低温缺血-再灌注对离体大鼠心房肌Kir2.1和CaMKⅡ表达的影响

doi:10.3969/j.issn.1006-5725.2023.21.010

Abstract

Abstract:

Objective To explore the molecular mechanism of prolonged atrial repolarization in rats with reperfusion atrial arrhythmia. Methods Sixteen Langendorff isolated heart perfusion models made by male SD rats were randomly divided into control group （group C，n = 8） and hypothermic ischemia-reperfusion group （group IR，n = 8）. According to the occurrence of atrial arrhythmia after reperfusion，group IR was further subdivided into reperfusion non-atrial arrhythmia subgroup （group N-RAA） and reperfusion atrial arrhythmia subgroup （group R-AA ）.Group C was perfused with 37 ℃ K-H solution for 120 min. In group IR， the isolated heart was perfused with 37 ℃ K-H solution for 30 min and stopped， and the isolated heart was perfused with 4 ℃ Thomas solution （20 mL/kg） for 60 mins. When the heart stopped for 30 mins， the isolated heart was perfused with a half dose of 4 ℃ Thomas solution （10 ℃）. During cardioplegia， the isolated heart was protected by low temperature Thomas solution （4 ℃）， and then reperfused for 30 mins with 37 ℃ K-H solution. The monophasic action potential （MAP） of the right atrium was recorded at balanced perfusion for 30 mins （T₀），balanced perfusion for 105 mins in group C/reperfusion for 15 mins in group IR（T₁） and balanced perfusion for 120 mins in group C/reperfusion for 30 min in group IR（T₂）； The duration of 50% and 90% repolarization of monophasic action potential （MAPD₅₀ and MAPD₉₀） was measured. After electrophysiological monitoring， the expression of Kir2.1 and CaMKⅡ in right atrium was detected by Western blot. Results Compared with T₀， MAPD₅₀ and MAPD₉₀ at T₁ and T₂ were significantly prolonged in group R-AA （P < 0.05）， and MAPD₉₀ at T₁ and T₂ in group R-NAA and group R-AA were significantly longer than those in group C （P < 0.05）.Compared with group R-NAA， MAPD₅₀ and MAPD₉₀ in group R-AA were significantly prolonged at T₁ and T₂ （P < 0.05）.The results of Western blot showed that the expression of Kir2.1 in group R-NAA and group R-AA was significantly lower than that in group C （P < 0.05）， and that in group R-AA was significantly lower than that in group R-NAA （P < 0.05）.The expression of CaMKⅡ in group R-NAA and group R-AA was significantly higher than that in group C （P < 0.05）， and the expression of CaMKⅡ in group R-AA was significantly higher than that in group R-NAA. Conclusion The prolonged duration of atrial repolarization in rats with hypothermic ischemia-reperfusion atrial arrhythmia may be related to the down-regulation of Kir2.1 expression and the up-regulation of CaMKⅡ expression.

Key words: ischemia-reperfusion, atrial myocardium, duration of repolarization, inwardly rectifying K channels 2.1, Ca²⁺-calmodulin kinase Ⅱ

CLC Number:

Youqin HE,Hong GAO,Penggui CHONG,Yanqiu LIU,Rui TONG,Xueyan. WU. Effect of hypothermic ischemia⁃reperfusion on the expression of Kir2.1 and CaMKⅡ in isolated rat atrial myocardium[J]. The Journal of Practical Medicine, 2023, 39(21): 2750-2753.

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References 19

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项目	组别	n	T₀	T₁	T₂
MAPD₅₀	C组	8	19.15 ± 2.03	19.42 ± 1.99	20.10 ± 2.23
	R-NAA组	5	19.21 ± 2.17	23.95 ± 2.10^*▲	21.69 ± 2.71
	R-AA组	3	19.09 ± 2.51	29.05 ± 3.81^*△▲	28.22 ± 3.37^*△▲
MAPD₉₀	C组	8	42.26 ± 1.62	43.82 ± 2.85	43.14 ± 3.74
	R-NAA组	5	43.34 ± 2.46	48.76 ± 2.66^*▲	47.58 ± 4.56^*▲
	R-AA组	3	43.48 ± 3.81	54.22 ± 3.85^*△▲	52.15 ± 4.99^*△▲

组别	n	Kir2.1	CaMKⅡ
C组	8	1.99 ± 0.44	0.49 ± 0.15
R-NAA组	5	1.30 ± 0.39^*	1.14 ± 0.25^*
R-AA组	3	0.46 ± 0.23^*△	1.65 ± 0.30^*△

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Effect of hypothermic ischemia⁃reperfusion on the expression of Kir2.1 and CaMKⅡ in isolated rat atrial myocardium

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