Fujii T, Kojima S, Ohe T, Karakawa S, Iida T, Hirata Y, Kuramochi M, Shimomura K, Ito K, Omae T
Department of Medicine, National Cardiovascular Center Hospital, Osaka, Japan.
Nephron. 1991;57(3):262-7. doi: 10.1159/000186273.
Supraventricular tachycardia was induced in 10 patients by programmed cardiac stimulation through esophageal lead. Blood pressure, heart rate, renal function, and hormonal factors were measured before, during, and after tachycardia. The patients were divided into two groups, depending on whether antinatriuresis occurred during tachycardia; one group (n = 5) with antinatriuresis during tachycardia associated with a decrease in blood pressure and the other group (n = 5) with neither antinatriuresis nor changes in blood pressure. The urinary sodium excretion tended to increase after tachycardia only in the latter group. On the other hand, urine volume and free water clearance increased during or after tachycardia in both groups. Plasma levels of atrial natriuretic peptide significantly increased and the urinary vasopressin excretion significantly decreased during tachycardia in both groups. During tachycardia, natriuresis due to atrial natriuretic peptide secretion seems to be hampered by hypotension, but polyuria is preserved despite the fall in blood pressure probably related to suppression of vasopressin release.
通过食管导联程控心脏刺激在10例患者中诱发室上性心动过速。在心动过速发作前、发作期间和发作后测量血压、心率、肾功能和激素因素。根据心动过速期间是否发生钠利尿，将患者分为两组；一组（n = 5）在心动过速期间出现钠利尿且伴有血压下降，另一组（n = 5）既无钠利尿也无血压变化。仅在后一组中，心动过速后尿钠排泄有增加趋势。另一方面，两组在心动过速期间或之后尿量和自由水清除率均增加。两组在心动过速期间心房利钠肽血浆水平显著升高，尿血管加压素排泄显著减少。在心动过速期间，心房利钠肽分泌引起的钠利尿似乎因低血压而受阻，但尽管血压下降，多尿现象仍存在，这可能与血管加压素释放受抑制有关。
