PEDIATRICS Vol. 26 No. 6 December 1960, pp. 925-938
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STUDIES IN EXPERIMENTAL HYPERTONICITY

I. Pathogenesis of the Clinical Syndrome, Biochemical Abnormalities and Cause of Death

Juan F. Sotos M.D.1, Philip R. Dodge M.D.1, Patricia Meara 1, and Nathan B. Talbot M.D.1

1 Departments of Pediatrics and Neurology, Harvard Medical School, the Children's Medical and Neurology Services and the Joseph P. Kennedy, Jr. Laboratories, Massachusetts General Hospital, Boston

Hypertonicity of the body fluids was induced in rabbits by the intravenous infusion of different hypertonic solutions (NaCl. NaCl plus NaHCO3, sucrose, mannitol and urea). The results obtained in this study indicate the following.

There is no significant correlation between the clinical syndrome or death and values for total body water, total body solutes, total extracellular or intracellular volume, or concentration of sodium or chloride in the plasma. The clinical manifestations and death can occur in the absence of in tracranial hemorrhage.

Hypertonicity, by creating an osmotic gradient between extracellular fluid and brain, is the important factor in producing the characteristic clinical syndrome and death, but is not the immediate cause of these abnormalities. The osmolality necessary to produce these alterations was greater in animals infused with urea.

Hypertonicity produces these alterations by decreasing water and increasing ion concentration in the brain. The resulting functional impairment of neurones accounts for the clinical and electroencephalographic abnormalities. The increased values of sodium and chloride in the brain reflect an impairment of function of either brain cells, "blood-brain barrier," or both. Acidosis, hyperkalemia and hyerphosphatemia ensue as a result of hypertonicity.

Unless death is imminent, all of the abnormalities described are reversible.




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