体内心脏神经交感活动的代谢调节：钾和腺苷的作用。

Metabolic modulation of cardiac neurosympathetic activity in vivo: effects of potassium and adenosine.

作者信息

Forfar J C, Riemersma R A

机构信息

Cardiovascular Research Unit, University of Edinburgh.

出版信息

Cardiovasc Res. 1987 Nov;21(11):821-9. doi: 10.1093/cvr/21.11.821.

DOI:10.1093/cvr/21.11.821

PMID:3370665

Abstract

The effects of intracoronary (LAD) infusion of potassium and adenosine on changes in coronary vascular resistance and regional cardiac noradrenaline overflow during graded cardiac sympathetic stimulation were assessed in non-ischaemic myocardium in the open chest anaesthetised dog. Intracoronary potassium at three concentration (10, 25, 75 mmol.litre-1) progressively increased the potassium content of local venous effluent from 3.6 to 9.4 mmol.litre-1 and produced biphasic effects on nerve stimulated regional noradrenaline overflow. At low dose it was inhibitory (peak overflow at 20 Hz stimulation being reduced from (mean(SEM)) 10.2(2.6) to 2.9(1.8) pmol.ml-1 with 10 mmol.litre-1 potassium chloride; p less than 0.01). At high dose, overflow was potentiated to 13.3(2.7) pmol.ml-1 with 75 mmol.litre-1 potassium chloride (p less than 0.05). Noradrenaline overflow from and the potassium content of circumflex territory venous effluent was unchanged. Intracoronary adenosine at high concentration (10(-3) and 10(-2) mol.litre-1) potentiated basal noradrenaline overflow from the heart producing a small negative arteriovenous concentration difference of 0.6(0.7) and 1.0(0.6) pmol.ml-1 respectively. However, noradrenaline overflow during maximal sympathetic stimulation was inhibited from 3.8(1.4) to 0.4(0.7) pmol.ml-1 with 10(-3) mol.litre-1 adenosine and to 0.7(0.6) pmol.ml-1 with 10(-2) mol.litre-1 adenosine (p less than 0.05). The changes in blood flow and coronary vascular resistance seen with sympathetic stimulation were not modified by adenosine, despite major alteration in basal coronary vascular tone. Thus both metabolites may potentially alter local neurosympathetic activity in ischaemic myocardium and act diversely to determine noradrenaline release at the nerve terminal.

摘要

在开胸麻醉犬的非缺血心肌中，评估了冠状动脉（左前降支）内输注钾和腺苷对分级心脏交感神经刺激期间冠状动脉血管阻力变化和局部心脏去甲肾上腺素溢出的影响。三种浓度（10、25、75 mmol·L⁻¹）的冠状动脉内钾使局部静脉流出液中的钾含量从3.6 mmol·L⁻¹逐渐增加到9.4 mmol·L⁻¹，并对神经刺激的局部去甲肾上腺素溢出产生双相作用。低剂量时具有抑制作用（20 Hz刺激时的峰值溢出量从（均值（标准误））10.2(2.6) pmol·ml⁻¹降低到2.9(1.8) pmol·ml⁻¹，使用10 mmol·L⁻¹氯化钾；p<0.01）。高剂量时，75 mmol·L⁻¹氯化钾使溢出量增强至13.3(2.7) pmol·ml⁻¹（p<0.05）。回旋支区域静脉流出液中的去甲肾上腺素溢出量和钾含量未发生变化。高浓度（10⁻³和10⁻² mol·L⁻¹）的冠状动脉内腺苷增强了心脏的基础去甲肾上腺素溢出，分别产生了0.6(0.7)和1.0(0.6) pmol·ml⁻¹的小负动静脉浓度差。然而，最大交感神经刺激期间的去甲肾上腺素溢出量在使用10⁻³ mol·L⁻¹腺苷时从3.8(1.4) pmol·ml⁻¹抑制到0.4(0.7) pmol·ml⁻¹，在使用10⁻² mol·L⁻¹腺苷时抑制到0.7(0.6) pmol·ml⁻¹（p<0.05）。尽管基础冠状动脉血管张力发生了重大改变，但腺苷并未改变交感神经刺激时观察到的血流和冠状动脉血管阻力变化。因此，这两种代谢产物都可能潜在地改变缺血心肌中的局部神经交感活动，并以不同方式决定神经末梢去甲肾上腺素的释放。