A system for the application of general anaesthetics and other volatile agents to superfused, isolated tissue preparations

Girdlestone, D.; Cruickshank, S; Winlow, William

doi:10.1016/0742-8413(89)90198-9

Cited by 7 publications

(11 citation statements)

References 7 publications

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“…To prepare semi-intact preparations, animals were first anaesthetized by bubbling 2% halothane into pond water as described by Girdlestone et al (1989). Snails were assumed to be anaesthetized when they either dropped to the bottom of the chamber or exhibited no withdrawal response when stimulated with a glass rod.…”

Section: The Semi-intact Preparationmentioning

confidence: 99%

Respiratory behavior in the pond snail Lymnaea stagnalis

1991

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This study describes the neural basis of respiratory behavior in a pulmonate mollusc, Lymnaea stagnalis. We describe and identify muscles of the respiratory orifice (pneumostome) and mantle cavity as well as relevant motor neurons innervating these muscles. All of these identified motor neurons are active during spontaneously occurring respiratory behavior and a sporadically occurring synaptic input, termed Input 3, controls the activities of these motor neurons. This spontaneous input can also be recorded from isolated brain preparations, suggesting that the respiratory motor program is generated centrally. However, evidence is also presented that in semi-intact preparations the role of peripheral feedback is important for the initiation and termination of respiratory behavior in Lymnaea.

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Section: The Semi-intact Preparationmentioning

confidence: 99%

Respiratory behavior in the pond snail Lymnaea stagnalis

1991

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“…31 In most experiments, halothane was introduced into the above solution as described by Girdlestone, Cruickshank and Winlow. 32 Briefly, the salt solution was bubbled with a vapour stream containing 2% halothane until the concentration of halothane had reached equilibrium (generally 15-20 min). The final concentration of halothane in the salt solution was measured by gas liquid chromatography.…”

Section: Solutionsmentioning

confidence: 99%

Mechanisms underlying the inotropic action of halothane on intact rat ventricular myocytes

Harrison

Robinson

Davies

et al. 1999

British Journal of Anaesthesia

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The mechanisms contributing to the negative inotropic effect of halothane were studied in isolated rate ventricular myocytes. Contraction and intracellular Ca2+ transients were measured optically in these cells. The initial application of halothane (2% or 0.5 mmol litre-1) led to short-lived increases in the Ca2+ transient and contraction, which were abolished by ryanodine. Continued application of halothane led to a sustained decrease in contraction: this resulted from: (i) a decrease in myofilament Ca2+ sensitivity; (ii) a decrease in the Ca2+ transient; and (iii) a decrease in the Ca2+ content of the sarcoplasmic reticulum. Although halothane reduced action potential duration, the sustained negative inotropic effect was similar when action potentials or voltage clamp pulses of constant duration were used to trigger contractions. In cells exposed to nifedipine 0.5 mumol litre-1 (which decreases the L-type Ca2+ current, ICa), Ca2+ transients, sarcoplasmic reticulum Ca2+ content and fractional release (the fraction of sarcoplasmic reticulum Ca2+ content released during each stimulus) were reduced. Halothane 0.5 mmol litre-1 (which also decreases ICa) decreased Ca2+ transients to a lesser extent and reduced sarcoplasmic reticulum Ca2+ content to a greater extent than nifedipine, whereas fractional release was unchanged compared with control. These data suggest that halothane sensitizes Ca(2+)-induced Ca2+ release from the sarcoplasmic reticulum in addition to reducing ICa.

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“…Sevoflurane (Maruishi Pharmaceutical, Japan) was vaporized in 100% O 2 using a sevoflurane Type-s MK III-VII (Acoma) vaporizer and bubbled for at least 15 min into the reservoirs containing Lymnaea saline (see Girdlestone et al 1989a). To minimize gas loss over time, all anesthetic solutions were prepared fresh in sealed glass reservoirs.…”

Section: Gas Chromatographymentioning

confidence: 99%

Sevoflurane Induced Suppression of Inhibitory Synaptic Transmission Between Soma-Soma PairedLymnaeaNeurons

Hamakawa

Feng

Grigoriv

et al. 1999

Journal of Neurophysiology

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The cellular and synaptic mechanisms by which general anesthetics affect cell-cell communications in the nervous system remain poorly defined. In this study, we sought to determine how clinically relevant concentrations of sevoflurane affected inhibitory synaptic transmission between identified Lymnaea neurons in vitro. Inhibitory synapses were reconstructed in cell culture, between the somata of two functionally well-characterized neurons, right pedal dorsal 1 (RPeD1, the giant dopaminergic neuron) and visceral dorsal 4 (VD4). Clinically relevant concentrations of sevoflurane (1-4%) were tested for their effects on synaptic transmission and the intrinsic membrane properties of soma-soma paired cells. RPeD1- induced inhibitory postsynaptic potentials (IPSPs) in VD4 were completely and reversibly blocked by sevoflurane (4%). Sevoflurane also suppressed action potentials in both RPeD1 and VD4 cells. To determine whether the anesthetic-induced synaptic depression involved postsynaptic transmitter receptors, dopamine was pressure applied to VD4, either in the presence or absence of sevoflurane. Dopamine (10(-]5) M) activated a voltage-insensitive K(+) current in VD4. The same K(+) current was also altered by sevoflurane; however, the effects of two compounds were nonadditive. Because transmitter release from RPeD1 requires Ca(2+) influx through voltage-gated Ca(2+) channels, we next tested whether the anesthetic-induced synaptic depression involved these channels. Individually isolated RPeD1 somata were whole cell voltage clamped, and Ca(2+) currents were analyzed in control and various anesthetic conditions. Clinically relevant concentrations of sevoflurane did not significantly affect voltage-activated Ca(2+) channels in RPeD1. Taken together, this study provides the first direct evidence that sevoflurane-induced synaptic depression involves both pre- and postsynaptic ion channels.

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A system for the application of general anaesthetics and other volatile agents to superfused, isolated tissue preparations

Cited by 7 publications

References 7 publications

Respiratory behavior in the pond snail Lymnaea stagnalis

Respiratory behavior in the pond snail Lymnaea stagnalis

Mechanisms underlying the inotropic action of halothane on intact rat ventricular myocytes

Sevoflurane Induced Suppression of Inhibitory Synaptic Transmission Between Soma-Soma PairedLymnaeaNeurons

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