Bell F R, Doris P A, Simmonds A
Department of Physiology and Biochemistry, University of Reading, UK.
Neuroendocrinology. 1988 Sep;48(3):217-22. doi: 10.1159/000125014.
Angiotensin II (AII), arginine vasopressin (AVP) and prolactin (PRL) were measured by radioimmunoassay in plasma and cerebrospinal fluid (CSF) in concurrent daily samples from conscious unrestrained steers. Packed cell volume, [Na+] and osmolality were also measured from these samples. Salt appetite was assessed during a 5-min daily session of operant conditioning. Food and water was always available. Unilateral parotid duct fistulation was effected under xylazine analgesia and halothane/O2 anaesthesia. To prevent a sodium deficit developing from loss of [Na+] in the extruded saliva, 0.3 M NaHCO3 was available ad libitum so that each animal could ingest sufficiently to balance the salivary loss. A week later epidural cannulae were implanted in the cisternae magna using the same anaesthesia. Three days afterwards when the saliva [Na] was 78 mmol/1, the 0.3-M NaHCO3 supplement was withdrawn for 7 days so that sodium deficiency developed to a degree which evoked salt appetite. When the NaHCO3 supplement was restored ad libitum, all aspects of [Na+] deficiency and salt appetite were completely ameliorated within 2-3 days. Packed cell volume increased and body weight decreased (p less than 0.05) during depletion, but rapidly returned to normal on day 2 of repletion. Both plasma and CSF osmolality were reduced during depletion as were plasma [Na+] (p less than 0.01) and CSF [Na+] (p less than 0.001). From a basal value of 64.7 +/- 9.35 fmol/ml on day 0, plasma AII increased to 229.2 +/- 46.65 fmol/ml (p less than 0.001) on day 3, prior to the onset of salt appetite on days 4-7. In marked contrast to plasma AII during sodium depletion, CSF AII was unchanged during salt appetite. There was no correlation between plasma and CSF AII during behavioural salt appetite.(ABSTRACT TRUNCATED AT 250 WORDS)
通过放射免疫分析法,对清醒自由活动的公牛每日采集的血浆和脑脊液样本中的血管紧张素II(AII)、精氨酸加压素(AVP)和催乳素(PRL)进行了测量。同时还对这些样本的血细胞比容、[Na⁺]和渗透压进行了测量。在每天5分钟的操作性条件反射实验中评估盐食欲。食物和水随时可得。在赛拉嗪镇痛和氟烷/O₂麻醉下进行单侧腮腺导管造瘘术。为防止因挤出唾液中[Na⁺]流失而出现钠缺乏,随意提供0.3M的NaHCO₃,以便每只动物能够摄入足够量以平衡唾液流失。一周后,在相同麻醉下于枕大池植入硬膜外套管。三天后,当唾液[Na]为78 mmol/L时,停用0.3M的NaHCO₃补充剂7天,以使钠缺乏发展到引发盐食欲的程度。当恢复随意补充NaHCO₃时,[Na⁺]缺乏和盐食欲的所有方面在2 - 3天内完全得到改善。在缺钠期间,血细胞比容增加而体重下降(p < 0.05),但在补充的第2天迅速恢复正常。缺钠期间血浆和脑脊液渗透压均降低,血浆[Na⁺](p < 0.01)和脑脊液[Na⁺](p < 0.001)也降低。在第0天血浆AII的基础值为64.7±9.35 fmol/ml,在第3天,即在第4 - 7天出现盐食欲之前,血浆AII增加到229.2±46.65 fmol/ml(p < 0.001)。与缺钠期间的血浆AII形成显著对比的是,在有盐食欲期间脑脊液AII未发生变化。在行为性盐食欲期间,血浆和脑脊液AII之间无相关性。(摘要截取自250字)