β-adrenergic stimulation after rewarming does not mitigate hypothermia-induced contractile dysfunction in rat cardiomyocytes.

Autor: Schanche T; Department of Physiology & Biomedical Engineering, Mayo Clinic Rochester, MN, USA; Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037, Tromsø, Norway., Han YS; Department of Physiology & Biomedical Engineering, Mayo Clinic Rochester, MN, USA., Jensen CW; Department of Physiology & Biomedical Engineering, Mayo Clinic Rochester, MN, USA., Arteaga GM; Department of Physiology & Biomedical Engineering, Mayo Clinic Rochester, MN, USA., Tveita T; Department of Physiology & Biomedical Engineering, Mayo Clinic Rochester, MN, USA; Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037, Tromsø, Norway; Division of Surgical Medicine and Intensive Care, University Hospital of North Norway, 9038, Tromsø, Norway., Sieck GC; Department of Physiology & Biomedical Engineering, Mayo Clinic Rochester, MN, USA. Electronic address: Sieck.Gary@mayo.edu.
Jazyk: angličtina
Zdroj: Cryobiology [Cryobiology] 2024 Sep; Vol. 116, pp. 104927. Date of Electronic Publication: 2024 Jun 25.
DOI: 10.1016/j.cryobiol.2024.104927
Abstrakt: Victims of severe accidental hypothermia are frequently treated with catecholamines to counteract the hemodynamic instability associated with hypothermia-induced cardiac contractile dysfunction. However, we previously reported that the inotropic effects of epinephrine are diminished after hypothermia and rewarming (H/R) in an intact animal model. Thus, the goal of this study was to investigate the effects of Epi treatment on excitation-contraction coupling in isolated rat cardiomyocytes after H/R. In adult male rats, cardiomyocytes isolated from the left ventricle were electrically stimulated at 0.5 Hz and evoked cytosolic [Ca 2+ ] and contractile responses (sarcomere length shortening) were measured. In initial experiments, the effects of varying concentrations of epinephrine on evoked cytosolic [Ca 2+ ] and contractile responses at 37 °C were measured. In a second series of experiments, cardiomyocytes were cooled from 37 °C to 15 °C, maintained at 15 °C for 2 h, then rewarmed to 37 °C (H/R protocol). Immediately after rewarming, the effects of epinephrine treatment on evoked cytosolic [Ca 2+ ] and contractile responses of cardiomyocytes were determined. At 37 °C, epinephrine treatment increased both cytosolic [Ca 2+ ] and contractile responses of cardiomyocytes in a concentration-dependent manner peaking at 25-50 nM. The evoked contractile response of cardiomyocytes after H/R was reduced while the cytosolic [Ca 2+ ] response was slightly elevated. The diminished contractile response of cardiomyocytes after H/R was not mitigated by epinephrine (25 nM) and epinephrine treatment reduced the exponential time decay constant (Tau), but did not increase the cytosolic [Ca 2+ ] response. We conclude that epinephrine treatment does not mitigate H/R-induced contractile dysfunction in cardiomyocytes.
(Copyright © 2024 Society for Cryobiology. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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