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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Effects of cyclic GMP and its protein kinase on the contraction of ventricular myocytes from hearts after cardiopulmonary arrest.
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Effects of cyclic GMP and its protein kinase on the contraction of ventricular myocytes from hearts after cardiopulmonary arrest.

机译：循环GMP及其蛋白激酶对心肺停搏后心脏心室肌细胞收缩的影响。

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摘要

Hearts undergoing cardiopulmonary arrest and resuscitation have depressed function and may have changes in signal transduction. We hypothesized that the cyclic GMP (cGMP) signaling pathway would be altered in the post-resuscitation heart. This was studied in ventricular myocytes from 7 anesthetized open-chest rabbits. Cardiopulmonary arrest was achieved for 10 min through ventricular fibrillation and respirator shutdown. After cardiopulmonary arrest, respiration was resumed, the heart was defibrillated, and the heart recovered for 15 min. Seven additional rabbits served as controls. Myocyte function was measured via a video edge detector. Myocytes were treated with 8-bromo-cGMP (10(-5)-10(-6) mol/L) followed by KT5823 (10(-6) mol/L, cGMP protein kinase inhibitor). The baseline percent shortening was significantly depressed in the cardiac arrest myocytes compared with control (3.3 +/- 0.1 vs. 5.5 +/- 0.3%). Treatment with 8-Br-cGMP similarly and dose-dependently reduced cell contraction in both cardiac arrest (-24%) and control (-25%) myocytes. The negative effect of 8-Br-cGMP was partially reversed by KT5823 in control myocytes, but not in the arrest group, indicating reduced involvement of cGMP protein kinase. Multiple proteins were specifically phosphorylated when cGMP was present, but the degree of phosphorylation was significantly less in myocytes after cardiac arrest. The data suggested that the basal contraction was reduced, but the functional response to 8-Br-cGMP was preserved in myocytes from cardiopulmonary arrested hearts. The results also indicated that the action of cGMP appeared to be mainly through non-cGMP protein kinase pathways in the post-resuscitation heart.
机译：进行心肺停止和复苏的心脏功能低下，信号传导可能发生变化。我们假设循环后GMP（cGMP）信号通路将在复苏后心脏发生改变。在来自7只麻醉的开胸兔子的心室肌细胞中进行了研究。通过心室纤颤和呼吸机关闭，实现了10分钟的心肺骤停。心肺停搏后，呼吸恢复，心脏除颤，心脏恢复15分钟。另外七只兔子作为对照。通过视频边缘检测器测量肌细胞功能。依次用8-溴-cGMP（10（-5）-10（-6）mol / L）和KT5823（10（-6）mol / L，cGMP蛋白激酶抑制剂）处理心肌细胞。与对照组相比，心脏骤停心肌细胞的基线缩短百分比显着降低（3.3 +/- 0.1与5.5 +/- 0.3％）。用8-Br-cGMP进行的治疗在心脏骤停（-24％）和对照（-25％）的心肌细胞中均相似且剂量依赖性地减少了细胞收缩。 KT5823在对照肌细胞中部分逆转了8-Br-cGMP的负作用，但在停搏组中却没有，这表明cGMP蛋白激酶的参与减少。当存在cGMP时，多种蛋白质被特异性磷酸化，但心脏骤停后心肌细胞的磷酸化程度明显降低。数据表明，基础收缩减少，但是对心律失常的心肌细胞对8-Br-cGMP的功能反应得以保留。结果还表明，cGMP的作用似乎主要是通过复苏后心脏中的非cGMP蛋白激酶途径进行的。

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