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

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2024-06-25 DOI:10.1016/j.cryobiol.2024.104927
Torstein Schanche , Young Soo Han , Cole W. Jensen , Grace M. Arteaga , Torkjel Tveita , Gary C. Sieck
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Abstract

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 [Ca2+] and contractile responses (sarcomere length shortening) were measured. In initial experiments, the effects of varying concentrations of epinephrine on evoked cytosolic [Ca2+] 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 [Ca2+] and contractile responses of cardiomyocytes were determined. At 37 °C, epinephrine treatment increased both cytosolic [Ca2+] 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 [Ca2+] 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 [Ca2+] response. We conclude that epinephrine treatment does not mitigate H/R-induced contractile dysfunction in cardiomyocytes.

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复温后β肾上腺素能刺激不会减轻低体温引起的大鼠心肌细胞收缩功能障碍。
严重意外低体温症患者通常会接受儿茶酚胺治疗,以对抗低体温引起的心脏收缩功能障碍所导致的血流动力学不稳定。然而,我们以前曾报道过,在一个完整的动物模型中,低体温和复温(H/R)后肾上腺素的肌力作用会减弱。因此,本研究的目的是探讨 H/R 后 Epi 处理对离体大鼠心肌细胞兴奋-收缩耦联的影响。在成年雄性大鼠体内,以 0.5 Hz 的频率电刺激从左心室分离的心肌细胞,并测量诱发的细胞膜[Ca2+]和收缩反应(肌节长度缩短)。在最初的实验中,测量了不同浓度的肾上腺素对 37° 下诱发的细胞膜[Ca2+]和收缩反应的影响。在第二系列实验中,将心肌细胞从 37°降温至 15°C,在 15°C 下维持 2 小时,然后再回温至 37°C(H/R 方案)。复温后,立即测定肾上腺素处理对诱发心肌细胞胞质[Ca2+]和收缩反应的影响。在 37°C 时,肾上腺素以浓度依赖的方式增加心肌细胞的细胞膜[Ca2+]和收缩反应,在 25-50 nM 时达到峰值。H/R 后心肌细胞的诱发收缩反应减弱,而细胞膜[Ca2+]反应略有增强。肾上腺素(25 nM)不能减轻 H/R 后心肌细胞收缩反应的减弱,肾上腺素处理可降低指数时间衰减常数(Tau),但不会增加细胞膜[Ca2+]反应。我们的结论是,肾上腺素处理不会减轻 H/R 诱导的心肌细胞收缩功能障碍。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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