Role of central nervous system monoamines in cardiopulmonary effects of Althesin in rabbit and man

Quail, Anthony W.; White, Saxon William; Traugott, F. M.; Moore, P. G.

doi:10.1016/0165-1838(85)90058-x

Cited by 2 publications

(5 citation statements)

References 24 publications

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“…During anaesthesia with alphaxalone‐based anaesthetics reductions in hind limb conductance and mean arterial pressure (Quail et al , 1985), modification of baroreceptor reflexes (Blake & Korner, 1981), Valsalva‐heart rate reflexes (Blake et al , 1982) and of sympathetic responses evoked by cerebellar stimulation (Paton & Gilbey, 1992) have been observed. The plasma concentration of alphaxalone during anaesthesia is in the range 2–12 μ m (Sear & Prys‐Roberts, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…Saffan is likely also to affect other central neurones involved in autonomic control which could facilitate or oppose its effects on SPNs. Changes in hind limb conductance and arterial pressure occurring during Saffan anaesthesia have been localized to central sympathetic sites and appear to require the presence of noradrenergic and 5‐hydroxytryptaminergic neurones (Quail et al , 1985), both of which synapse onto SPNs (Chiba & Masuko, 1986; Bacon & Smith, 1988). Further experiments in vivo would be required to show exactly which neurones are affected during anaesthesia.…”

Section: Discussionmentioning

confidence: 99%

“…Changes in the functioning of the autonomic nervous system often accompany general anaesthesia. Such changes include modification of basal sympathetic discharge and of sympathetic reflexes (Blake & Korner, 1981; Kollai & Koizumi, 1981; Quail et al , 1985; Paton & Gilbey, 1992). In order to understand how these changes occur it is important to determine the actions of anaesthetics on individual neurones.…”

Section: Introductionmentioning

confidence: 99%

“…Alphaxalone‐based anaesthetics have the advantage of a high therapeutic index, short action and quick recovery (Davis & Pearce, 1972). However, they have undesirable autonomic effects, including a rise in heart rate (Kollai & Koizumi, 1981), dose‐dependent changes in mean arterial pressure (Quail et al , 1985) and modification of autonomic reflexes (Paton & Gilbey, 1992). A number of these effects have been suggested to result from actions within CNS regions involved in sympathetic regulation (Quail et al , 1985).…”

Section: Introductionmentioning

confidence: 99%

“…However, they have undesirable autonomic effects, including a rise in heart rate (Kollai & Koizumi, 1981), dose‐dependent changes in mean arterial pressure (Quail et al , 1985) and modification of autonomic reflexes (Paton & Gilbey, 1992). A number of these effects have been suggested to result from actions within CNS regions involved in sympathetic regulation (Quail et al , 1985). Alphaxalone acts at GABA A receptors in vivo at similar concentrations to which it occurs in vivo during anaesthesia with Saffan (reviewed in Lambert et al , 1987).…”

Section: Introductionmentioning

confidence: 99%

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Actions of the anaesthetic Saffan on rat sympathetic preganglionic neurones in vitro

Nolan

Gıbson

Logan

1997

British J Pharmacology

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2ZD1 Whole-cell patch-clamp recordings were used to investigate the e ects of the anaesthetic Sa an on the electrophysiological properties of sympathetic preganglionic neurones (SPNs) in rat spinal cord slices. 2 Sa an (1 ± 54 mM) abolished or reduced the frequency of spontaneous action potential ®ring and abolished spontaneous, sub-threshold membrane potential oscillations. Sa an caused dose-dependent decreases in input resistance and depending upon the initial resting membrane potential, either a depolarization, a hyperpolarization or no change in membrane potential. 3 Responses to Sa an were blocked by the GABA A receptor antagonists bicuculline (5 ± 20 mM) and picrotoxin (20 mM), but not by the glycine receptor antagonist strychnine (20 mM) indicating that they were mediated by GABA A receptors. 4 Changes in the properties of SPN action potentials were also observed. In the presence of Sa an the amplitude and duration of the action potential after-hyperpolarization were reduced and larger depolarizations were required in order to evoke trains of action potentials. 5 To examine the e ects of Sa an on electrotonic coupling between SPNs, experiments were performed with the Na + channel blocker QX-314 in the intracellular solution and antidromic oscillations were evoked by ventral root stimulation. Sa an failed to abolish antidromic oscillations, but reduced their amplitude and duration. This indicates that the abolition of spontaneous membrane potential oscillations was not a direct e ect on the coupling between SPNs, but was a result of the abolition of spontaneous activity by Sa an. 6 The responses to Sa an occurred within the plasma concentration range of Sa an during anaesthesia, suggesting that the electrophysiological properties of SPNs may be altered during anaesthesia with Sa an. This would be expected to lead to changes in sympathetic tone and in the integration of sympathetic output.

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