We were interested in determining the infusion rate of mivacurium required to maintain approximately 95% neuromuscular blockade during nitrous oxide-halothane (0.8% end-tidal or nitrous oxide-narcotic anesthesia. Neuromuscular blockade was monitored by recording the electromyographic activity (Datex NMT) of the adductor pollicis muscle resulting from supramaximal stimulation of the ulnar nerve at 2 Hz for 2 s at 10-s intervals. Mivacurium steady-state infusion requirements averaged 315 ± 26 μg·m−2·min−1 during nitrous oxide-halothane anesthesia arid 375 ± 19 μg·m−2·min−1 (mean ± sem) during nitrous oxide-narcotic anesthesia. Higher levels of pseudocholinesterase activity were generally associated with a higher mivacurium infusion requirement. During both anesthetics, younger age was associated with a higher infusion requirement when the infusion requirement was calculated in terms of μg·kg−1·min−1. This difference was not present when the infusion rate was calculated in terms of μg·m−2·min−1. There was no evidence of cumulation during prolonged mivacurium infusion. There was no difference in the rates of spontaneous or reversal-mediated recovery between anesthetic groups. After the termination of the infusion, spontaneous recovery to T4/T1 ≥ 0.75 occurred in 9.8 ± 0.4 min, with a recovery index, T25–75, of 4.0 ± 0.2 min (mean ± sem). In summary, pseudocholinesterase activity is the major factor influencing mivacurium infusion rate in children during nitrous oxide-narcotic or nitrous oxide-halothane (0.8% end-tidal) anesthesia.
1. Hyperpolarization following single and repetitive excitation of dorsal spinocerebellar tract (DSCT) neurones of the cat was studied by intracellular recording.2. Hyperpolarization following an antidromic action potential consisted of an initial, brief phase (undershoot) and a late, prolonged phase. The latter hyperpolarization was independent of the membrane potential, whereas the former was reversed in polarity by hyperpolarizing pulses applied across the DSCT cell membrane.3. DSCT neurones showed a prolonged hyperpolarization after a train of antidromic action potentials. The amplitude and duration of the hyperpolarization were dependent on the number and the frequency of action potentials. A similar hyperpolarization was observed following a train of impulses evoked by depolarizing pulses applied through the intracellular electrode.4. There was no detectable conductance change during the post-tetanic hyperpolarization. The latter showed no reversal potential when the membrane potential was altered.5. The half-decay time of the post-tetanic hyperpolarization was lengthened when the cord temperature was lowered. The temperature coefficient (Q(10)) was 2.4 within the range of 31-40 degrees C.6. The amplitude of the undershoot following each action potential was assumed to provide a criterion for the accumulation of the extracellular K(+). Alterations in the amplitude of undershoots during repetitive excitation suggested that the duration of post-tetanic hyperpolarization depends on the accumulation of extracellular K(+) as well as of intracellular Na(+) associated with a train of impulses.7. It is suggested that post-tetanic hyperpolarization is produced by an electrogenic sodium pump. A possible significance of such a hyperpolarization in impulse coding is discussed.
Recent studies suggest that the number of nerve terminals maintained per motoneuron and perhaps other motoneuron properties (Grinnell and Herrera, 1980a; Grinnell and Trussell, 1983) influence transmitter release. We have examined, in detail, the structure and function of motoneurons innervating two different twitch muscles, the sartorius and the ext. long. dig. IV (e.l.d.) in the adult frog using histochemical and electrophysiological techniques. These studies were undertaken with a view towards learning whether differences in the number of nerve terminals per motoneuron were correlated with differences in transmitter release between motoneurons innervating these two muscles. Moreover, these studies provide detailed, quantitative data that are a necessary prerequisite for carrying out additional studies to examine the possible influence of muscle on transmitter release properties. In low Ca2+-high Mg2+ Ringer's solution, mean quantal content (m) and miniature end-plate potential (MEPP) frequency were larger at sartorius than at e.l.d. end-plates. The mean length of nerve terminals was also found to be greater in sartorius than in e.l.d. muscles. When release was normalized for the difference in terminal length, m remained larger in the sartorius, whereas MEPP frequency in the two muscles was similar. Cell bodies of individual sartorius motoneurons were greater in cross-sectional area and maintained approximately 5.6-fold greater aggregate length of nerve terminals per motoneuron than did e.l.d. motoneurons. This greater aggregate length of nerve terminal contact with their respective target muscles is primarily a result of a greater number of nerve terminals supported by sartorius than by e.l.d. motoneurons.(ABSTRACT TRUNCATED AT 250 WORDS)
1. Descending tracts and primary afferent fibres were chronically degenerated in the lumbosacral cord of the cat, and attempts were made to evoke monosynaptic e.p.s.p.s in motoneurones by stimulation of interneurones with a pair of fine electrodes inserted into the cord.2. The reversal potential of monosynaptic e.p.s.p.s so produced was more negative than that measured for monosynaptic e.p.s.p.s produced by afferent impulses.3. Monosynaptic e.p.s.p.s evoked in motoneurones by internuncial impulses showed a significantly greater facilitation than those produced by afferent impulses.4. Monosynaptic e.p.s.p.s in a motoneurone produced by supramaximal intraspinal stimuli often revealed a fluctuation in amplitude. In such cases, when two successive stimuli were applied at a short interval, the mean amplitude of the second e.p.s.p.s was greater than that of the first e.p.s.p.s. This facilitation was associated with a decrease in the coefficient of variation of the e.p.s.p. amplitude fluctuation.5. The degree of facilitation of monosynaptic e.p.s.p.s evoked by internuncial impulses was not related to the amount of transmitter released by the preceding impulses.6. It is concluded that facilitation of monosynaptic e.p.s.p.s evoked by both afferent and internuncial impulses is based on the same mechanism and that the degree of facilitation of e.p.s.p.s is entirely determined by the nature of presynaptic elements.
1. Monosynaptic i.p.s.p.s were produced in spinal motoneurones of the cat by stimulation of a pool of interneurones following chronic degeneration of descending tracts and primary afferent fibres in the lumbosacral cord.2. Monosynaptic i.p.s.p.s so evoked by supramaximal stimuli often showed a fluctuation in amplitude with occasional failures of response.3. When two successive stimuli were applied at a short interval, the mean amplitude of the second i.p.s.p.s was greater than that of the first. This facilitation was associated with a decrease in the number of failures, a decrease in the coefficient of variation of the amplitude distribution and an increase in the probability of occurrences of large i.p.s.p.s.4. A statistical analysis of the i.p.s.p. amplitude fluctuation showed that the monosynaptic i.p.s.p. is composed of discrete unit potentials evoked with a certain probability in a manner described by a binomial law.5. The application of strychnine decreased the mean amplitude of i.p.s.p.s with little change in the coefficient of variation of the i.p.s.p. amplitude distribution.6. It is concluded that the release of inhibitory transmitter occurs in quantal steps and that strychnine blocks primarily the post-synaptic receptors for the inhibitory transmitter.
