English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

To determine whether accumulation of long-chain acyl carnitine contributes to electrophysiological abnormalities induced by hypoxia, we characterized effects of normoxic and hypoxic perfusion on the subcellular distribution of endogenous long-chain acyl carnitine and transmembrane potentials of cultured rat neonatal myocytes. Hypoxia increased long-chain acyl carnitine more than 5-fold. Sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (10 microM), a carnitine acyltransferase inhibitor, precluded accumulation of long-chain acyl carnitine induced by hypoxia. Tissue was processed for electron microscopy by a procedure specifically developed for selective extraction of endogenous short-chain and free carnitine but retention of endogenous long-chain acyl carnitine. In normoxic-perfused cells, long-chain acyl carnitine was concentrated in mitochondria and cytoplasmic membranous components. Only small amounts were present in sarcolemma. Hypoxia increased mitochondrial long-chain acyl carnitine by 10-fold and sarcolemmal long-chain acyl carnitine by 70-fold. After 60 minutes of hypoxia, sarcolemma contained 1.4 X 10(7) long-chain acyl carnitine molecules/micron 3 of membrane volume, a value corresponding to approximately 3.5% of total sarcolemmal phospholipid. Hypoxia also significantly decreased maximum diastolic potential, action potential amplitude and maximum upstroke velocity of phase 0. Sodium 2-[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate inhibited accumulation of long-chain acyl carnitine in each subcellular compartment and prevented the depression of electrophysiological function induced by hypoxia. These results strongly implicate endogenous long-chain acyl carnitine as a mediator of electrophysiological alterations induced by hypoxia.

The dependence of electrophysiological derangements on accumulation of endogenous long-chain acyl carnitine in hypoxic neonatal rat myocytes.