| Literature DB >> 30150463 |
Christian Koch1, Jennifer Jersch2, Emmanuel Schneck2, Fabian Edinger2, Hagen Maxeiner2, Florian Uhle3, Markus A Weigand3, Melanie Markmann2, Michael Sander2, Michael Henrich4.
Abstract
Recent studies showed that critically ill patients might be at risk for hemodynamic impairment during caspofungin (CAS) therapy. The aim of our present study was to examine the mechanisms behind CAS-induced cardiac alterations. We revealed a dose-dependent increase in intracellular Ca2+ concentration ([Ca2+]i) after CAS treatment. Ca2+ ions were found to be released from intracellular caffeine-sensitive stores, most probably via the activation of ryanodine receptors.Entities:
Keywords: adverse drug reaction; antifungal agents; cardiac output; cardiac toxicity
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Year: 2018 PMID: 30150463 PMCID: PMC6201063 DOI: 10.1128/AAC.01114-18
Source DB: PubMed Journal: Antimicrob Agents Chemother ISSN: 0066-4804 Impact factor: 5.191