Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Vic 3010, Australia.
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Vic 3010, Australia; Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, Vic 3010, Australia; Baker IDI Heart and Diabetes Institute, Melbourne, Vic 3010, Australia.
Brain Res. 2021 Feb 1;1752:147223. doi: 10.1016/j.brainres.2020.147223. Epub 2020 Dec 23.
Previous experiments in rodents showed that ablation of the septal brain region caused hyperdipsia. We investigated which part of the septal region needs ablation to produce hyperdipsia in sheep, and whether increased drinking was a primary hyperdipsia. Following ablation of the medial septal region (n = 5), but not parts of the lateral septal region (n = 4), daily water intake increased from ~2.5-5 L/day up to 10 L/day for up to 3 months post-lesion. In hyperdipsic sheep, plasma osmolality increased on the first day post-lesion and body weight fell, suggesting that initial hyperdipsia was secondary to fluid loss. However hyperosmolality was not sustained long-term and plasma hypo-osmolality persisted from 0.5 to 3 months post-lesion. Acute dipsogenic responses to intravenous hypertonic saline, intravenous or intracerebroventricular angiotensin II, water deprivation for 2 days, or feeding over 5 h were not potentiated by medial septal lesions, showing that the rapid pre-systemic inhibitory influences that cause satiation of thirst upon the act of drinking were intact. However, hyperdipsic sheep continued to ingest water when hyponatremic (plasma [Na] was 127-132 mmol/l) and plasma osmolality was 262-268 mosmol/kg due to retention of ingested fluid resulting from intravenous infusion of vasopressin administered to maintain a basal blood level of antidiuretic hormone. The results show that septal lesion-induced hyperdipsia is not due to disruption of acute pre-systemic influences associated with drinking water that initiates rapid satiation of thirst. Rather, inhibitory influences of hyponatremia, hypo-osmolality or hypervolemia on drinking appear to be disrupted by medial septal lesions.
先前在啮齿动物中的实验表明，隔区脑区的消融会导致多饮症。我们研究了在绵羊中需要消融隔区的哪个部位才能产生多饮症，以及增加的饮水量是否是原发性多饮症。在消融内侧隔区（n=5）后，但不消融外侧隔区的部分区域（n=4），绵羊的日饮水量从~2.5-5 L/天增加到 10 L/天，持续了 3 个月。在多饮性绵羊中，损伤后第一天血浆渗透压升高，体重下降，表明最初的多饮症继发于液体丢失。然而，高渗血症并未长期持续，并且血浆低渗血症从损伤后 0.5 个月持续到 3 个月。静脉内高渗盐水、静脉内或脑室内血管紧张素 II、2 天禁水或 5 小时以上进食等急性引起饮水的刺激反应，并未因内侧隔区损伤而增强，表明在饮水时快速的全身前抑制性影响会使口渴感得到满足。然而，由于给予抗利尿激素以维持基础血液水平的血管加压素的静脉输注导致摄入的液体潴留，低钠血症（血浆[Na]为 127-132 mmol/l）和血浆渗透压为 262-268 mosmol/kg 的情况下，多饮性绵羊仍继续饮水。结果表明，隔区损伤引起的多饮症不是由于与饮水相关的急性全身前抑制性影响的破坏引起的，而这种影响会迅速使口渴感得到满足。相反，低钠血症、低渗透压或高血容量对饮水的抑制性影响似乎被内侧隔区损伤所破坏。
