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清醒大鼠低血压和高渗状态下中枢神经系统去甲肾上腺素的释放

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

作者信息

Van Huysse J W, Bealer S L

机构信息

Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.

出版信息

Am J Physiol. 1991 Jun;260(6 Pt 2):R1071-6. doi: 10.1152/ajpregu.1991.260.6.R1071.

Abstract

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.

摘要

通过体内微透析技术,对清醒的斯普拉格-道利大鼠在持续性低血压(平均动脉压75mmHg)产生前、产生期间和产生后,测量其室旁/下丘脑前部区域(P/A)和延髓背内侧(DM)的细胞外去甲肾上腺素(NE)水平。持续性低血压由出血(Hem)或静脉输注2-氯腺苷(2-Cl-ADO,2.6 - 26.0微克/分钟)引起。在静脉输注高渗盐水(HTS;1.5M NaCl,10微升/100克体重·分钟)前、期间和之后,也对P/A和DM NE进行了测量。在Hem和2-Cl-ADO过程中,P/A和DM NE均升高,在回输出血的血液或停止输注2-Cl-ADO后恢复至基线水平。然而,尽管血压下降程度相同,但Hem引起的P/A NE升高幅度大于2-Cl-ADO。Hem和2-Cl-ADO引起的DM NE变化相当。尽管血压升高约15mmHg且血浆渗透压升高约30mOsmol/kgH₂O,但HTS并未改变P/A或DM NE。我们得出以下结论:1)低血压会增加P/A和DM NE,这可能介导代偿反应;2)与2-Cl-ADO诱导的等容性低血压相比,Hem是P/A中NE释放的更强刺激因素;3)对HTS的高血压反应不涉及P/A或DM NE的变化。

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