Spinal cord injury enhances arterial expression and reactivity of α1-adrenergic receptors—mechanistic investigation into autonomic dysreflexia

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• 作者：Jung-Shun Lee ; MD ; MSc^a ; Shih-Yuan Fang ; MD^b ; Jun-Neng Roan ; MD^c ; I-Ming Jou ; MD^d ; Chen-Fuh Lam ; MD ; PhD^b ; ^e ; ^{lamcf@mail.tcu.edu.tw" class="auth_mail" title="E-mail the corresponding author}
• 关键词：α-1 adrenergic receptor ; Autonomic dysreflexia ; Autonomic hyperreflexia ; Hypertension ; Neuroaxial denervation ; Phenylephrine ; Spinal cord injury ; Sympathetic activity ; Vasoreactivity ; Vascular smooth muscle
• 刊名：The Spine Journal
• 出版年：2016
• 出版时间：1 January 2016
• 年：2016
• 卷：16
• 期：1
• 页码：65-71
• 全文大小：1354 K

文摘

Autonomic dysreflexia (AD) usually presents with a significant increase in blood pressure, and uncontrollable autonomic response to stimuli below the level of spinal cord injury (SCI).

Purpose

This study analyzed the vasomotor function and molecular changes in the peripheral arteries below the lesion of SCI to characterize the mechanism of autonomic dysreflexia.

Study Design

This was a randomized experimental study in rats.

Methods

Contusive SCI was induced using a force-calibrated weight-drop device at the T10 level in anesthetized rats. Two weeks after severe SCI, blood flow in the femoral arteries was measured, and the vasomotor function and expression of α1-adrenergic receptors were analyzed.

Results

Blood flow in the femoral artery was significantly reduced in rats with SCI (8.0±2 vs. 17.5±4 mL/min, SCI vs. control, respectively; p=.016). The contraction responses of femoral artery segments to cumulative addition of α1-adrenergic agonist phenylephrine were significantly enhanced in rats with SCI. Expression of α1-adrenergic receptor was upregulated in the medial layer of femoral artery vascular homogenates of these rats.

Conclusion

Our study provides evidence demonstrating that prolonged denervation below the lesion level following SCI results in a compensatory increased expression of α1-adrenergic receptors in the arterial smooth muscle layer, thereby enhancing the responsiveness to α1-adrenergic agonist and potentiating the development of AD.