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Myocardial subcellular glycogen distribution and sarcoplasmic reticulum Ca 2+ handling: effects of ischaemia, reperfusion and ischaemic preconditioning
Journal of Muscle Research and Cell Motility ( IF 2.7 ) Pub Date : 2019-10-19 , DOI: 10.1007/s10974-019-09557-3
Joachim Nielsen 1 , Jacob Johnsen 2 , Kasper Pryds 2 , Niels Ørtenblad 1 , Hans Erik Bøtker 2
Affiliation  

Ischaemic preconditioning (IPC) protects against myocardial ischaemia–reperfusion injury. The metabolic and ionic effects of IPC remain to be clarified in detail. We aimed to investigate the effect of IPC (2 times 5 min ischaemia) on the subcellular distribution of glycogen and Ca2+-uptake and leakiness by the sarcoplasmic reticulum (SR) in response to ischaemia–reperfusion in cardiomyocytes of isolated perfused rat hearts (Wistar rats, 335 ± 25 g). As estimated by quantitative transmission electron microscopy, the pre-ischaemic contribution [%, mean (95% CI)] of three sub-fractions of glycogen relative to total glycogen was 50 (39:61) as subsarcolemmal, 41 (31:50) as intermyofibrillar, and 9 (5:13) as intramyofibrillar glycogen. After 25 min of ischaemia, the relative contribution (%) of subsarcolemmal glycogen decreased to 39 (32:47) in control hearts (Con) and to 38 (31:45) in IPC. After 15 min reperfusion the contribution of subsarcolemmal glycogen was restored to pre-ischaemic levels in IPC hearts, but not in Con hearts. IPC increased the left ventricular developed pressure following ischaemia–reperfusion compared with Con. In saponin-skinned cardiomyocyte bundles, ischaemia reduced the SR Ca2+-uptake rate, with no effect of IPC. However, IPC reduced a SR Ca2+-leakage at pre-ischaemia, after ischaemia and during reperfusion. In conclusion, subsarcolemmal glycogen was preferentially utilised during sustained myocardial ischaemia. IPC improved left ventricular function reflecting reduced ischaemia–reperfusion injury, mediated a re-distribution of glycogen towards a preferential storage within the subsarcolemmal space during reperfusion, and lowered SR Ca2+-leakage. Under the present conditions, we found no temporal associations between alterations in glycogen localisation and SR Ca2+ kinetics.



中文翻译:

心肌亚细胞糖原分布和肌浆网 Ca 2+ 处理:缺血、再灌注和缺血预处理的影响

缺血预处理 (IPC) 可防止心肌缺血再灌注损伤。IPC 的代谢和离子效应仍有待详细阐明。我们旨在研究 IPC(2 次 5 分钟缺血)对糖原和 Ca 2+亚细胞分布的影响- 肌浆网 (SR) 对离体灌注大鼠心脏(Wistar 大鼠,335 ± 25 g)心肌细胞缺血再灌注的吸收和渗漏。根据定量透射电子显微镜估计,糖原的三个亚部分相对于总糖原的缺血前贡献 [%,平均 (95% CI)] 为 50 (39:61),作为肌膜下的 41 (31:50)作为肌原纤维间,和 9 (5:13) 作为肌原纤维内糖原。缺血 25 分钟后,肌膜下糖原的相对贡献 (%) 在对照心脏 (Con) 中降至 39 (32:47),在 IPC 中降至 38 (31:45)。再灌注 15 分钟后,肌膜下糖原的贡献在 IPC 心脏中恢复到缺血前水平,但在 Con 心脏中没有。与 Con 相比,IPC 增加了缺血再灌注后的左心室发展压力。在皂苷皮肤心肌细胞束中,缺血降低了 SR Ca2+ -吸收率,不受 IPC 影响。然而,IPC 减少了缺血前、缺血后和再灌注期间的 SR Ca 2+ -泄漏。总之,在持续的心肌缺血期间优先利用肌膜下糖原。IPC 改善了左心室功能,反映了缺血-再灌注损伤的减少,介导了再灌注过程中糖原向肌膜下空间优先储存的重新分布,并降低了 SR Ca 2+泄漏。在目前的条件下,我们发现糖原定位的改变和 SR Ca 2+动力学之间没有时间关联。

更新日期:2019-10-19
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