Kojima S, Fujii T, Ohe T, Yoshitomi Y, Kuramochi M, Shimomura K, Omae T
Department of Clinical Research, Tohsei National Hospital, Shizuoka, Japan.
Jpn Heart J. 1995 Jul;36(4):429-37. doi: 10.1536/ihj.36.429.
Supraventricular tachycardia (SVT) was induced in 7 patients by programmed cardiac stimulation via an esophageal lead. Blood pressure, renal function, and hormonal factors were measured before, during, and after SVT. The glomerular filtration rate increased during SVT, while renal blood flow did not change. The parameters of glomerular hemodynamics were calculated according to the method of Gomez. Glomerular pressure was 64 +/- 3 (mean +/- SE) mmHg before SVT, and rose significantly (p < 0.01) to 76 +/- 5 during SVT. This rise in glomerular pressure was associated with a decrease in afferent vascular resistance (from 3355 +/- 610 to 1770 +/- 517 dynes x sec/cm5, p < 0.05) and an increase in efferent vascular resistance (from 3726 +/- 758 to 4814 +/- 780 dynes x sec/cm5, p < 0.05). Since atrial natriuretic peptide (ANP) increased during SVT (from 40 +/- 15 to 208 +/- 72 pg/ml, p < 0.01), these changes in glomerular hemodynamics may be attributed to the physiologic action of ANP. Despite the changes in glomerular hemodynamics during SVT, natriuresis appeared after SVT and not during SVT. This suggests that natriuresis accompanying SVT could not be attributed to the changes in glomerular hemodynamics.
通过食管导联进行程控心脏刺激，在7例患者中诱发了室上性心动过速（SVT）。在SVT发作前、发作期间和发作后测量血压、肾功能和激素因素。SVT发作期间肾小球滤过率增加，而肾血流量未发生变化。根据戈麦斯方法计算肾小球血流动力学参数。SVT发作前肾小球压力为64±3（平均值±标准误）mmHg，在SVT发作期间显著升高（p<0.01）至76±5。肾小球压力的升高与入球血管阻力降低（从3355±610降至1770±517达因×秒/厘米⁵，p<0.05）和出球血管阻力增加（从3726±758增至4814±780达因×秒/厘米⁵，p<0.05）有关。由于SVT发作期间心房利钠肽（ANP）增加（从40±15增至208±72 pg/ml，p<0.01），肾小球血流动力学的这些变化可能归因于ANP的生理作用。尽管SVT发作期间肾小球血流动力学发生了变化，但利钠作用出现在SVT发作后而非发作期间。这表明伴随SVT的利钠作用不能归因于肾小球血流动力学的变化。
