Translational research : the journal of laboratory and clinical medicine · 2026
Cervical Cord Compression-Induced Hypertension: A Treatable Neurogenic Vascular Disorder.
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Lin Chi-Wei, Huang Shiang-Suo, Kuo Terry B J, She Sheng-Chieh, Chen Chun-Hsiu, Yang Cheryl C H, Chu Ya-Chun
Аннотация
BACKGROUND: Decompression surgery has been reported to attenuate hypertension in patients with cervical cord stenosis; however, the causal relationship and underlying neurobiological mechanisms remain unclear. We investigated whether cervical spinal cord compression induces blood pressure (BP) elevation and evaluated the therapeutic effects of decompression in a rodent model.
METHODS: Male Wistar Kyoto rats (17-week-old) were randomized into sham (n=13) or compression (Com) groups after baseline (Bas) assessments. Following 3 weeks of compression, the Com group was subdivided into persistent compression (n=10) or decompression (n=11) groups. BP, heart rate variability (HRV) derived autonomic function and sensorimotor behaviors were monitored at Bas, post-compression week 3 (Comp-W3) and decompression week 2 (Decomp-W2). Spinal cord tissues were collected after Decomp-W2 for biochemical analysis.
RESULTS: BP significantly increased following persistent compression and returned to baseline levels after decompression. Spinal cord norepinephrine (NE) levels increased with compression but normalized following decompression. In contrast, neuropeptide Y (NPY) and NPY type 2 receptor (NPY2R) expression increased after compression and remained upregulated despite decompression. Compression-induced reactive astrogliosis and amoeboid microglial activation were significantly reversed following decompression. Notably, in contrast to the BP normalization, a reduction in cardiac sympathetic activity persisted throughout the post-decompression phase.
CONCLUSIONS: Our findings revealed the potential relationship between mechanical cervical spinal cord compression and hypertension, identifying local NE accumulation and neuroinflammation as key drivers. We demonstrate that surgical decompression effectively mitigates cardiovascular risks by restoring the spinal microenvironment, providing a novel clinical rationale for BP management in patients with cervical cord stenosis.
METHODS: Male Wistar Kyoto rats (17-week-old) were randomized into sham (n=13) or compression (Com) groups after baseline (Bas) assessments. Following 3 weeks of compression, the Com group was subdivided into persistent compression (n=10) or decompression (n=11) groups. BP, heart rate variability (HRV) derived autonomic function and sensorimotor behaviors were monitored at Bas, post-compression week 3 (Comp-W3) and decompression week 2 (Decomp-W2). Spinal cord tissues were collected after Decomp-W2 for biochemical analysis.
RESULTS: BP significantly increased following persistent compression and returned to baseline levels after decompression. Spinal cord norepinephrine (NE) levels increased with compression but normalized following decompression. In contrast, neuropeptide Y (NPY) and NPY type 2 receptor (NPY2R) expression increased after compression and remained upregulated despite decompression. Compression-induced reactive astrogliosis and amoeboid microglial activation were significantly reversed following decompression. Notably, in contrast to the BP normalization, a reduction in cardiac sympathetic activity persisted throughout the post-decompression phase.
CONCLUSIONS: Our findings revealed the potential relationship between mechanical cervical spinal cord compression and hypertension, identifying local NE accumulation and neuroinflammation as key drivers. We demonstrate that surgical decompression effectively mitigates cardiovascular risks by restoring the spinal microenvironment, providing a novel clinical rationale for BP management in patients with cervical cord stenosis.