Abstract
The effect of experimental acute hyponatraemia on severe traumatic brain injury (TBI) was studied in a modified impact-acceleration model. The cortical contusional volume was quantified by image analysis on serial sections, injured axons were visualized and quantified by β-Amyloid Precursor Protein (β-APP) immuno-histochemical staining. Regional brain water content was estimated by the wet-dry weight method. The experiment was conducted in Group I (injury only) and Group II (injury followed by acute hyponatraemia). Comparison between the two groups showed that acute hyponatraemia significantly increased contusional volume (3.24 ± 0.70 mm3 vs. 1.80 ± 0.65 mm3, P = 0.009) and the number of injured axons (128.7 ± 44.3 vs. 41.7 ± 50.1, P = 0.04) in the right thalamus & basal ganglia region. Water content of the brain stem region was also significantly increased by acute hyponatraemia (73.71 ± 0.14% vs. 72.28 ± 0.93%, P = 0.004). These results suggest that acute hyponatraemia potentiates secondary brain damage in severe TBI by augmentation of both focal contusion and diffuse axonal injury. The injured brain stem region is more susceptible to edema formation induced by experimental acute hyponatraemia.
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References
Adler S, Verbalis JG, Williams D (1993) Effect of acute and chronic hyponatraemia on brain buffering in rats. Am J Physiol 264: F968–F974
Atchison JW, Wachendorf J, Haddock D, Mysiw WJ, Gribble M, Cornigan JD (1993) Hyponatraemia-associated cognitive impairment in traumatic brain injury. Brain Inj 7: 347–352
Auer RN, Kalimo H, Olsson Y, Siesjö BK (1985) The temporal evolution of hypoglycemic brain damage. I. Light- and electron-microscopic findings in the rat cerebral cortex. Acta Neuro-pathol (Berl) 67: 13–24
Dila CJ and Pappius HM (1972) Cerebral water and electrolytes. An experimental model of inappropriate secretion of antidiuretic hormone. Arch Neurol 26: 85–90
Dóczi T, Tarjányi J, Huszka E, Kiss J (1982) Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after head injury. Neurosurgery 10: 685–688
Dohanics J, Hoffman GE, Verbalis JG (1996) Chronic hyponatremia reduced survival of magnocellular vasopressin and oxytocin neurons after axonal injury. J Neurosci 16: 2373–2380
Marmarou A, Foda MAA, van den Brink W, Campbell J, Kita H, Demetriou K (1994) A new model of diffuse brain injury in rat: part I: pathophysiology and biomechanics. J Neurosurg 80: 291–300
Maxwell WL, Povlishock JT, Graham DL (1997) A mechanistic analysis of non disruptive axonal injury: a review. J Neurotrauma 14: 419–440
Vexler ZS, Ayus JC, Roberts TPL, Fraser CL, Kucharczk J, Arieff AI (1994) Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals. J Clin Invest 93: 256–264
Yang GY, Betz AL, Chenevert TL, Brunberg JA, Hoff JT (1994) Experimental intracerebral hemorrhage: relationship between brain edema, blood flow and blood-brain barier permeability in rats. J Neurosurg 81: 93–102
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© 2000 Springer-Verlag Wien
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Ke, C. et al. (2000). The Impact of Acute Hyponatraemia on Severe Traumatic Brain Injury in Rats. In: Mendelow, A.D., et al. Brain Edema XI. Acta Neurochirurgica Supplements, vol 76. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6346-7_84
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DOI: https://doi.org/10.1007/978-3-7091-6346-7_84
Publisher Name: Springer, Vienna
Print ISBN: 978-3-7091-7257-5
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