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  • Title: [Local spinal cord glucose utilization and extracellular potassium activity changes after spinal cord injury in rats].
    Author: Murai H, Itoh C, Wagai N, Nakamura T, Yamaura A, Makino H.
    Journal: No To Shinkei; 1991 Apr; 43(4):337-42. PubMed ID: 1888573.
    Abstract:
    Spinal microenvironment and metabolic alterations after experimental contusional injury of the spinal cord were evaluated in the same Wistar rats. Severe spinal cord injury was made under light GOF anesthesia with a 10 g weight drop onto the exposed Th-8 spinal cord from a 10 cm height and then halothane was ceased. The author studied extracellular potassium activity ([K+]e) and DC potential for 2 hours after paraplegic spinal cord injury in conscious rats. Furthermore, at 2 hours after cord injury, local spinal cord glucose utilization (1-SCGU) was measured with quantitative autoradiographic 2-[14C] deoxy-glucose method (Sokoloff et al.). [K+]e in injured spinal cords was 59 +/- 5 (mean +/- S.E.M.) mEq at 10 min after injury and was cleared with an exponential half-life of 1 hour. At 2 hours after injury [K+]e was still high with a value of 16 +/- 1 mEq compared with 4 mEq of control animals. DC potential changes was a mirror image of that of [K+]e. DC potential changed by a mean of 10.7 mV positively from 10 min. to 2 hours after injury. 1-SCGU at the impact site was extremely low in both white and gray matters. At 6mm rostral from the impact center 1-SCGU was remarkably reduced in the gray matter, and in the lateral white matter. But at 3 mm rostral 1-SCGU was well preserved. And at 20 mm rostral there was no difference in 1-SCGU with control animals. Massive potassium efflux from the injured spinal cord to the adjacent spinal segment was clarified at this experiment.(ABSTRACT TRUNCATED AT 250 WORDS)
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