UMLS:C0432222 - FACTA Search

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Query: UMLS:C0432222 (SEM)
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To determine whether the dose of atropine affects the rate of neostigmine-induced recovery from vecuronium-induced neuromuscular blockade, the authors monitored isometric adductor pollicis mechanical activity in 36 anesthetized (thiopental, fentanyl, nitrous oxide) adult patients (ASA physical status 1 or 2). Once surgery was completed and twitch height had spontaneously regained 25% of its initial value, the patients were randomly allocated into three groups (A10, A15, A20; n = 12 in each group) according to the dose of atropine (10, 15, or 20 micrograms/kg) that was mixed with 40 micrograms/kg neostigmine. Twitch height, train-of-four, and 50- and 100-Hz tetanic fade were recorded for 15 min after the administration of the reversal agents. No significant differences were found among the three groups in the final twitch height (95% +/- 2%), train-of-four (87% +/- 1%, 88% +/- 2%, 89% +/- 1%), and 50-Hz tetanic fade (90% +/- 1%, 94% +/- 1%, 93% +/- 1%) (mean +/- SEM). Fifteen minutes after reversal, fade in response to 100-Hz tetanus was statistically greater in the A10 group than in the two other groups (70% +/- 3% of control versus 84% +/- 4% and 81% +/- 2%) (mean +/- SEM, P less than 0.05). The present results demonstrate that larger doses of atropine facilitate neostigmine's reversal of vecuronium neuromuscular blockade. The clinical implications of the differences observed in this study remain to be determined.
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PMID:The influence of atropine dose on recovery from vecuronium-induced neuromuscular blockade. 809 86

The effects of increasing the extracellular K+ concentration on the capacity to generate action potentials and to contract were tested on unfatigued muscle fibers isolated from frog sartorius muscle. The goal of this study was to investigate further the role of K+ in muscle fatigue by testing whether an increased extracellular K+ concentration in unfatigued muscle fibers causes a decrease in force similar to the decrease observed during fatigue. Resting and action potentials were measured with conventional microelectrodes. Twitch and tetanic force was elicited by field stimulation. At pHo (extracellular pH) 7.8 and 3 mmol K+.L-1 (control), the mean resting potential was -86.6 +/- 1.7 mV (mean +/- SEM) and the mean overshoot of the action potential was 5.6 +/- 2.5 mV. An increased K+ concentration from 3 to 8.0 mmol.L-1 depolarized the sarcolemma to -72.2 +/- 1.4 mV, abolished the overshoot as the peak potential during an action potential was -12.0 +/- 3.9 mV, potentiated the twitch force by 48.0 +/- 5.7%, but did not affect the tetanic force (maximum force) and the ability to maintain a constant force during the plateau phase of a tetanus. An increase to 10 mmol K+.L-1 depolarized the sarcolemma to -70.1 +/- 1.7 mV and caused large decreases in twitch (31.6 +/- 26.1%) and tetanic (74.6 +/- 12.1%) force. Between 3 and 9 mmol K+.L-1, the effects of K+ at pHo 7.2 (a pHo mimicking the change in interstitial pH during fatigue) and 6.4 (a pHo known to inhibit force recovery following fatigue) on resting and action potentials as well as on the twitch and tetanic force were similar to those at pHo 7.8. Above 9 mmol K+.L-1 significant differences were found in the effect of K+ between pHo 7.8 and 7.2 or 6.4. In general, the decrease in peak action potential and twitch and tetanic force occurred at higher K+ concentrations as the pHo was more acidic. The results obtained in this study do not support the hypothesis that an accumulation of K+ at the surface of the sarcolemma is sufficiently large to suppress force development during fatigue. The possibility that the K+ concentration in the T tubules reaches the critical K+ concentration necessary to cause a failure of the excitation-contraction coupling mechanism is discussed.
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PMID:Effects of K+ on the twitch and tetanic contraction in the sartorius muscle of the frog, Rana pipiens. Implication for fatigue in vivo. 149 91

Subparalyzing doses of d-tubocurarine (dTC) given before succinylcholine decrease the duration of neuromuscular blockade. In animal preparations, they also abolish succinylcholine-induced twitch augmentation, defined as a greater-than-maximal contraction in response to a single stimulus. To determine quantitatively the effect of dTC on succinylcholine potency and on twitch augmentation in humans, 60 adult patients, ASA physical status I or II, were assigned randomly to receive either 0.05 mg/kg of dTC or saline 2 min before induction of anesthesia with fentanyl and thiopental. Train-of-four stimulation was applied every 12 s to the ulnar nerve and the force of contraction of the adductor pollicis muscle was measured. One minute after induction of anesthesia, 0.15, 0.20, 0.25, 0.35, or 0.50 mg/kg of succinylcholine was given. The height of the first twitch (T1) reached 121% +/- 6% (mean +/- SEM) of control without dTC, and was virtually abolished by dTC pretreatment (105% +/- 1%, P less than 0.01). Twitch augmentation was more noticeable with lower doses of succinylcholine, and was not observed in the response to the fourth stimulus of the train of four (T4). The potency of succinylcholine was decreased by approximately one-half in the dTC-pretreated groups. The ED50 was 0.27 +/- 0.04 mg/kg without dTC and 0.50 +/- 0.06 mg/kg with dTC (P less than 0.002). The corresponding values for ED90 were 0.51 +/- 0.07 and 1.02 +/- 0.12 mg/kg, respectively (P less than 0.02). The ED95 values were 0.63 +/- 0.09 and 1.28 +/- 0.15 mg/kg, respectively (P less than 0.02). The slopes of the regression lines did not deviate significantly from parallelism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of d-tubocurarine pretreatment on succinylcholine twitch augmentation and neuromuscular blockade. 236 29

We developed a two-compartment model to simulate neuromuscular function and heart rate following the administration of four nondepolarizing neuromuscular blocking agents (atracurium, vecuronium, pancuronium, and d-tubocurarine), three neuromuscular block reversal agents (edrophonium, neostigmine, and pyridostigmine), and two anticholinergic agents (atropine and glycopyrrolate). Twitch depression, train-of-four ratio, and heart rate were modeled during fentanyl, halothane, enflurane, or isoflurane anesthesia, optionally supplemented with nitrous oxide. Simulation results, compared with published values for each drug, fell within the clinical accuracy range (onset time 6.1 +/- 3.9% [mean +/- SEM]; duration, 1.7 +/- 3.5%, 50% effective dose, 0.5 +/- 5.7%; and 95% effective dose, 2.1 +/- 1.1%). The simulation graphically demonstrates the pharmacokinetics, pharmacodynamics, and interactions between neuromuscular blocking agents, reversal agents, and anticholinergic agents. During a simulation, the need for frequent monitoring and repeated delivery of a neuromuscular blocking agent to keep neuromuscular blockade stable becomes apparent, especially with the intermediate-acting neuromuscular blocking agents. When inhalational agents are given concomitantly, the task becomes even more difficult, since potentiation changes with anesthetic uptake. Recurarization, tachycardia, or bradycardia may be seen with the simulation if an improper drug regimen is followed. Concurrent simulation of two identical patients allows comparison of different modes of administration, choice of anesthetic agents, and drug doses.
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PMID:A simulation of neuromuscular function and heart rate during induction, maintenance, and reversal of neuromuscular blockade. 240 85

Thumb adductor twitch response to train-of-four (2 Hz for 2 seconds) stimulation of the ulnar nerve was used to assess the clinical characteristics of long-term neuromuscular blockade induced with continuous infusion of succinylcholine during balanced (N2O-O2-narcotic-thiopental) anesthesia. Twitch depression of 80 to 90% was maintained for 86 to 365 minutes by continuous infusion of succinylcholine at 86 +/- 5(SEM) micrograms/kg/min. Of 32 patients, 24 developed phase II block, defined as a train-of-four ratio of less than 50%. There was a large degree of individual variability in sensitivity to development of phase II block. This precluded defining a narrow dose range where transition from phase I to phase II occurred. Tachyphylaxis occurred in 25% of patients and was independent of the type of block. Neither dose nor duration of infusion was predictive of spontaneous recovery rate from phase II block. Of 24 patients who developed phase II block, 50% recovered spontaneously at a rate comparable to the recovery rate from a phase I block. The other 50% manifested prolonged recovery of neuromuscular function. After observing spontaneous recovery in these patients for 31 +/- 5(SEM) minutes, successful antagonism of residual phase II block with anticholinesterase agents was achieved.
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PMID:Clinical characteristics of long-term succinylcholine neuromuscular blockade during balanced anesthesia. 718 31

In 24 ASA I-II adults anaesthetized with thiopentone, fentanyl and nitrous oxide in oxygen, we studied neuromuscular transmission with isometric adductor pollicis monitoring. Patients received mivacurium 0.2 mg kg-1 followed by an infusion lasting at least 60 min and adjusted to maintain twitch height at 1-5%. After termination of the mivacurium infusion, when twitch height spontaneously regained 25% of its control value, the patients were allocated to two groups of 12 patients each. In group NEO patients received neostigmine 40 micrograms kg-1 and atropine 15 micrograms kg-1 and in group SPO neuromuscular transmission was allowed to recover spontaneously. Twitch height was measured every 10 s and train-of-four (TOF) (2 Hz) every 3 min. After 15 min, residual force after tetanic stimulation (50 and 100 Hz, 5-s duration (RF50HZ, RF100HZ), 1 min apart) were recorded sequentially. At 15 min, mean TOF ratio was greater in group NEO (0.94 (SEM 0.01)) than in group SPO (0.87 (0.02)) (P < 0.01). All patients in group NEO recovered to a TOF ratio greater than 0.7 after 6 min compared with 15 min in group SPO (P < 0.005). A TOF ratio greater than 0.9 was observed in all patients in group NEO compared with only six in group SPO (P < 0.025). Nevertheless, RF50HZ and RF100HZ did not differ significantly (0.92 (0.01) (group NEO), 0.91 (0.01) (group SPO) and 0.83 (0.02) (group NEO), 0.78 (0.03) (group SPO), respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of neostigmine-induced recovery with spontaneous recovery from mivacurium-induced neuromuscular block. 788 Jun 68

In order to study the neuromuscular interactions between suxamethonium and magnesium sulphate (MgSO4), we have determined the dose-response relationship of suxamethonium and the neuromuscular actions of 1.25 x ED50 dose of suxamethonium, both before and after pretreatment with MgSO4. We have also compared the effect of 1.25 x ED50 dose of suxamethonium in the absence and in the presence of 50% neuromuscular block, established previously by infusion of MgSO4. Twenty-one cats were anaesthetized with urethane. Train-of-four stimulation was applied every 12 s to the sciatic nerve and the force of contraction of the tibialis anterior muscle was measured. The potency of suxamethonium decreased in each instance with pretreatment with MgSO4. The ED50 of suxamethonium increased significantly from mean 21.0 (SEM 1.9) micrograms kg-1 before MgSO4 to 25.6 (2.3) micrograms kg-1 after MgSO4 60 mg kg-1 and to 26.6 (2.2) micrograms kg-1 after MgSO4 90 mg kg-1 (P < 0.05). Twitch depression produced by 1.25 x ED50 dose of suxamethonium decreased significantly with MgSO4 pretreatment, from 76.7 (2.6)% before MgSO4 to 61.7 (6.4)% after MgSO4 60 mg kg-1 and 48.7 (7.5)% after MgSO4 90 mg kg-1 (P < 0.05). With stable 50% neuromuscular block, established previously by infusion of MgSO4, the 1.25 x ED50 dose of suxamethonium produced more twitch augmentation (133 (6.3)% vs 108.3 (1.3)%; P < 0.05) and less twitch depression (31.6 (9.6)% vs 74.1 (0.6)%, P < 0.05) than in the absence of MgSO4. The results of all three methods demonstrated that the pharmacological interaction between suxamethonium and magnesium was antagonistic.
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PMID:Neuromuscular interactions between suxamethonium and magnesium sulphate in the cat. 802 15

Anesthesia was induced in 8 healthy llamas by administration of guaifenesin and ketamine, and was maintained with halothane in oxygen. On 2 separate experimental days, atracurium was given to induce 95 to 99% reduction of evoked hind limb digital extensor tension (twitch). For the first part of the study, atracurium was given IV as repeat boluses, with muscle twitch strength being allowed to return without intervention to 75% of baseline after each bolus before the subsequent bolus was given. A total of 5 bolus doses of atracurium was given. For the first bolus, 0.15 mg/kg of body weight IV, and for subsequent boluses, 0.08 mg/kg, induced desired relaxation. Onset of relaxation was slightly more rapid for repeat, compared with initial, bolus. Duration of relaxation and recovery time were similar to initial and repeat doses. Maximal twitch reduction was observed in 4 +/- 0.2 minutes (mean +/- SEM). Duration from maximal twitch reduction to 10% recovery was 6.3 +/- 0.4 minutes. Twitch recovery from 10 to 50% of baseline took 11.6 +/- 0.6 minutes. Twitch recovery from 10 to 75% recovery took 19.5 +/- 1.1 minutes. Recovery from 10% twitch to 50% fade took 12.8 +/- 0.5 minutes. Fade at 50% recovery of twitch was 39 +/- 0.02%. Significant (P < 0.05) animal-to-animal variation was observed in twitch recovery times. For the second part of the study, atracurium was initially given IV as a 0.15-mg/kg bolus, followed by infusion for 1 to 2 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuromuscular blockade by use of atracurium in anesthetized llamas. 849 48

Bundles of 10-100 fibers were dissected from the extensor digitorum longus muscle of mouse, mounted in an apparatus for optical recording, and stretched to long sarcomere length (> or = 3.6 microns). One fiber within the bundle was microinjected with furaptra, a fluorescent indicator that responds rapidly to changes in myoplasmic free [Ca2+] (delta [Ca2+]). Twitches and brief tetani were initiated by external stimulation. At myoplasmic furaptra concentrations of approximately 0.1 mM, the indicator's fluorescence signal during fiber activity (delta F/F) was well resolved. delta F/F was converted to delta [Ca2+] under the assumption that furaptra's myoplasmic dissociation constant for Ca2+ is 98 microM at 16 degrees C and 109 microM at 28 degrees C. At 16 degrees C, the peak amplitude of delta [Ca2+] during a twitch was 17.8 +/- 0.4 microM (+/-SEM; n = 8) and the half-width of delta [Ca2+] was 4.6 +/- 0.3 ms. At 28 degrees C, the peak and half-width values were 22.1 +/- 1.8 microM and 2.0 +/- 0.1 ms, respectively (n = 4). During a brief high-frequency tetanus, individual peaks of delta [Ca2+] were also well resolved and reached approximately the same amplitude that resulted from a single shock; the initial decays of delta [Ca2+] from peak slowed substantially during the tetanus. For a single twitch at 16 degrees C, the amplitude of delta [Ca2+] in fast-twitch fibers of mouse is not significantly different from that recently measured in fast-twitch fibers of frog (16.5 +/- 0.9 microM; Zhao, M., S. Hollingworth, and S.M. Baylor. 1996. Biophys. J. 70:896-916); in contrast, the half-width of delta [Ca2+] is surprisingly brief in mouse fibers, only about half that measured in frog (9.6 +/- 0.6 ms). The estimated peak rate at which Ca2+ is released from the sarcoplasmic reticulum in response to an action potential is also similar in mouse and frog, 140-150 microM/ms (16 degrees C).
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PMID:The amplitude and time course of the myoplasmic free [Ca2+] transient in fast-twitch fibers of mouse muscle. 892 69

The [Ca2+]i transient in heart is now thought to involve the recruitment and summation of discrete and independent "units" of Ca2+ release (Ca2+ "sparks") from the sarcoplasmic reticulum, each of which is controlled locally by single coassociated L-type Ca2+ channels ("local control theory of excitation-contraction coupling"). All prior studies on Ca2+ sparks, however, have been performed in single enzymatically dissociated heart cells under nonphysiological conditions. In order to understand the possible significance of Ca2+ sparks to normal working cardiac muscle, we used confocal microscopy to record Ca2+ sparks, spatially averaged [Ca2+]i transients and Ca2+ waves in individual cells of intact rat right ventricular trabeculae (composed of < 15 cells in cross section) microinjected with the Ca2+ indicator fluo 3 under physiological conditions ([Ca2+]o, 1 mmol/L; temperature, 33 +/- 1 degree C). Twitch force was recorded simultaneously. When stretched to optimal length (sarcomere length, 2.2 microns) and stimulated at 0.2 Hz, the trabeculae generated approximately equal to 700 micrograms of force per cell. Spatially averaged [Ca2+]i transients recorded from individual cells within a trabecula were similar to those recorded previously from single cells. The amplitude distribution of the peak ratio of Ca2+ sparks was bimodal, with maxima at ratios of 1.8 +/- 0.3 and 2.7 +/- 0.2 (mean +/- SD), respectively. The amplitude of the peak of Ca2+ sparks was approximately equal to 170 nmol/L. Ca2+ sparks occurred at a frequency of 12.0 +/- 0.8/s (mean +/- SEM) in line scans covering 94 sarcomeres. Ca2+ waves occurred randomly at a frequency of 0.57 +/- 0.08/s and propagated with a velocity of 29.5 +/- 1.7 microns/s. The extent of Ca2+ wave propagation was 3.9 +/- 0.3 sarcomere lengths (sarcomere length, 2.2 microns). Ca2+ sparks could be identified along the leading edge of the waves at intervals of 1.30 +/- 0.11 sarcomere length. Our observations suggest that (1) Ca2+ sparks, similar to those recorded in single cells, occur in trabeculae under physiological conditions and (2) coupling of Ca2+ spark generation between neighboring sites occurs and may lead to (3) the development of Ca2+ waves, which propagate under physiological conditions at a low velocity over limited distances. The results suggest that concepts of excitation-contraction coupling recently derived from isolated myocytes are applicable to intact cardiac trabeculae [corrected].
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PMID:Ca2+ 'sparks' and waves in intact ventricular muscle resolved by confocal imaging. 931 46

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