Sevoflurane preconditioning limits intracellular/mitochondrial Ca 2+ in ischemic newborn myocardium

Hong Liu, Lianguo Wang, Matt Eaton, Saul Schaefer

Research output: Contribution to journalArticle

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Abstract

Sevoflurane preconditioning (SPC) in adult hearts reduces myocardial ischemia/reperfusion (I/R) injury, an effect that may be mediated by reductions in intracellular Ca2+ ([Ca2+]i) and/or mitochondrial Ca2+ ([Ca2+]m) accumulation during ischemia and reperfusion. Because the physiology, pharmacology, and metabolic responses of the newborn differ from adults, we tested the hypothesis that SPC protects newborn myocardium by limiting [Ca2+]i and [Ca2+]m by a KATP channel-dependent mechanism. Fluorescence spectrofluorometry and nuclear magnetic resonance spectroscopy were used to measure [Ca2+]i, [Ca 2+]m, and adenosine triphosphate (ATP) in 4- to 7-day-old Langendorff-perfused rabbit hearts. Three experimental groups were used to study the effect of SPC on [Ca2+]m/[Ca2+] i, ATP, as well as hemodynamics and ischemic injury. The role of mitochondrial KATP channels was assessed by exposing the SPC hearts to the mitochondrial KATP channel blocker 5-hydroxydecanoic acid. Our results show that SPC significantly decreased [Ca2+]i and [Ca2+]m, during I/R, as well as decreased creatine kinase release during reperfusion and resulted in higher ATP. 5-Hydroxydecanoic acid abolished the effect of SPC on [Ca2+], hemodynamics, ATP, and creatine kinase release. In conclusion, decreased [Ca2+]i and [Ca2+]m, observed with SPC is associated with greater ATP recovery as well as diminished cell injury. Mitochondrial KATP channel blockade attenuates the SPC effect during I/R, suggesting that these channels are involved in the protective effects of SPC in the newborn.

Original languageEnglish (US)
Pages (from-to)349-355
Number of pages7
JournalAnesthesia and Analgesia
Volume101
Issue number2
DOIs
StatePublished - Aug 2005

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Myocardium
Adenosine Triphosphate
Reperfusion
Ischemia
Creatine Kinase
Hemodynamics
Adenosine Kinase
Myocardial Reperfusion Injury
sevoflurane
KATP Channels
Fluorescence Spectrometry
Wounds and Injuries
Reperfusion Injury
Myocardial Ischemia
Magnetic Resonance Spectroscopy
Fluorescence
Pharmacology
Rabbits
mitochondrial K(ATP) channel

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Sevoflurane preconditioning limits intracellular/mitochondrial Ca 2+ in ischemic newborn myocardium. / Liu, Hong; Wang, Lianguo; Eaton, Matt; Schaefer, Saul.

In: Anesthesia and Analgesia, Vol. 101, No. 2, 08.2005, p. 349-355.

Research output: Contribution to journalArticle

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AB - Sevoflurane preconditioning (SPC) in adult hearts reduces myocardial ischemia/reperfusion (I/R) injury, an effect that may be mediated by reductions in intracellular Ca2+ ([Ca2+]i) and/or mitochondrial Ca2+ ([Ca2+]m) accumulation during ischemia and reperfusion. Because the physiology, pharmacology, and metabolic responses of the newborn differ from adults, we tested the hypothesis that SPC protects newborn myocardium by limiting [Ca2+]i and [Ca2+]m by a KATP channel-dependent mechanism. Fluorescence spectrofluorometry and nuclear magnetic resonance spectroscopy were used to measure [Ca2+]i, [Ca 2+]m, and adenosine triphosphate (ATP) in 4- to 7-day-old Langendorff-perfused rabbit hearts. Three experimental groups were used to study the effect of SPC on [Ca2+]m/[Ca2+] i, ATP, as well as hemodynamics and ischemic injury. The role of mitochondrial KATP channels was assessed by exposing the SPC hearts to the mitochondrial KATP channel blocker 5-hydroxydecanoic acid. Our results show that SPC significantly decreased [Ca2+]i and [Ca2+]m, during I/R, as well as decreased creatine kinase release during reperfusion and resulted in higher ATP. 5-Hydroxydecanoic acid abolished the effect of SPC on [Ca2+], hemodynamics, ATP, and creatine kinase release. In conclusion, decreased [Ca2+]i and [Ca2+]m, observed with SPC is associated with greater ATP recovery as well as diminished cell injury. Mitochondrial KATP channel blockade attenuates the SPC effect during I/R, suggesting that these channels are involved in the protective effects of SPC in the newborn.

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