Stable inhibition of brain synaptic plasma membrane calcium ATPpase in rats anesthetized with halothane

J. J. Franks, J. L. Horn, Piotr Janicki, G. Singh

Research output: Contribution to journalArticle

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Abstract

Background: The authors recently showed that plasma membrane Ca2+- ATPase (PMCA) activity in cerebral synaptic plasma membrane (SPM) is diminished in a dose-related fashion during exposure in vitro to halothane, isoflurane, xenon, and nitrous oxide at clinically relevant partial pressures. They have now extended their work to in vivo studies, examining PMCA pumping in SPM obtained from control rats decapitated without anesthetic exposure, from rats decapitated during halothane anesthesia, and from rats decapitated after recovery from halothane anesthesia. Methods: Three treatment groups were studied: 1) C, control rats that were decapitated without anesthetic exposure, 2) A, anesthetized rats exposed to 1 minimum effective dose (MED) for 20 min and then decapitated, and 3) R, rats exposed to 1 MED for 20 min and then decapitated after recovery from anesthesia, defined as beginning to groom. Plasma membrane Ca2+-ATPase pumping and Ca2+-dependent ATPase hydrolytic activity, as well as sodium-calcium exchanger activity and Na+K+ -ATPase hydrolytic activity, were assessed in cerebral SPM. In addition, halothane effect on smooth endoplasmic reticulum Ca2+-ATPase (SERCA) was examined. Results: Plasma membrane Ca2+-ATPase transport of Ca2+ into SPM vesicles from anesthetized rats was reduced to 71% of control (P < 0.01) compared with 113% of control for the recovered group (NS). No depression by halothane of SERCA activity, sodium-calcium exchanger, or Na+ -K+-ATPase activity was noted among the CAR treatment groups. Conclusions: Plasma membrane Ca2+-ATPase is selectively and stably inhibited in cerebral SPM from rats killed while anesthetized with halothane, compared with rats killed without anesthesia or after recovery from anesthesia. The studies described in this report, in conjunction with previously re-ported inhibition of PMCA activity in vitro by a wide range of anesthetic agents, indicate a relationship between inhibition of PMCA and action of inhalational anesthetics.

Original languageEnglish (US)
Pages (from-to)118-128
Number of pages11
JournalAnesthesiology
Volume82
Issue number1
DOIs
StatePublished - Feb 3 1995

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Synaptic Membranes
Halothane
Calcium-Transporting ATPases
Cell Membrane
Calcium
Brain
Anesthesia
Anesthetics
Sodium-Calcium Exchanger
Smooth Endoplasmic Reticulum
Xenon
Partial Pressure
Isoflurane
Nitrous Oxide

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

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title = "Stable inhibition of brain synaptic plasma membrane calcium ATPpase in rats anesthetized with halothane",
abstract = "Background: The authors recently showed that plasma membrane Ca2+- ATPase (PMCA) activity in cerebral synaptic plasma membrane (SPM) is diminished in a dose-related fashion during exposure in vitro to halothane, isoflurane, xenon, and nitrous oxide at clinically relevant partial pressures. They have now extended their work to in vivo studies, examining PMCA pumping in SPM obtained from control rats decapitated without anesthetic exposure, from rats decapitated during halothane anesthesia, and from rats decapitated after recovery from halothane anesthesia. Methods: Three treatment groups were studied: 1) C, control rats that were decapitated without anesthetic exposure, 2) A, anesthetized rats exposed to 1 minimum effective dose (MED) for 20 min and then decapitated, and 3) R, rats exposed to 1 MED for 20 min and then decapitated after recovery from anesthesia, defined as beginning to groom. Plasma membrane Ca2+-ATPase pumping and Ca2+-dependent ATPase hydrolytic activity, as well as sodium-calcium exchanger activity and Na+K+ -ATPase hydrolytic activity, were assessed in cerebral SPM. In addition, halothane effect on smooth endoplasmic reticulum Ca2+-ATPase (SERCA) was examined. Results: Plasma membrane Ca2+-ATPase transport of Ca2+ into SPM vesicles from anesthetized rats was reduced to 71{\%} of control (P < 0.01) compared with 113{\%} of control for the recovered group (NS). No depression by halothane of SERCA activity, sodium-calcium exchanger, or Na+ -K+-ATPase activity was noted among the CAR treatment groups. Conclusions: Plasma membrane Ca2+-ATPase is selectively and stably inhibited in cerebral SPM from rats killed while anesthetized with halothane, compared with rats killed without anesthesia or after recovery from anesthesia. The studies described in this report, in conjunction with previously re-ported inhibition of PMCA activity in vitro by a wide range of anesthetic agents, indicate a relationship between inhibition of PMCA and action of inhalational anesthetics.",
author = "Franks, {J. J.} and Horn, {J. L.} and Piotr Janicki and G. Singh",
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Stable inhibition of brain synaptic plasma membrane calcium ATPpase in rats anesthetized with halothane. / Franks, J. J.; Horn, J. L.; Janicki, Piotr; Singh, G.

In: Anesthesiology, Vol. 82, No. 1, 03.02.1995, p. 118-128.

Research output: Contribution to journalArticle

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T1 - Stable inhibition of brain synaptic plasma membrane calcium ATPpase in rats anesthetized with halothane

AU - Franks, J. J.

AU - Horn, J. L.

AU - Janicki, Piotr

AU - Singh, G.

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N2 - Background: The authors recently showed that plasma membrane Ca2+- ATPase (PMCA) activity in cerebral synaptic plasma membrane (SPM) is diminished in a dose-related fashion during exposure in vitro to halothane, isoflurane, xenon, and nitrous oxide at clinically relevant partial pressures. They have now extended their work to in vivo studies, examining PMCA pumping in SPM obtained from control rats decapitated without anesthetic exposure, from rats decapitated during halothane anesthesia, and from rats decapitated after recovery from halothane anesthesia. Methods: Three treatment groups were studied: 1) C, control rats that were decapitated without anesthetic exposure, 2) A, anesthetized rats exposed to 1 minimum effective dose (MED) for 20 min and then decapitated, and 3) R, rats exposed to 1 MED for 20 min and then decapitated after recovery from anesthesia, defined as beginning to groom. Plasma membrane Ca2+-ATPase pumping and Ca2+-dependent ATPase hydrolytic activity, as well as sodium-calcium exchanger activity and Na+K+ -ATPase hydrolytic activity, were assessed in cerebral SPM. In addition, halothane effect on smooth endoplasmic reticulum Ca2+-ATPase (SERCA) was examined. Results: Plasma membrane Ca2+-ATPase transport of Ca2+ into SPM vesicles from anesthetized rats was reduced to 71% of control (P < 0.01) compared with 113% of control for the recovered group (NS). No depression by halothane of SERCA activity, sodium-calcium exchanger, or Na+ -K+-ATPase activity was noted among the CAR treatment groups. Conclusions: Plasma membrane Ca2+-ATPase is selectively and stably inhibited in cerebral SPM from rats killed while anesthetized with halothane, compared with rats killed without anesthesia or after recovery from anesthesia. The studies described in this report, in conjunction with previously re-ported inhibition of PMCA activity in vitro by a wide range of anesthetic agents, indicate a relationship between inhibition of PMCA and action of inhalational anesthetics.

AB - Background: The authors recently showed that plasma membrane Ca2+- ATPase (PMCA) activity in cerebral synaptic plasma membrane (SPM) is diminished in a dose-related fashion during exposure in vitro to halothane, isoflurane, xenon, and nitrous oxide at clinically relevant partial pressures. They have now extended their work to in vivo studies, examining PMCA pumping in SPM obtained from control rats decapitated without anesthetic exposure, from rats decapitated during halothane anesthesia, and from rats decapitated after recovery from halothane anesthesia. Methods: Three treatment groups were studied: 1) C, control rats that were decapitated without anesthetic exposure, 2) A, anesthetized rats exposed to 1 minimum effective dose (MED) for 20 min and then decapitated, and 3) R, rats exposed to 1 MED for 20 min and then decapitated after recovery from anesthesia, defined as beginning to groom. Plasma membrane Ca2+-ATPase pumping and Ca2+-dependent ATPase hydrolytic activity, as well as sodium-calcium exchanger activity and Na+K+ -ATPase hydrolytic activity, were assessed in cerebral SPM. In addition, halothane effect on smooth endoplasmic reticulum Ca2+-ATPase (SERCA) was examined. Results: Plasma membrane Ca2+-ATPase transport of Ca2+ into SPM vesicles from anesthetized rats was reduced to 71% of control (P < 0.01) compared with 113% of control for the recovered group (NS). No depression by halothane of SERCA activity, sodium-calcium exchanger, or Na+ -K+-ATPase activity was noted among the CAR treatment groups. Conclusions: Plasma membrane Ca2+-ATPase is selectively and stably inhibited in cerebral SPM from rats killed while anesthetized with halothane, compared with rats killed without anesthesia or after recovery from anesthesia. The studies described in this report, in conjunction with previously re-ported inhibition of PMCA activity in vitro by a wide range of anesthetic agents, indicate a relationship between inhibition of PMCA and action of inhalational anesthetics.

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