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Experimental Delayed Postischemic Spinal Cord Hypoperfusion After Aortic Cross-clamping

Published online by Cambridge University Press:  18 September 2015

F. Follis ,
K. Miller ,
O.U. Scremin ,
S. Pett ,
R. Kessler ,
T. Temes  and
J.A. Wernly
F. Follis*
Affiliation:
Department of Thoracic and Cardiovascular Surgery, University of New Mexico, Albuquerque
K. Miller
Affiliation:
Department of Thoracic and Cardiovascular Surgery, University of New Mexico, Albuquerque
O.U. Scremin
Affiliation:
West Los Angeles V.A. Medical Center and Department of Physiology, University of California, Los Angeles School of Medicine, Los Angeles
S. Pett
Affiliation:
Department of Thoracic and Cardiovascular Surgery, University of New Mexico, Albuquerque
R. Kessler
Affiliation:
Department of Thoracic and Cardiovascular Surgery, University of New Mexico, Albuquerque
T. Temes
Affiliation:
Department of Thoracic and Cardiovascular Surgery, University of New Mexico, Albuquerque
J.A. Wernly
Affiliation:
Department of Thoracic and Cardiovascular Surgery, University of New Mexico, Albuquerque
*
University of New Mexico. Department of Thoracic and Cardiovascular Surgery, 2211 Lomas Boulevard, Albuquerque, New Mexico 87131 U.S.A.
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Abstract

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Background

As in the brain, recent evidence has suggested a defect in the microcirculation during the reperfusion period after spinal cord ischemia. This investigation was undertaken in order to delineate blood flow dynamics in the postischemic spinal cord of the rat.

Methods

Male Sprague-Dawley rats underwent cross-clamping of the aorta and subclavian arteries (XC) for 11 minutes. Spinal cord blood flow (SCBF) was measured by autoradiography in the gray and white matter of cervical (Ce), thoracic (Th) and lumbar (Lu) regions during XC, 1 h, 6 h and 24 h (XC n = 8, 1 h n = 9, 6 h n = 9, and 24 h n = 11, groups) after XC. Control groups underwent surgical manipulations and SCBF measurement but no XC (Sham 1, n = 8), or clamping of the subclavian arteries only (Sham 2, n = 8).

Results

In Ce cord, there was no difference between SCBF of 1 h, 6 h, 24 h and Sham 1. In Th cord, SCBF was reduced during XC (P < 0.003 vs. Sham 2), 1 h, 6 h (P < 0.04 and P < 0.01 vs. Sham 1). In Lu cord, SCBF was not detectable in XC, and depressed in 1 h (P < 0.003) and 6 h (P < 0.003). There was no difference between 24 h and Sham 1 in Ce, Th, and Lu cords.

Conclusions

The study demonstrated a period of delayed postischemic hypoperfusion in the white and gray matter of Th and Lu cord segments lasting 6 h after XC. The phenomenon may play an important role in the ultimate fate of neural elements with borderline viability after ischemic injury.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 22 , Issue 3 , August 1995 , pp. 202 - 207
Copyright
Copyright © Canadian Neurological Sciences Federation 1995

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