from fatigued values (P < 0.05). Compared with Group 1, Pdi at 20-Hz stimulation decreased from fatigued values (P < 0.05) during propofol administration in Groups 2 and 3. The decrease in Pdi was more in Group 3 than in Group 2 (P < 0.05). We conclude that propofol decreases the contractility of fatigued canine diaphragm in a dose-related fashion. IMPLICATIONS: Propofol is a widely used IV anesthetic for the induction and maintenance of general anesthesia and sedation. It decreases, in a dose-related fashion, the contractility of fatigued diaphragm in dogs.

Midazolam versus propofol for reducing contractility of fatigued canine diaphragm.

The effects of midazolam and propofol on the contractility of fatigued canine diaphragm were examined. Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. After fatigue had been induced, group I (n=10) received no study drug, group II (n=10) was given a propofol infusion (0.1 mg kg(-1) loading dose plus 1.5 mg kg(-1) h(-1) maintenance dose) and group III (n=10) was given a midazolam infusion (0.1 mg kg(-1) loading dose plus 0.1 mg kg(-1) h(-1) maintenance dose). Diaphragmatic contractility was assessed by measuring transdiaphragmatic pressure (Pdi). After the fatigue-inducing period in each group, Pdi at low-frequency (20 Hz) stimulation was lower than the baseline values (P<0.05), whereas no change in Pdi at high-frequency (100 Hz) stimulation was observed. In group II, Pdi at 20 Hz stimulation was lower than fatigued values (P<0.05); Pdi at 100 Hz stimulation did not change. In group III, Pdi at both stimulation frequencies was lower than fatigued values (P<0.05). Compared with group I, Pdi at 20 Hz stimulation was lower than fatigued values (P<0.05) during administration of the study drug in groups II and III. The decrease in Pdi was greater in group III than in group II (P<0.05). In conclusion, midazolam compared with propofol is associated with an inhibitory effect on contractility in the fatigued canine diaphragm.

The formalin test: effects of formalin concentration and short-term halothane inhalation.

BACKGROUND AND OBJECTIVES: In order to evaluate the effects of formalin concentration and inhalational anesthetics in formalin tests, we injected 5 concentrations of formalin into awake and anesthetized rats and investigated their behavior and the c-fos immunoreactivity of their spinal cords. METHODS: Sixty adult male Sprague-Dawley rats were divided into 10 experimental groups. Each rat was either manually restrained or subdued through several minutes of 2% to 2.5% halothane inhalation, and then 1 of 5 concentrations of 0%, 5%, 10%, 27%, or 100% formalin (0%, 1.85%, 3.7%, 10%, or 37% formaldehyde solutions) was injected into its rear paw. Nociceptive behaviors were checked for 1 hour, 6 times for each 5-minute period. Two hours after the formalin injections, the rats were killed and c-fos immunoreactivity was measured. RESULTS: Typical responses were observed in the 5% and 10% formalin (1.85% and 3.7% formaldehyde) groups, and nociceptive behaviors were lower in the 27% and 100% formalin (10% and 37% formaldehyde) groups. The number of c-fos-positive cells increased as the formalin concentration increased. Halothane inhalation affected the results of both the behavior and the c-fos immunoreactivity, especially in the 10% formalin (3.7% formaldehyde) group. CONCLUSIONS: It is desirable to describe both formalin and formaldehyde concentrations simultaneously and to do formalin tests without inhalational anesthetics.

The residual effects of hemorrhagic shock on pain reaction and c-fos expression in rats.

UNLABELLED: To investigate the residual effects of hemorrhagic shock on pain reaction and c-fos expression, we performed formalin tests after hemorrhage and reinfusion in rats. Twenty adult male Sprague-Dawley rats were divided into Control (n = 10) and Postshock (n = 10) groups. The mean blood pressure of the Control group was 100-120 mm Hg, and that of the Postshock group was kept at 50-60 mm Hg for 30 min by draining blood. After 15 min of returning mean blood pressure to normal levels in the Postshock group, 10% formalin (3.7% formaldehyde solution, 100 microL) was injected into the left rear paw of both groups. Nociceptive behaviors were observed for 1 h after the formalin injection. The rats were killed at 2 h after the formalin injection, and the lumbar spinal cord was then stained for c-fos immunohistochemistry by using the avidin-biotin-peroxidase method. Animals in the Postshock group showed considerably less nociceptive behavior than those in the Control group. C-fos expression in the deep layer (IV-VI) of the spinal cord was significantly less in the Postshock group. In conclusion, decreases of nociceptive behaviors and c-fos expression were observed under normotensive conditions after hemorrhagic shock. The mechanisms governing these reactions remain unclear. IMPLICATIONS: Formalin tests were performed after hemorrhage and reinfusion in rats. A stress-induced analgesia was observed under normotensive conditions after hemorrhagic shock. The mechanisms remain unclear.

Repeated administration of protamine does not attenuate circulatory changes caused by protamine reversal of heparin in dogs.

OBJECTIVE: To determine whether repeated administration of protamine attenuates circulatory changes caused by protamine reversal of heparin and to evaluate the significance of nitric oxide generation. DESIGN: Prospective, randomized, controlled, animal study. SETTING: University research laboratory. PARTICIPANTS: Twenty-seven adult mongrel dogs. INTERVENTIONS: The animals were randomly assigned to 3 groups (n = 9 in each) according to the pretreatment. The control group was pretreated with normal saline, and the 2 other groups were given 2 different doses of protamine: protamine 0.1 (protamine, 0.1 mg/kg) and protamine 1.0 (protamine, 1.0 mg/kg). Under general anesthesia, all animals were anticoagulated with intravenous heparin, 200 IU/kg. Five minutes after heparin injection, preadministered saline (control) or protamine in saline was infused during 60 seconds. Five minutes after the pretreatment, protamine, 2.0 mg/kg in control, 1.9 mg/kg in protamine 0.1, or 1.0 mg/kg in protamine 1.0, was administered intravenously during 10 seconds. MEASUREMENTS AND MAIN RESULTS: Percent changes in mean arterial blood pressure among the 3 groups at each period were not significantly different except 60 minutes after protamine infusion. Mean pulmonary arterial pressure in the protamine 1.0 group at 5, 15, 20, and 60 minutes was higher than in the control group. Serum nitrate concentration was not significantly different among the 3 groups at baseline and 10 minutes after protamine injection. CONCLUSION: Repeated administration of protamine does not attenuate circulatory changes caused by protamine reversal of heparin in dogs. Nitric oxide generation does not appear to be responsible for the phenomenon.

Dose-response characteristics of midazolam for reducing diaphragmatic contractility.

A sedative dose of midazolam decreases contractility of the diaphragm, but no data are available concerning the relationship between dose and diaphragmatic contractility. We studied the dose-response characteristics of midazolam for reducing the diaphragmatic contractility in dogs. Animals were divided into three groups of eight each: Group 1 received no study drug, Group 2 was infused with a sedative dose of midazolam (0.1 mg/kg initial dose plus 0.1 mg x kg(-1) x h(-1) maintenance dose), and Group 3 was infused with an anesthetic dose of midazolam (0.1 mg/kg initial dose plus 0.5 mg x kg(-1) x h(-1) maintenance dose). We assessed the diaphragmatic contractility by transdiaphragmatic pressure (Pdi). With an infusion of midazolam in Groups 2 and 3, Pdi at low-frequency (20 Hz) and high-frequency (100 Hz) stimulation decreased from the baseline values (P < 0.05), and the integrated electrical activity of diaphragm (Edi) at 100-Hz stimulation decreased from the baseline values, whereas Edi at 20-Hz stimulation did not change. Compared with Group 1, Pdi and Edi for each stimulus decreased during midazolam infusion in Groups 2 and 3 (P < 0.05). The decrease in Pdi and Edi was more in Group 3 than in Group 2 (P < 0.05). We conclude that midazolam decreases, in a dose-dependent manner, contractility of the diaphragm in dogs.