Central nervous system norepinephrine release during hypotension and hyperosmolality in conscious rats.

Central nervous system norepinephrine release during hypotension and hyperosmolality in conscious rats.
复制标题

清醒大鼠低血压和高渗透压期间中枢神经系统去甲肾上腺素释放。

DOI:
10.1152/ajpregu.1991.260.6.r1071
复制
发表时间:
1991
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Bealer,SL
Bealer,SL
中科院分区:
--
文献类型:
--
作者:
VanHuysse,JW;Bealer,SL

文献摘要

被引文献

相似文献

通过体内微透析,在出血(Hem)或2-氯腺苷(2-Cl-ADO, 2.6-26.0微克/分静脉注射)引起的持续低血压(平均动脉压75 mmHg)之前、期间和之后,评估清醒的Sprague-Dawley大鼠室旁/下丘脑前区(P/A)和髓内背内侧(DM)的细胞外去甲肾上腺素(NE)水平。同时测定高渗盐水输注(HTS)前、中、后的P/A和DM NE。100努力解决。最低为1(四)。P/A和DM NE在Hem和2-Cl-ADO期间均升高,在回输出血或2-Cl-ADO停止后恢复到基线水平。然而,Hem比2-Cl-ADO引起的P/A - NE的增加更大,尽管血压也相应降低。Hem和2-Cl-ADO在DM NE中产生相同的变化。尽管血压升高约15 mmHg,血浆渗透压升高约30 mosmol/kgH2O, HTS并未改变P/A或DM NE。我们得出结论:1)低血压增加P/A和DM NE,这可能介导代偿反应;2)Hem比2- cl - ado诱导的等容性低血压更有效地刺激P/A中NE的释放;3)高血压对HTS的反应不涉及P/A或DM NE的改变。
Extracellular norepinephrine (NE) levels in the paraventricular/anterior hypothalamic area (P/A) and in the dorsomedial medulla (DM) in conscious Sprague-Dawley rats were estimated by in vivo microdialysis before, during, and after sustained hypotension (75 mmHg mean arterial pressure) produced either by hemorrhage (Hem) or by 2-chloroadenosine infusion (2-Cl-ADO, 2.6-26.0 micrograms/min iv). P/A and DM NE were also measured before, during, and after hypertonic saline infusion (HTS; 1.5 M NaCl at 10 microliters.100 g-1.min-1 iv). P/A and DM NE increased during both Hem and 2-Cl-ADO and returned to baseline after reinfusion of hemorrhaged blood or after 2-Cl-ADO was stopped. However, Hem caused greater increases in P/A NE than 2-Cl-ADO despite equivalent decreases in blood pressure. Hem and 2-Cl-ADO produced equivalent changes in DM NE. HTS did not change P/A or DM NE despite increases in blood pressure of approximately 15 mmHg and plasma osmolality of approximately 30 mosmol/kgH2O. We conclude that 1) hypotension increases P/A and DM NE, which may mediate compensatory responses, 2) Hem is a more potent stimulus for NE release in the P/A than isovolemic hypotension induced by 2-Cl-ADO, and 3) the hypertensive response to HTS does not involve changes in P/A or DM NE.