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麻醉大鼠使用腺苷或硝普钠诱导低血压期间的节前和节后交感神经活动

Pre- and postganglionic sympathetic nerve activity during induced hypotension with adenosine or sodium nitroprusside in the anesthetized rat.

作者信息

Delle M, Ricksten S E, Delbro D

机构信息

Department of Physiology and Anesthesia, Sahlgren's Hospital, University of Göteborg, Sweden.

出版信息

Anesth Analg. 1988 Apr;67(4):307-12.

PMID:2833134
Abstract

The aim of this study was to examine the effects of adenosine (AD)-induced hypotension on preganglionic adrenal (aSNA) and postganglionic renal (rSNA) sympathetic nerve activity. rSNA (n = 10) and aSNA (n = 6) were recorded together with mean arterial pressure (MAP) and heart rate (HR) in chloralose-anesthetized, artificially ventilated rats. In each experiment, hypotension was induced by equihypotensive doses of AD (0.03-2.0 mg.kg-1.min-1) and sodium nitroprusside (SNP) (1-10 micrograms.kg-1.min-1). SNP induced a progressive reflex tachycardia and a reflex increase in rSNA to levels 159 +/- 35% above control at a MAP reduction of 55% of the normotensive control value. Equipotent doses of AD induced a decrease in HR and significantly less pronounced reflex increase in rSNA. The maximal increase in rSNA with AD was 55 +/- 19% at a MAP reduction of 30%. At higher infusions rates of AD, rSNA progressively declined toward the normotensive control values. However, AD elicited a progressive increase in preganglionic aSNA that was not significantly different from the increase seen during SNP infusion. It is concluded that AD-induced hypotension is associated with a suppression of postganglionic sympathetic nerve activity caused by an inhibition of ganglionic neurotransmission.

摘要

本研究的目的是检验腺苷(AD)诱导的低血压对节前肾上腺(aSNA)和节后肾(rSNA)交感神经活动的影响。在水合氯醛麻醉、人工通气的大鼠中,同时记录rSNA(n = 10)和aSNA(n = 6)以及平均动脉压(MAP)和心率(HR)。在每个实验中,通过等降压剂量的AD(0.03 - 2.0 mg·kg⁻¹·min⁻¹)和硝普钠(SNP)(1 - 10 μg·kg⁻¹·min⁻¹)诱导低血压。SNP诱导渐进性反射性心动过速,且在MAP降至正常血压对照值的55%时,rSNA反射性增加至比对照水平高159±35%。等剂量的AD导致心率降低,且rSNA反射性增加明显较弱。AD使rSNA最大增加为55±19%,此时MAP降低30%。在更高的AD输注速率下,rSNA逐渐降至正常血压对照值。然而,AD引起节前aSNA逐渐增加,这与SNP输注期间所见的增加无显著差异。结论是,AD诱导的低血压与神经节神经传递受抑制导致的节后交感神经活动受抑制有关。

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