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Advances in neurology · Jan 1990
Comparative StudySpinal cord edema and changes in tissue content of Na+, K+, and Mg2+ after impact trauma in rats.
- P Demediuk, M Lemke, and A I Faden.
- Department of Neurology, University of California, San Francisco, School of Medicine 94121.
- Adv Neurol. 1990 Jan 1; 52: 225-32.
AbstractChanges in the tissue content of water, Na+, K+, and Mg2+ were measured in spinal cord samples from anesthetized rats subjected to impact trauma (T9 spinal segment) of varying severity: 25 g-cm (low injury), 100 g-cm (high injury). Laminectomized animals served as controls. Rats with high injury were killed at 15 min, 60 min, 4 hr, 24 hr, 3 days, or 7 days after trauma. Those with low injury were killed at 24-hr postinjury. In all groups, spinal cord tissue was rapidly removed (less than 30 sec), frozen in liquid nitrogen, and dissected into the injured segment and adjacent two caudal and rostral segments. Water content was determined as wet weight/dry weight ratios, and cations were measured by atomic absorption spectrophotometry. High injury resulted in statistically significant increases in water content as early as 15 min after trauma. There were concomitant increases in Na+ and decreases in K+ that were apparent at 15 min and were statistically significant by 60-min posttrauma. The increases in water content and Na+ were present to a similar degree in the 4-hr, 24-hr, 3-day, and 7-day groups. In contrast, tissue Mg2+ was reduced and significantly decreased at 4 hr and 24 hr; Mg2+ levels had recovered partially by 3 days and completely by 7 days. Whereas changes in the tissue content of water, Na+, and K+ occurred at 24 hr regardless of the injury severity, changes in total Mg2+ were correlated with the degree of injury. These data are consistent with the conclusion that edema formation (and associated Na+ and K+ changes) after spinal cord trauma may be an epiphenomenon and does not significantly contribute to injury progression. In contrast, reductions in Mg2+ content may represent an important factor in the development of irreversible tissue damage.
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