The effect of intracerebroventricular indomethacin on osmotically stimulated vasopressin release.

The effect of intracerebroventricular indomethacin on osmotically stimulated vasopressin release.
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脑室内吲哚美辛对渗透刺激加压素释放的影响。

DOI:
10.1159/000123290
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发表时间:
1982
期刊:
影响因子:
4.1
通讯作者:
Shade,RE
Shade,RE
中科院分区:
医学2区
文献类型:
--
作者:
Hoffman,PK;Share,L;Crofton,JT;Shade,RE

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本实验研究了侧脑室注射前列腺素合成抑制剂对加压素(ADH)分泌的渗透压调节作用。在用吲哚美辛(7.6 μg/min)或溶剂进行脑室-脑池灌注期间,向犬静脉输注2.5或0.15 M NaCl。高渗盐水输注使血浆渗透压升高约60 mosm/kg H2O。相应地,在用溶剂进行脑室脑池灌注的动物中,血浆ADH浓度显著增加(从2.1 ± 0.7 μU/ml增加至7.3 ± 1.3 μU/ml);然而,在用吲哚美辛进行灌注的动物中,该反应显著减弱(从1.0 ± 0.2 μU/ml增加至2.2 ± 0.4 μU/ml)。等渗盐水输注引起血浆ADH浓度下降,这是相似的吲哚美辛和车辆灌注组。平均动脉血压在实验过程中没有变化。在一项配套研究中,发现在存在吲哚美辛的情况下,以152 ng PGE 2/min的速度进行脑室池灌注在刺激ADH释放方面与不存在吲哚美辛的情况下一样有效,这表明在第一项研究中吲哚美辛的作用不是非特异性的。脑室内注射吲哚美辛对肾上腺素诱导的ADH释放的抑制作用表明,内源性脑内肾上腺素在渗透压控制ADH分泌中起着重要的中介作用。
Experiments were carried out to investigate the effect of intracerebroventricular administration of a prostaglandin synthesis inhibitor on the osmotic control of vasopressin (ADH) secretion. During ventriculocisternal perfusion with indomethacin (7.6 μg/min) or vehicle, dogs were infused intravenously with either 2.5 or 0.15 M NaCl. Hypertonic saline infusion elevated plasma osmolality approximately 60 mosm/kg H2O. In accordance, the plasma ADH concentration increased substantially in animals perfused ventriculocisternally with the vehicle (from 2.1 ± 0.7 to 7.3 ± 1.3 μU/ml); this response was markedly attenuated, however, in animals perfused with indomethacin (from 1.0 ± 0.2 to 2.2 ± 0.4 μU/ml). Isotonic saline infusion caused a decline in plasma ADH concentration which was similar in the indomethacin- and vehicle-perfused groups. Mean arterial blood pressure was unchanged during the experiments. In a companion study, ventriculocisternal perfusion with 152 ng PGE2/min was found to be as effective in stimulating ADH release in the presence of indomethacin as in its absence, indicating that the action of indomethacin in the first study was not nonspecific. The suppression of osmotically induced ADH release by intracerebroventricular indomethacin suggests that endogenous brain prostaglandins play a critical intermediary role in the osmotic control of ADH secretion.