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

Hong Liu, Lianguo Wang, Matt Eaton, Saul Schaefer

Research output: Contribution to journalArticle

20 Scopus citations

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

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

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