Emanuelsson H, Mannheimer C, Waagstein F
Division of Cardiology, Sahlgrenska Hospital, Göteborg, Sweden.
Clin Cardiol. 1991 Jul;14(7):567-72.
In order to elucidate the effects of atrial pacing on cardiac catecholamine metabolism, 11 patients were studied during cardiac catheterization. Blood samples were drawn from a peripheral artery and the coronary sinus for estimation of catecholamine concentrations. Heart rate was increased by 10 beats/min each minute, and all patients experienced chest pain at maximal pacing rate. Coronary sinus blood flow rose from 122 +/- 19 at rest to 208 +/- 25 ml/min at final pacing rate, and myocardial lactate extraction ratio decreased. There was no significant change in arterial epinephrine levels, whereas the extraction ratio decreased (p less than 0.05). The norepinephrine arterial levels increased at the final pacing rate (p less than 0.01). The calculated myocardial release increased as well, but not to a statistically significant degree. The exact mechanisms of the rise in sympathetic activity and arterial norepinephrine levels cannot be ascertained with the present study design. Myocardial ischemia with subsequent chest pain seems to be a probably cause for the increased sympathetic outflow.
为了阐明心房起搏对心脏儿茶酚胺代谢的影响,在心脏导管插入术期间对11例患者进行了研究。从外周动脉和冠状窦采集血样以估计儿茶酚胺浓度。心率每分钟增加10次,所有患者在最大起搏速率时均出现胸痛。冠状窦血流量从静息时的122±19增加到最终起搏速率时的208±25 ml/min,心肌乳酸摄取率降低。动脉肾上腺素水平无显著变化,而摄取率降低(p<0.05)。最终起搏速率时动脉去甲肾上腺素水平升高(p<0.01)。计算得出的心肌释放也增加,但未达到统计学显著程度。本研究设计无法确定交感神经活动和动脉去甲肾上腺素水平升高的确切机制。心肌缺血及随后的胸痛似乎是交感神经流出增加的一个可能原因。