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

IT is generally accepted that malignant hyperthermia (MH) susceptibility is caused by an abnormal Ca metabolism within the skeletal muscle cell. Ca homeostasis in skeletal muscles is regulated by two main receptors, the ryanodine receptor type I and the dihydropyridine receptor, and by a variety of intracellular second messenger systems. They have a direct or indirect Ca releasing potency from the sarcoplasmic reticulum in common. However, it is not known whether a passive accumulation of Ca might also be a relevant mechanism in MH. Hence, the aim of this study was to examine whether the blockade of the Ca reuptake in the sarcoplasmic reticulum is a potent method to induce in vitro contractures in MH susceptible (MHS) and MH normal (MHN) skeletal muscle specimens. To answer this question in porcine in vitro contracture tests we used cyclopiazonic acid (CPA). We examined the in vitro effects of CPA in a cumulative pattern in MHS and MHN porcine skeletal muscle specimens.

anesthesiology

Inhibition of Sarcoplasmic Ca2+Adenosine Triphosphatase in Porcine Skeletal Muscle Samples with Cyclopiazonic Acid Enables In Vitro Malignant Hyperthermia Discrimination