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去氧皮质酮盐性高血压大鼠对出血应激的交感肾上腺反应增强。

Enhanced sympathoadrenal reactivity to haemorrhagic stress in DOCA-salt hypertensive rats.

作者信息

Drolet G, Bouvier M, de Champlain J

机构信息

Département de Physiologie, Faculté de Médecine, Université de Montréal, Québec, Canada.

出版信息

J Hypertens. 1989 Mar;7(3):237-42. doi: 10.1097/00004872-198903000-00011.

Abstract

The effect of haemorrhagic hypotension on plasma catecholamine levels was studied in anesthetized normotensive and DOCA-salt hypertensive rats. The basal levels of plasma norepinephrine (NE) were significantly higher in DOCA-salt hypertensive rats than in normotensive rats. Moreover, the elevations in plasma NE and epinephrine (E) levels induced by haemorrhagic hypotension were found to be markedly potentiated in DOCA-salt hypertensive rats. Pretreatment with the re-uptake blocker (desmethylimipramine) increased both basal and haemorrhage NE levels in DOCA-salt hypertensive as well as in normotensive rats. Consequently, basal and haemorrhage NE plasma levels remained significantly higher in the DOCA-salt hypertensive animals than in the normotensive rats even following neuronal re-uptake blockage. This suggests that the elevated NE concentrations found in the plasma of DOCA-salt hypertensive rats both under basal condition and during haemorrhagic hypotension do not reflect a defective re-uptake. Moreover, in contrast with what is observed in normotensive animals, bilateral adrenalectomy did not induce any increase in basal or haemorrhage NE levels in the DOCA-salt hypertensive rats. This constitutes yet more evidence supporting the existence of an impaired balance of the sympatho-adrenal axis in this hypertension model. The present study therefore suggests that the potentiated plasma catecholamine response to haemorrhage in DOCA-salt hypertensive rats is the consequence of an increased sympathoadrenal reactivity and not of an altered neuronal uptake. This hyperreactivity may result from an impaired regulation of the sympatho-adrenal axis in that hypertension model.

摘要

在麻醉的正常血压大鼠和去氧皮质酮-盐高血压大鼠中研究了出血性低血压对血浆儿茶酚胺水平的影响。去氧皮质酮-盐高血压大鼠的血浆去甲肾上腺素(NE)基础水平显著高于正常血压大鼠。此外,发现出血性低血压诱导的血浆NE和肾上腺素(E)水平升高在去氧皮质酮-盐高血压大鼠中明显增强。用再摄取阻滞剂(去甲丙咪嗪)预处理可增加去氧皮质酮-盐高血压大鼠和正常血压大鼠的基础NE水平和出血后NE水平。因此,即使在神经元再摄取受阻后,去氧皮质酮-盐高血压动物的基础和出血后NE血浆水平仍显著高于正常血压大鼠。这表明在基础状态和出血性低血压期间,去氧皮质酮-盐高血压大鼠血浆中升高的NE浓度并不反映再摄取缺陷。此外,与正常血压动物中观察到的情况相反,双侧肾上腺切除术并未导致去氧皮质酮-盐高血压大鼠的基础或出血后NE水平升高。这构成了更多证据,支持该高血压模型中交感-肾上腺轴平衡受损的存在。因此,本研究表明,去氧皮质酮-盐高血压大鼠对出血的血浆儿茶酚胺反应增强是交感肾上腺反应性增加的结果,而非神经元摄取改变的结果。这种高反应性可能是由于该高血压模型中交感-肾上腺轴调节受损所致。

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