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多系统萎缩中渗透性口渴丧失:与窦主动脉压力感受器传入神经阻滞的关联。

Loss of osmotic thirst in multiple system atrophy: association with sinoaortic baroreceptor deafferentation.

作者信息

Bevilacqua M, Norbiato G, Righini V, Vago T, Castelli L, Carella F, Caraceni T

机构信息

Servizio di Endocrinologia, Luigi Sacco Hospital, Vialba, Italy.

出版信息

Am J Physiol. 1994 Jun;266(6 Pt 2):R1752-8. doi: 10.1152/ajpregu.1994.266.6.R1752.

Abstract

We evaluated plasma osmolality (pOsm), thirst, and vasopressin response to hypertonic saline infusion in 14 patients with multiple system atrophy (MSA). This disease is characterized by the degeneration of noradrenergic neurons in the central nervous system and severe orthostatic hypotension. Seven patients were also characterized by the lack of vasopressin response to hypotension (group B) and seven by a preserved response (group A). In group A pOsm rose from 290 +/- 2 to 312 +/- 6 mosmol/kgH2O, vasopressin from 0.9 +/- 0.3 to 5.7 +/- 0.5 pmol/l, and thirst from 1.1 +/- 0.1 to 8.7 +/- 1.1 cm on the visual analog scale. After saline, patients drank 1,215 +/- 150 ml of water (no different from healthy controls). In group B patients' pOsm rose from 296 +/- 3 to 325 +/- 6 mosmol/kgH2O and vasopressin from 1.2 +/- 0.1 to 19.6 +/- 0.4 pmol/l (P < 0.01 vs. group A and controls). Group B patients had no thirst during saline and drank little after the challenge (175 +/- 50 ml; P < 0.01 vs. group A and control). Forced drinking decreased vasopressin in patients before changes in pOsm, showing that inhibitory afferents from oropharyngeal mucosa were intact. In MSA patients with altered afferent control of vasopressin there is a dissociation between the osmotic control of thirst and the osmotic control of vasopressin.

摘要

我们评估了14例多系统萎缩(MSA)患者输注高渗盐水后的血浆渗透压(pOsm)、口渴感及血管加压素反应。该疾病的特征为中枢神经系统去甲肾上腺素能神经元变性及严重直立性低血压。7例患者血管加压素对低血压无反应(B组),7例反应保留(A组)。A组中,pOsm从290±2升至312±6 mosmol/kgH₂O,血管加压素从0.9±0.3升至5.7±0.5 pmol/l,视觉模拟量表上的口渴感从1.1±0.1升至8.7±1.1 cm。输注盐水后,患者饮水1215±150 ml(与健康对照无差异)。B组患者pOsm从296±3升至325±6 mosmol/kgH₂O,血管加压素从1.2±0.1升至19.6±0.4 pmol/l(与A组及对照组相比,P<0.01)。B组患者在输注盐水期间无口渴感,刺激后饮水少(175±50 ml;与A组及对照组相比,P<0.01)。强制饮水在pOsm改变前降低了患者的血管加压素,表明口咽黏膜的抑制性传入神经完整。在血管加压素传入控制改变的MSA患者中,口渴的渗透控制与血管加压素的渗透控制之间存在分离。

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