Fujii T, Kojima S, Imanishi M, Ohe T, Omae T
Division of Cardiology, National Hiroshima Chest Hospital, Japan.
Am J Cardiol. 1991 Aug 1;68(4):343-8. doi: 10.1016/0002-9149(91)90829-a.
The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.
对8例阵发性室上性心动过速(SVT)相关的多尿机制进行了研究。人工诱发并维持SVT 60分钟。每30分钟采集尿液和血液样本。在SVT的后半段,SVT前的对照受试者尿流量增加了两倍。SVT后30分钟内尿钠排泄显著增加(p<0.01)。抗利尿激素(ADH)的尿排泄在SVT后半段减少(p<0.01),在SVT后增加(p<0.01)。SVT期间ADH的血浆水平没有变化,但在SVT后增加(p<0.05)。在SVT结束前,血浆心钠素(ANP)浓度显著增加(p<0.05)。SVT终止后,前列腺素E2的尿排泄显著增加(p<0.05)。前列腺素E2尿排泄的百分比变化与ADH的百分比变化相关(r=0.713,p<0.001)。前列腺素E2尿排泄的百分比变化与钠的百分比变化之间也存在相关性(r=0.6,p<0.001)。他们的研究结果表明,SVT期间的多尿主要归因于ADH释放的抑制,SVT后的利钠作用不仅归因于ANP的增加,还归因于可能由ADH刺激的肾前列腺素E2的增加。