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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
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Extracellular vesicles isolated from patients undergoing remote ischemic preconditioning decrease hypoxia-evoked
Frederik Abel1, Florian Murke2, Morten Gaida1
1Klinik für Anästhesiologie und Intensivmedizin, Universität Duisburg-Essen & Universitätsklinikum Essen, Essen, Germany.
Plos One
|February 15, 2020
Summary
Remote ischemic preconditioning (RIPC) generates extracellular vesicles (EVs) that protect heart cells from damage. However, propofol anesthesia may block this protective effect, impacting RIPC signaling.
Area of Science:
- Cardiovascular Science
- Cell Biology
- Anesthesiology
Background:
- Remote ischemic preconditioning (RIPC) offers cardioprotection against ischemia/reperfusion injury.
- The anesthetic used during RIPC may influence its protective effects.
- Extracellular vesicles (EVs) are implicated in cell-to-cell communication and may mediate RIPC's benefits.
Purpose of the Study:
- To investigate if EVs from RIPC patients protect cardiomyoblasts from hypoxia-induced apoptosis.
- To determine if isoflurane or propofol exposure alters the protective effects of these EVs.
Main Methods:
- EVs were isolated from patients undergoing coronary artery bypass graft surgery with isoflurane anesthesia before and after RIPC or Sham.
- EVs were quantified using Nanoparticle Tracking Analysis.
- Rat H9c2 cardiomyoblasts were treated with EVs and exposed to isoflurane or propofol, followed by normoxic or hypoxic culture to assess apoptosis via flow cytometry.
Main Results:
- RIPC increased serum nanoparticle concentrations compared to Sham.
- Hypoxia significantly increased cardiomyoblast apoptosis.
- EVs from RIPC patients reduced apoptosis, an effect enhanced by in vitro isoflurane exposure but abrogated by propofol.
Conclusions:
- Human RIPC-generated EVs possess cardioprotective properties against hypoxia-induced apoptosis.
- The anesthetic agent significantly influences EV-mediated cardioprotection, with propofol potentially acting as a confounder in RIPC signaling via EVs.
