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与房性心动过速相关的利尿反应机制。

Mechanism of diuretic response associated with atrial tachycardia.

作者信息

Boykin J, Cadnapaphornchai P, McDonald K M, Schrier R W

出版信息

Am J Physiol. 1975 Dec;229(6):1486-91. doi: 10.1152/ajplegacy.1975.229.6.1486.

Abstract

Left atrial pacing was performed in three groups of anesthetized dogs. In the first group of eight intact dogs a mean increase in atrial rate (AR) from 140 +/- 7 to 244 +/- 6 was associated with a decrease in urinary osmolality (U osmol) from 631 +/- 72 to 264 +/- 43 mosmol/kg (P less than .001), and free-water clearance (CH20) increased from -.325 +/- .06 to +.355 +/- .15 ml/min (P less than .001). At the same time left atrial pressure (LAP) increased from 6 +/- 1 to 15 +/- 1 mmHg (P less than .001). A second group of studies was performed in six hypophysectomized, steroid-replaced animals receiving 40-50 muU/kg per min of antidiuretic hormone (ADH). In these animals AR was increased from 148 +/- 17 to 250 +/- 17 but diuresis did not occur. In these studies Uosmol was 690 +/- 55 before and 704 +/- 49 mosmol/kg after atrial pacing and CH20 also did not change. Left atrial pressure increased from 10 +/- 2 to 19 +/- 2 mmHg during atrial pacing. A third group of studies was performed in five animals with bilateral cervical vagotomy. In these animals AR was increased from 159 +/- 6 to 258 +/- 17 and LAP increased from 7 +/- 1 to 16 +/- 2 mmHg. Osmolality increased from 808 +/- 72 to 1,049 +/- 65 musmol/kg (P less than .005) and CH20 was unchanged. These results, therefore, indicate that atrial tachycardia primarily increases renal water excretion by suppressing ADH release. This reflex is dependent on the integrity of cervical vagal pathways.

摘要

对三组麻醉犬进行左心房起搏。在第一组8只完整的犬中,心房率(AR)平均从140±7次/分钟增加到244±6次/分钟,同时尿渗透压(U osmol)从631±72毫摩尔/千克降至264±43毫摩尔/千克(P<0.001),自由水清除率(CH20)从-0.325±0.06毫升/分钟增加到+0.355±0.15毫升/分钟(P<0.001)。同时,左心房压力(LAP)从6±1毫米汞柱增加到15±1毫米汞柱(P<0.001)。在第二组研究中,对6只垂体切除并用类固醇替代、接受每分钟40-50微单位/千克抗利尿激素(ADH)的动物进行实验。在这些动物中,AR从148±17次/分钟增加到250±17次/分钟,但未出现利尿现象。在这些研究中,心房起搏前Uosmol为690±55,起搏后为704±49毫摩尔/千克,CH20也未改变。心房起搏期间,LAP从10±2毫米汞柱增加到19±2毫米汞柱。在第三组研究中,对5只双侧颈迷走神经切断的动物进行实验。在这些动物中,AR从159±6次/分钟增加到258±17次/分钟,LAP从7±1毫米汞柱增加到16±2毫米汞柱。渗透压从808±72微摩尔/千克增加到1049±65微摩尔/千克(P<0.005),CH20未改变。因此,这些结果表明,房性心动过速主要通过抑制ADH释放来增加肾脏水排泄。这种反射依赖于颈迷走神经通路的完整性。

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