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纳洛酮对自发性高血压大鼠低血压性出血期间脑功能的影响。

The effects of naloxone on cerebral function in spontaneously hypertensive rats during hypotensive haemorrhage.

作者信息

Skarphedinsson J O, Thorén P

出版信息

Acta Physiol Scand. 1986 Dec;128(4):597-604. doi: 10.1111/j.1748-1716.1986.tb08017.x.

Abstract

The purpose of this study was to examine the effects of naloxone on signs of relative cerebral ischaemia induced by hypotensive haemorrhage. Mean arterial blood pressure (MAP), heart rate (HR), renal sympathetic nerve activity (rSNA) and somatosensory evoked potentials (SEP) were recorded in chloralose-anaesthetized spontaneously hypertensive rats exposed to graded bleeding. Hypotensive haemorrhage resulted, after a very brief sympathetic excitation, in marked sympathetic inhibition and bradycardia and a considerable reduction of SEP, indicating relative cerebral ischaemia. However, after 25-30 min this sympatho-inhibitory response was reversed to pronounced sympathetic excitation and tachycardia, which was accompanied by a further attenuation of SEP. A single bolus of naloxone (10 mg kg-1) caused transient sympathetic inhibition and bradycardia, which was accompanied by an improvement of SEP. A bolus injection (5-10 mg kg-1) followed by a 30 min infusion of naloxone (25-35 mg kg-1 h-1) caused a sustained SEP improvement despite the fact that MAP was kept constant during naloxone administration. We conclude that naloxone can have beneficial effects on brain function during cerebral ischaemia, effects that are probably due to blockade of opioid receptors. Our model of relative cerebral ischaemia might be useful for evaluating the mechanisms behind the naloxone effects during this condition.

摘要

本研究的目的是检验纳洛酮对低血压性出血所致相对脑缺血体征的影响。在给予水合氯醛麻醉的自发性高血压大鼠进行分级出血时,记录平均动脉血压(MAP)、心率(HR)、肾交感神经活动(rSNA)和体感诱发电位(SEP)。低血压性出血在经过非常短暂的交感神经兴奋后,导致明显的交感神经抑制、心动过缓和SEP显著降低,提示相对脑缺血。然而,25 - 30分钟后,这种交感神经抑制反应转变为明显的交感神经兴奋和心动过速,同时伴有SEP的进一步衰减。单次静脉注射纳洛酮(10 mg kg-1)引起短暂的交感神经抑制和心动过缓,同时SEP有所改善。静脉注射一次(5 - 10 mg kg-1)后,持续输注纳洛酮30分钟(25 - 35 mg kg-1 h-1),尽管在输注纳洛酮期间MAP保持恒定,但SEP仍持续改善。我们得出结论,纳洛酮在脑缺血期间可对脑功能产生有益影响,这些影响可能是由于阿片受体被阻断所致。我们的相对脑缺血模型可能有助于评估在此情况下纳洛酮作用背后的机制。

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