Retraction Note to: Monitoring of vecuronium-induced neuromuscular block at the sternocleidomastoid muscle in anesthetized patients.

The Editor-in-Chief has retracted this article [1] because the three studies included in the meta-analysis [2,3 and 4] (cited as references 16, 17 and 18) have been retracted due to concerns regarding the data, which has rendered the results of this meta-analysis invalid.

Assessment of neuromuscular block at the orbicularis oris, corrugator supercilii, and adductor pollicis muscles.

PURPOSE: We studied neuromuscular block at the orbicularis oris, corrugator supercilii, and adductor pollicis muscles in anesthetized patients. METHODS: Fifty-four adult patients undergoing air-oxygen-sevoflurane-fentanyl and epidural anesthesia were randomly divided into orbicularis oris, corrugator supercilii, and adductor pollicis groups of 18 patients each. In the three groups, the degree of neuromuscular block caused by rocuronium 0.6 mg/kg was monitored at the orbicularis oris, corrugator supercilii, and adductor pollicis muscles acceleromyographically. RESULTS: Onset of neuromuscular block did not significantly differ among the three groups [157 ± 60, 186 ± 73, and 148 ± 45 s; mean ± standard deviation (SD)]. Minimum value of 1st stimulation in train-of-four (T1)/control at the corrugator supercilii group was significantly higher than in the orbicularis oris and adductor pollicis groups (0.108 ± 0.066 vs. 0.021 ± 0.024 and 0.002 ± 0.007; P < 0.001). T1/control at the orbicularis oris group was significantly higher than at the adductor pollicis group 30 min after rocuronium (P < 0.05). T1/control at the corrugator supercilii group was significantly higher than at the orbicularis oris and adductor pollicis groups 10-30 and 10-40 min, respectively, after rocuronium (P < 0.05). Train-of-four ratios at the orbicularis oris and corrugator supercilii groups were significantly higher than at the adductor pollicis group 40-120 min after rocuronium (P < 0.05). CONCLUSION: The corrugator supercilii muscle is more resistant to rocuronium than the orbicularis oris and adductor pollicis muscles. Recovery of neuromuscular block at the orbicularis oris muscle is slower than that at the corrugator supercilii muscle but was faster than that at the adductor pollicis muscle.

Blockade of 5-HT(2A) and/or 5-HT(2C) receptors modulates sevoflurane-induced immobility.

PURPOSE: Blockade of 5-hydroxytryptamine (5-HT)(2A) receptors reportedly mediates or modulates the ability of isoflurane to produce immobility during noxious stimulation and would thereby influence MAC (the minimum alveolar concentration required to suppress movement in response to noxious stimulation in 50% of subjects). However, no data are yet available regarding the role of this receptor in the immobilizing action of sevoflurane. In this study, we examined how prior intraperitoneal administration of either the 5-HT(2A) receptor antagonist altanserin or the 5-HT(2C/2B) receptor antagonist SB 206553 might affect sevoflurane MAC in rats. METHODS: Three groups of six male Wistar rats weighing 250-350 g each received one of the following drugs dissolved in dimethyl sulfoxide intraperitoneally 30 min before MAC testing: (1) altanserin 10 mg/kg; (2) SB 206553 10 mg/kg; (3) no drug (vehicle control). MAC was defined as the average of the concentrations that just prevented or just permitted movement in response to clamping the tail for 1 min. RESULTS: The rank order of MAC values obtained after intraperitoneal drug pretreatment and sevoflurane exposure was altanserin < SB 206553 < vehicle control. CONCLUSION: Considering the low levels of 5-HT(2B) receptors within the CNS, this result suggests that 5-HT(2A) and the 5-HT(2C) receptors are present within the neural circuitry influencing sevoflurane MAC. Blockade of 5-HT(2A) and/or 5-HT(2C) receptors may modulate the immobility produced by sevoflurane during noxious stimulation.

Monitoring of vecuronium-induced neuromuscular block at the sternocleidomastoid muscle in anesthetized patients.

PURPOSE: To assess the degree of neuromuscular block acceleromyographically at the sternocleidomastoid muscle. METHODS: Eighteen adult patients scheduled for air-oxygen-sevoflurane-fentanyl and epidural anesthesia were studied. In the patients, the right accessory nerve and the sternocleidomastoid muscle were stimulated and the contraction of the sternocleidomastoid muscle was evaluated acceleromyographically. Simultaneously, the response of the adductor pollicis muscle was measured electromyographically. Supramaximal stimulating current, degree of maximum neuromuscular block after vecuronium 0.1 mg/kg, and onset of or recovery from vecuronium-induced neuromuscular block were compared between the two muscles. RESULTS: The supramaximal stimulating current at the sternocleidomastoid muscle was significantly higher than that at the adductor pollicis muscle (54.8 ± 7.1 vs. 33.7 ± 10.3 mA, mean ± SD, P < 0.001). The onset of neuromuscular block at the sternocleidomastoid muscle did not significantly differ from that at the adductor pollicis muscle (214 ± 117 vs. 161 ± 87 s, P = 0.131). The degree of maximum neuromuscular block at the sternocleidomastoid muscle was significantly less than that at the adductor pollicis muscle (93.6 ± 3.1 vs. 99.2 ± 2.5%, P < 0.001). During recovery from neuromuscular block, T1/control and train-of-four ratio measured at the sternocleidomastoid muscle were significantly higher than those at the adductor pollicis muscle 10-30 and 40-120 min after vecuronium, respectively (P < 0.05). CONCLUSION: The sternocleidomastoid muscle is more resistant to vecuronium than the adductor pollicis muscle. Recovery from neuromuscular block is faster at the sternocleidomastoid muscle than at the adductor pollicis muscle.

Acceleromyographic monitoring of neuromuscular block over the orbicularis oris muscle in anesthetized patients receiving vecuronium.

STUDY OBJECTIVE: To evaluate the level of neuromuscular block acceleromyographically over the orbicularis oris muscle. DESIGN: Prospective, randomized, controlled study. SETTING: Operating room of a university-affiliated hospital. PATIENTS: 36 adult, ASA physical status I and II women scheduled for mastectomy with air-oxygen-isoflurane-fentanyl anesthesia. INTERVENTIONS: Patients were randomized to two groups. In the orbicularis oris group (n=18), the facial nerve was stimulated and movement of the orbicularis oris muscle was measured acceleromyographically. In the control group (n=18), adduction of the thumb was quantified mechanically. MEASUREMENTS: Onset and recovery of neuromuscular block caused by vecuronium 0.1 mg/kg were compared between the groups. MAIN RESULTS: Time to onset of neuromuscular block in the orbicularis oris group was significantly shorter than in the control group (176 + or - 52 vs. 220 + or - 34 sec, mean + or - SD; P = 0.004). Times to return of the first, second, third, or fourth (T1, T2, T3, or T4) response of train-of four (TOF), and recovery of T1/control were comparable between the groups. Train-of-four ratio (T4/T1) in the orbicularis oris group was significantly higher than in the control group 50 to 120 minutes after vecuronium administration (P < 0.05). CONCLUSION: Depth of neuromuscular block can be assessed acceleromyographically over the orbicularis oris muscle. Onset of neuromuscular block is quicker and recovery of TOF ratio is faster over the orbicularis oris muscle than at the thumb in patients receiving vecuronium.

Inhibitory effects of landiolol and nicardipine on thiopental-induced yawning in humans.

PURPOSE: Either the calcium (Ca(2+))-channel blocker nicardipine or the beta(1)-adrenoceptor antagonist landiolol may be intravenously (IV) administered to reduce the hemodynamic responses to tracheal intubation. In this study, we examined the effects of these drugs on the yawning response elicited by intravenous thiopental in humans. METHODS: After Institutional Review Board approval, 180 consenting American Society of Anesthesiologists (ASA) I or II patients undergoing elective surgery were recruited. In a double-blind, randomized design, three groups of 60 patients each received one of the following intravenous injections: (1) landiolol 0.1 mg/kg (L-group), (2) nicardipine 0.02 mg/kg (N-group), or (3) saline (S-group). In all patients, anesthesia was subsequently induced IV with 4 mg/kg thiopental. Thereafter, the occurrence of the yawning response (characterized by mouth opening) was continuously assessed as the only clinical endpoint for 1 min. Throughout the study, mean arterial blood pressure and heart rate were also recorded at 1-min intervals. RESULTS: The incidence of the yawning response was lower in both the L-group (6.7%) and the N-group (16.7%) than in the S-group (46.7%) (each, P < 0.01). CONCLUSIONS: Prior intravenous administration of either a Ca(2+)-channel blocker or a beta(1)-adrenoceptor antagonist can greatly reduce the thiopental-induced yawning response in humans.

Reversal of vecuronium with neostigmine: a comparison between male and female patients.

We investigated the differences between males and females in the reversal effect of neostigmine on neuromuscular blockade. Thirty male and 30 female patients undergoing elective general anesthesia were studied. Vecuronium was given in all patients anesthetized with nitrous oxide, oxygen, and sevoflurane. After the surgical procedure, when T1 (1st response in train-of-four (TOF))/control returned to 0.25, neostigmine 40 microg/kg in combination with atropine 20 microg/kg was given to antagonize residual neuromuscular blockade. Three, six, nine, 12, and 15 minutes after neostigmine reversal, T1/control or TOF ratio (T4/T1) did not significantly differ between the sexes. Also, 15 minutes after neostigmine administration, the number of patients in whom recovery from neuromuscular blockade was sufficient to guarantee good respiratory function, i.e., TOF ratio > 0.74, did not significantly differ between the sexes. In contrast, 15 minutes after neostigmine, the number of patients in whom recovery from neuromuscular blockade was adequate to ensure satisfactory recovery from neuromuscular blockade including the return of the faculty of sight, i.e., TOF ratio > 0.9, was significantly less in the males than in females (6 vs. 14, P = 0.028). In conclusion, 15 min after neostigmine, TOF ratio less often returns to a value of more than 0.9 in males than in females.

Monitoring of vecuronium-induced neuromuscular blockade during one-lung ventilation.

PURPOSE: We investigated the monitoring of neuromuscular blockade caused by vecuronium in patients receiving one-lung ventilation (OLV) anesthesia for lung surgery. METHODS: Eighteen adult patients requiring OLV for lung surgery (OLV group) and 18 undergoing two-lung ventilation (TLV) for colon surgery (control group) were enrolled in this study. In the two groups, anesthesia was maintained with sevoflurane, fentanyl, and epidural lidocaine. Time from vecuronium 0.1 mg.kg(-1) to the onset of neuromuscular blockade; times to the return of T1, T2, T3, or T4 (the first, second, third, or fourth response of the train-of-four [TOF]); and recovery of T1/control or TOF ratio (T4/T1) were compared between the two groups. RESULTS: Time to the onset of neuromuscular blockade in the OLV group was similar to that in the control group (289 +/- 74 vs 270 +/- 85 s [mean +/- SD]; P = 0.482). Times from vecuronium to the return of T1, T2, T3, or T4 in the OLV group did not significantly differ from those in the control group (21.9 +/- 7.0 vs 25.8 +/- 6.7 min for T1; P = 0.099). T1/control in the OLV group was significantly higher than that in the control group 50-120 min after vecuronium (P < 0.05). The TOF ratio did not differ significantly between the two groups. CONCLUSION: During OLV for lung surgery, recovery of T1/control is accelerated in anesthetized patients receiving vecuronium.

Recovery of neuromuscular blockade caused by vecuronium is delayed in patients with hypertriglyceridemia.

We investigated the effects of hypertriglyceridemia on the onset and recovery of neuromuscular blockade, induced by vecuronium, over the adductor pollicis muscle, electromyographically. Eighteen adult patients with hypertriglyceridemia (hypertriglyceridemia group) and 18 healthy patients with normal serum triglyceride (control group) were studied. The supramaximal stimulating current for train-of-four (TOF) in the hypertriglyceridemia group was significantly higher than that in the control group (45.7 +/- 16.7 vs 31.5 +/- 9.8 mA; mean +/- SD; P = 0.004). The onset of vecuronium 0.1 mg.kg(-1)-induced neuromuscular blockade in the hypertriglyceridemia group did not significantly differ from that in the control group (240 +/- 60 vs 279 +/- 88 s; P = 0.132). Times from vecuronium to the return of T1, T2, T3, and T4 in the hypertriglyceridemia group were significantly longer than those in the control group (31.4 +/- 6.2 vs 25.5 +/- 6.2 min for T1; P = 0.008). During recovery from neuromuscular blockade, T1/control did not differ between the two groups. However, the TOF ratios (T4/T1) in the hypertriglyceridemia group were significantly lower than those in the control group 80-120 min after vecuronium (P < 0.05). We conclude that, in patients with hypertriglycemidemia, a higher current is needed to elicit supramaximal response of the adductor pollicis muscle, and recovery from vecuronium-induced neuromuscular blockade is delayed.

Effects of olprinone on neuromuscular blockade caused by vecuronium.

We studied the effect of olprinone on neuromuscular blockade caused by vecuronium. Thirty women undergoing nitrous oxide-oxygen-isoflurane anesthesia were randomly divided into olprinone (n=15) or control group (n=15). In the olprinone group, the patients received an intravenous initial loading dose of olprinone at a rate of 2 microg/kg/minute for 5 minutes, followed by a continuous infusion of olprinone at 0.3 microg/kg/minute. In the control group, the patients received normal saline. Thirty minutes after the beginning of the infusion of olprinone or normal saline, vecuronium (0.1 mg/kg) was administered. The degree of neuromuscular blockade was monitored electromyographically at the adductor pollicis muscle. The time to the onset of neuromuscular blockade, and to the return of the first, second, third, or fourth response in train-of-four (TOF; T1, T2, T3, or T4, respectively), and the time course of recovery of T1/control did not differ significantly between the groups. After 50-70 minutes of vecuronium, the TOF ratio (T4/T1) in the olprinone group was significantly higher than in the control group. During this period, the mean TOF ratios in the control and olprinone groups were 0.15-0.39 and 0.40-0.57, respectively. In conclusion, olprinone accelerates the recovery of the TOF ratio, and the quickening effect of olprinone on the recovery of the TOF ratio may be apparent 50-70 minutes after vecuronium in anesthetized patients receiving vecuronium.

Recovery from vecuronium is delayed in patients with hypercholesterolemia.

PURPOSE: To examine the effects of hypercholesterolemia with respect to onset time and recovery from vecuronium-induced neuromuscular block. METHODS: A randomized controlled trial was undertaken in 20 adult patients with hypercholesterolemia (hypercholesterolemia group) and 20 healthy patients with normal serum cholesterolemia (control group). Following induction of anesthesia, vecuronium 0.1 mg.kg(-1) iv was administered. Onset of neuromuscular block and recovery times in the two groups were compared using supramaximal stimulation of the ulnar nerve. RESULTS: The supramaximal stimulating current in the hypercholesterolemia group was similar to that of the control group (38.1 +/- 15.5 vs 31.3 +/- 7.6 mA, P = 0.087). Onset of vecuronium-induced neuromuscular block (time to loss of response to T1) in the hypercholesterolemia group was similar to that observed in the control group (243 +/- 84 vs 249 +/- 56 sec, P = 0.792). Times from vecuronium administration to the return of T1 were also similar in the two groups (29.8 +/- 9.7 vs 25.3 +/- 6.8 min, P = 0.099). However, mean times for return of T2, T3, and T4 in the hypercholesterolemia group were longer than in the control group (44.5 +/- 14.4 vs 34.0 +/- 8.4 min for T2, P = 0.018). During recovery from neuromuscular block, T1/control and train-of-four ratio in the hypercholesterolemia group were less than in the control group, 90-120 min and 70-120 min after vecuronium, respectively (P < 0.05). CONCLUSION: Recovery from vecuronium-induced neuromuscular block is delayed in patients with hypercholesterolemia.

Drugs to facilitate recovery of neuromuscular blockade and muscle strength.

Several drugs that quicken recovery from neuromuscular blockade caused by vecuronium in anesthetized patients are reviewed. Ulinastatin, a protease inhibitor, is thought to promote the release of acetylcholine at the neuromuscular junction and increases hepatic blood flow and urine volume. For this reason, ulinastatin quickens recovery from neuromuscular blockade in anesthetized patients receiving vecuronium. Additionally, pretreatment with ulinastatin avoids prolongation of vecuronium-induced neuromuscular blockade in patients with hepatic cirrhosis. Gabexate mesilate is also a protease inhibitor. During a continuous infusion of gabexate mesilate, recovery from neuromuscular blockade was quickened. Amino acid-enriched solution supplies energy to the skeletal muscles and causes an increase in muscle strength. An infusion of amino acid-enriched solution hastens recovery from neuromuscular blockade in anesthetized patients. When amino acids supply energy to the skeletal muscles, they simultaneously produce heat in the skeletal muscles. This thermal generation may be closely related to fast recovery from neuromuscular blockade. Amino acid-enriched solution makes recovery from neuromuscular blockade quick and avoids hypothermia during general anesthesia. Milrinone, a phosphodiesterase III inhibitor, is supposed to increase the release of acetylcholine at the neuromuscular junction and make the neuromuscular junction sensitive to acetylcholine. Therefore, recovery from neuromuscular blockade is hastened. Nicorandil enhances membrane K+ conductance in skeletal muscle and increases contraction of the skeletal muscle. Thus, nicorandil quickens recovery from neuromuscular blockade.