Rigid and remodelled: cerebrovascular structure and function after experimental high-thoracic spinal cord transection

J Physiol, 2016 · DOI: 10.1113/JP270925 · Published: December 4, 2015

Spinal Cord Injury Cardiovascular Science Neurology

Simple Explanation

Spinal cord injury (SCI) is linked to a significantly higher risk of stroke and problems with how the brain regulates blood flow. However, it's not well understood how SCI affects the structure and function of blood vessels in the brain. This research used a rat model of SCI to show that SCI leads to changes in the structure of cerebral arteries, making them stiffer and less responsive. These changes involve an increase in collagen and a decrease in elastin, possibly driven by a protein called transforming growth factor β. The study found that these changes were not caused by disruption of nerve pathways to the brain's blood vessels. The authors suggest that SCI's effects on exercise capacity, blood volume, and reliance on the renin–angiotensin system may contribute to these vascular issues, potentially explaining the increased risk of stroke and cognitive problems after SCI.

Study Duration

7 weeks

Participants

25 male Wistar rats (15 T3-SCI, 10 Sham)

Evidence Level

Not specified

Key Findings

1
Experimental SCI leads to inward cerebrovascular remodeling, increased stiffness, and impaired reactivity of the largest cerebral artery.
2
SCI induces a profibrotic environment within the largest cerebral artery, characterized by greater collagen and less elastin.
3
Sympathetic innervation and endothelium-dependent dilatation of the MCA were not different between groups.

Research Summary

This study investigated the impact of high-thoracic SCI on cerebrovascular structure and function in rats. Seven weeks post-SCI, researchers assessed the middle cerebral artery (MCA) for structural and functional changes. The findings revealed inward remodeling of the MCA, reduced distensibility, and a trend toward decreased vasoconstrictive reactivity after SCI. The MCA also exhibited increased collagen and decreased elastin, indicating a profibrotic environment. The study concludes that high-thoracic SCI leads to cerebrovascular maladaptation, potentially contributing to the increased risk of stroke and impaired cerebral blood flow regulation observed in SCI patients.

Practical Implications

Therapeutic targets

The study suggests potential therapeutic targets, such as AT1/AT2 receptor blockade or exercise training, to mitigate cerebrovascular dysfunction after SCI.

Clinical interventions

These findings highlight the importance of managing blood pressure and promoting physical activity in individuals with SCI to preserve cerebrovascular health.

Risk mitigation

Understanding the mechanisms underlying cerebrovascular dysfunction after SCI may help develop strategies to reduce the risk of stroke, cognitive decline, and other cerebrovascular complications in this population.

Study Limitations

1
Behavioral outcomes related to cerebrovascular dysfunction were not assessed.
2
Quantification of protein expression was indirect (immunohistochemistry).
3
Greater between-group differences might have occurred for 5-HT if a range of doses were used.

Your Feedback

Was this summary helpful?

Back to Spinal Cord Injury