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等渗性中心血容量扩张抑制正常人血浆精氨酸加压素。

Isoosmotic central blood volume expansion suppresses plasma arginine vasopressin in normal man.

作者信息

Epstein M, Preston S, Weitzman R E

出版信息

J Clin Endocrinol Metab. 1981 Feb;52(2):256-62. doi: 10.1210/jcem-52-2-256.

Abstract

Despite numerous studies which have characterized the regulation of antidiuretic hormone (ADH), the role of volume in governing ADH release remains incompletely defined. Most studies have examined the quantitative effects of hypovolemia on arginine vasopressin (AVP). In contrast, few have assessed the role of hypervolemia on AVP regulation. Furthermore, there are no data to date on the effect of acute isoosmotic volume expansion on plasma AVP in man. The successful characterization of the water immersion model (NI) and the demonstration that it induces an acute central volume expansion without changes in plasma composition commended its utilization in the present study. Twelve normal subjects were studied after 14 h of dehydration on two occasions: control and during 4 h of NI. Blood was obtained every 30 min for AVP. AVP was unaltered during the control period. In contrast, there was a prompt and sustained suppression of AVP throughout NI (P < 0.05 vs. control). There were no concomitant changes in plasma osmolality. Since the changes in AVP occurred consequent to central volume expansion but in the absence of concomitant changes in plasma composition, the current data support the concept that acute isoosmotic central volume expansion in man results in a suppression of plasma AVP.

摘要

尽管已有大量研究对抗利尿激素(ADH)的调节机制进行了描述,但血容量在控制ADH释放中所起的作用仍未完全明确。大多数研究探讨了血容量过低对精氨酸加压素(AVP)的定量影响。相比之下,很少有研究评估血容量过高对AVP调节的作用。此外,迄今为止,尚无关于急性等渗性血容量扩张对人体血浆AVP影响的数据。成功建立的水浸模型(NI)以及该模型能诱导急性中枢血容量扩张且血浆成分无变化的特性,促使本研究采用该模型。对12名正常受试者进行了两次研究,每次研究均先进行14小时脱水:一次作为对照,另一次在水浸4小时期间进行。每隔30分钟采集血液检测AVP。对照期内AVP无变化。相比之下,在整个水浸期间AVP迅速且持续受到抑制(与对照相比,P < 0.05)。血浆渗透压没有相应变化。由于AVP的变化是中枢血容量扩张所致,且血浆成分没有相应改变,因此目前的数据支持这样的观点:人体急性等渗性中枢血容量扩张会导致血浆AVP受到抑制。

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