Dreyfuss D, Leviel F, Sperandio M, Paillard M, Marty J, Coste F
Service de Réanimation Médicale, Hôpital Louis Mourier, Colombes, France.
Intensive Care Med. 1990;16(5):323-7. doi: 10.1007/BF01706358.
The pathogenesis of excessive arginine vasopressin (AVP) release and hyponatraemia in euvolaemic intensive care unit (ICU) patients is poorly understood. Stress has frequently been proposed as a possible determinant, but its actual responsibility has not been adequately assessed. Therefore, water-load tests were prospectively performed in 11 patients admitted to the ICU for severe or potentially severe diseases, but who had no other condition which could result in excessive AVP release or impairment of renal diluting ability. Renal diluting ability was normal in 9 patients. Two patients exhibited very slight defects, which might be the consequence of subclinical haemodynamic alterations, since one had a pulmonary embolism and the other manifested a gastrointestinal haemorrhage just after the completion of the water load. Nevertheless, plasma AVP levels decreased in response to the water load in all the patients, resulting in a significant decrease in mean values. Plasma norepinephrine values were found to be elevated both before and after water loading. A highly significant correlation existed between the levels of norepinephrine and those of AVP measured before the load, but was lost after it. In addition, norepinephrine values were markedly elevated in two patients who exhibited strictly normal renal diluting abilities, and no correlation was found between plasma norepinephrine values and any parameter of renal water excretion. Our study shows that the stress of a serious illness and of admission to an ICU does not seem to interfere, by itself, with osmotic regulation of AVP secretion and renal diluting ability, and that sympathetic activation is not, under such circumstances, a predominant stimulus for AVP release.(ABSTRACT TRUNCATED AT 250 WORDS)
对于血容量正常的重症监护病房(ICU)患者,精氨酸血管加压素(AVP)分泌过多及低钠血症的发病机制目前尚不清楚。应激反应常被认为是一个可能的决定因素,但其实际作用尚未得到充分评估。因此,我们对11名因患严重或潜在严重疾病而入住ICU的患者进行了前瞻性水负荷试验,这些患者不存在其他可导致AVP分泌过多或肾稀释能力受损的情况。9名患者的肾稀释能力正常。两名患者存在非常轻微的缺陷,这可能是亚临床血流动力学改变的结果,因为其中一名患者发生了肺栓塞,另一名患者在水负荷试验结束后出现了胃肠道出血。然而,所有患者的血浆AVP水平在水负荷后均下降,导致平均值显著降低。发现水负荷前后血浆去甲肾上腺素值均升高。负荷前测量的去甲肾上腺素水平与AVP水平之间存在高度显著的相关性,但负荷后这种相关性消失。此外,两名肾稀释能力完全正常的患者的去甲肾上腺素值明显升高,且血浆去甲肾上腺素值与肾排水的任何参数之间均未发现相关性。我们的研究表明,重症疾病及入住ICU所带来的应激反应本身似乎并不干扰AVP分泌的渗透调节和肾稀释能力,在这种情况下,交感神经激活并不是AVP释放的主要刺激因素。(摘要截选至250字)