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突触后α1肾上腺素能受体超敏反应是否导致自主神经反射异常?

Does postsynaptic alpha 1-adrenergic receptor supersensitivity contribute to autonomic dysreflexia?

作者信息

Landrum L M, Thompson G M, Blair R W

机构信息

Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA.

出版信息

Am J Physiol. 1998 Apr;274(4):H1090-8. doi: 10.1152/ajpheart.1998.274.4.H1090.

DOI:10.1152/ajpheart.1998.274.4.H1090
PMID:9575911
Abstract

Quadriplegics often experience periods of severe hypertension known as autonomic dysreflexia. Clinically, these events have been well documented, but the mechanisms for mediating autonomic dysreflexia remain unclear. We used a chronic rat model to investigate the potential development of supersensitivity at postsynaptic alpha 1-adrenergic receptors as a contributing factor to the exaggerated sympathetic response characteristic of autonomic dysreflexia. Adult male Wistar and Sprague-Dawley rats were anesthetized and given spinal transection at T5. After 30 days, rats were reanesthetized and arterial and venous catheters implanted. Twenty-four hours later, colorectal distension (CRD) was used to evoke autonomic dysreflexia in conscious, spinalized rats. To gauge changes in alpha 1-receptor sensitivity, we assessed mean arterial pressure (MAP) in response to intravenous phenylephrine (PE) infusions. No consistent differences were observed between intact and spinalized rats. Therefore, supersensitivity of alpha 1-receptors cannot completely account for the hypertensive bouts associated with autonomic dysreflexia. In addition, while attempting to develop an appropriate model for autonomic dysreflexia, we discovered that spinalized Wistar rats exhibited MAP responses characteristic of autonomic dysreflexia, whereas lesioned Sprague-Dawley rats did not, when subjected to CRD. Thus Wistar rats provide a better animal model for autonomic dysreflexia.

摘要

四肢瘫痪者常经历称为自主神经反射异常的严重高血压期。临床上,这些事件已有充分记录,但介导自主神经反射异常的机制仍不清楚。我们使用慢性大鼠模型来研究突触后α1 - 肾上腺素能受体超敏反应的潜在发展,这是自主神经反射异常特征性交感反应过度的一个促成因素。成年雄性Wistar和Sprague - Dawley大鼠麻醉后在T5水平进行脊髓横断。30天后,大鼠再次麻醉并植入动脉和静脉导管。24小时后,对清醒的脊髓损伤大鼠使用结直肠扩张(CRD)诱发自主神经反射异常。为了评估α1受体敏感性的变化,我们评估了静脉注射去氧肾上腺素(PE)时的平均动脉压(MAP)。完整大鼠和脊髓损伤大鼠之间未观察到一致的差异。因此,α1受体超敏反应不能完全解释与自主神经反射异常相关的高血压发作。此外,在尝试建立自主神经反射异常的合适模型时,我们发现脊髓损伤的Wistar大鼠在接受CRD时表现出自主神经反射异常的MAP反应特征,而损伤的Sprague - Dawley大鼠则没有。因此,Wistar大鼠为自主神经反射异常提供了更好的动物模型。

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