Jung-Shun Lee1, Shih-Yuan Fang2, Jun-Neng Roan3, I-Ming Jou4, Chen-Fuh Lam5. 1. Divisions of Neurosurgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Rd, Tainan 704, Taiwan. 2. Department of Anesthesiology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Rd, Tainan 704, Taiwan. 3. Divisions of Cardiovascular Surgery, Department of Surgery, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Rd, Tainan 704, Taiwan. 4. Department of Orthopedics, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Rd, Tainan 704, Taiwan. 5. Department of Anesthesiology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, 138 Sheng Li Rd, Tainan 704, Taiwan; Department of Anesthesiology, Buddhist Tzu Chi General Hospital and Tzu Chi University School of Medicine, 707 Chung Yang Rd Section 3, Hualien 907, Taiwan. Electronic address: lamcf@mail.tcu.edu.tw.
Abstract
BACKGROUND CONTEXT: 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.
BACKGROUND CONTEXT: 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.
Authors: Syed A Quadri; Mudassir Farooqui; Asad Ikram; Atif Zafar; Muhammad Adnan Khan; Sajid S Suriya; Chad F Claus; Brian Fiani; Mohammed Rahman; Anirudh Ramachandran; Ian I T Armstrong; Muhammad A Taqi; Martin M Mortazavi Journal: Neurosurg Rev Date: 2018-07-11 Impact factor: 3.042