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Reproducible Motor Deficit Following Aortic Occlusion in a Rat Model Of Spinal Cord Ischemia
Published on: July 22, 2017
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Profound Hypotension before Aortic Clamping Can Exacerbate Spinal Cord Ischemic Injury after Aortic Surgery in Rats
Chang-Hoon Koo1, Jung-Hee Ryu1,2, Jin-Young Hwang2,3
1Department of Anesthesiology & Pain medicine, Seoul National University Bundang Hospital, Seongnam 13620, Korea.
Journal of Clinical Medicine
|October 29, 2020
Summary
Profound hypotension before aortic clamping worsens spinal cord injury after aortic surgery. This exacerbates neurological deficits and reduces motor neuron survival, highlighting the critical role of maintaining blood pressure.
Area of Science:
- Cardiovascular Surgery
- Neurology
- Pathophysiology
Background:
- Spinal cord ischemia is a severe complication following aortic repair in acute aortic syndrome.
- The impact of pre-aortic clamping hypotension on spinal cord injury remains unclear.
Purpose of the Study:
- To investigate the effect of varying degrees of hypotension before aortic clamping on spinal cord injury.
- To evaluate neurological function, histopathology, oxidative stress, and inflammation.
Main Methods:
- 48 male Sprague-Dawley rats were divided into sham, control, mild hypotension, and profound hypotension groups.
- Spinal cord ischemia was induced via aortic catheterization.
- Neurological function (Motor Deficit Index), spinal cord histology, oxidative stress (malondialdehyde), and inflammation (TNF-α) were assessed.
Main Results:
- Profound hypotension significantly increased Motor Deficit Index 48 hours post-reperfusion.
- The profound hypotension group showed a lower number of normal motor neurons.
- Increased levels of malondialdehyde and TNF-α were observed in the profound hypotension group.
Conclusions:
- Profound hypotension before aortic clamping aggravates neurological outcomes after aortic surgery.
- This is mediated by increased neurological injury, reduced motor neuron count, oxidative stress, and inflammation.

