scholarly journals Brain Uptake of Myoinositol after Exogenous Administration

2002 ◽  
Vol 13 (5) ◽  
pp. 1255-1260
Author(s):  
Stephen M. Silver ◽  
Barbara M. Schroeder ◽  
Richard H. Sterns

ABSTRACT. An acute increase in plasma tonicity results in an adaptive increase in brain organic osmolyte content, but this process requires several days to occur. Slow reaccumulation of brain organic osmolytes may contribute to osmotic demyelination. It was investigated whether administration of intravenous myoinositol in rats could speed entry of the osmolyte into the brain. Two groups of animals were studied: normonatremic animals and animals with hyponatremia (105 mmol/L) of 3–d duration. Animals were intravenously administered either 1 M NaCl to induce a 25 to 28 mM increase in serum sodium concentration over 200 min or an infusate that maintained serum sodium concentration. In some animals, myoinositol was administered intravenously over the same time period to raise plasma myoinositol levels by 5 to 10 mM. Brain myoinositol, electrolyte, and water contents were determined at the end of the infusions. In both normonatremic and hyponatremic rats, infusion of hypertonic saline without myoinositol or infusion of myoinositol without hypertonic saline did not increase brain myoinositol levels above control levels. In normonatremic animals, concurrent infusion of hypertonic saline and myoinositol increased brain myoinositol levels by about 50% above control levels. Brain myoinositol content in animals with uncorrected hyponatremia was about 50% of that found in normonatremic controls; concurrent infusion of hypertonic saline and myoinositol increased brain myoinositol to levels similar to those found in normonatremic controls. Intravenous infusion of myoinositol did not alter brain water content compared with animals not infused with myoinositol. In conclusion, systemic infusion of myoinositol can rapidly increase brain myoinositol content, but only when plasma tonicity is concomitantly increased.

Author(s):  
V Georgy ◽  
D Mullhi ◽  
A F Jones

Central pontine myelinolyis (CPM), an acute demyelinating condition of the brain stem, is a recognized complication of the treatment of patients with chronic hyponatraemia (hyponatraemia >48 h), particularly in those who abuse alcohol. The risk of CPM is believed to be associated with a rapid (>8 mmol/L/day) correction of the serum sodium concentration, which is said to lead to an osmotically-induced demyelination. CPM is also commonly believed to have a poor, and often fatal, outcome. We report the case of a 37-year-old female alcoholic patient who presented following a collapse, and who was hyponatraemic (serum sodium concentration 105 mmol/L). The rate at which the serum sodium concentration was corrected to normal was less than the 8 mmol/L/day guideline, but nonetheless she developed the clinical and radiological features of CPM. She made a good neurological recovery, however, and was able to be discharged from hospital. CPM does not necessarily have a bleak prognosis, and may occur even with optimal rates of correction of the serum sodium concentration. Clinicians should recognize that the outcome of CPM is not inevitably poor, and the complication may occur despite appropriate management. It is possible that CPM is a complication of the hyponatraemia itself, rather than the treatment of the biochemical disturbance.


2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  

1991 ◽  
Vol 261 (2) ◽  
pp. E252-E256 ◽  
Author(s):  
B. A. Clark ◽  
D. Elahi ◽  
L. Fish ◽  
M. McAloon-Dyke ◽  
K. Davis ◽  
...  

Atrial natriuretic peptide (ANP) may suppress vasopressin release, but the dynamics of this interaction as well as the influence of age have not been defined. We studied six or seven young (19-40 yr old) and seven elderly volunteers (65-83 yr old) under two circumstances: 1) after infusion of 5% saline (0.04 ml.kg-1.min-1) for 2 h and 2) after the same infusion given with simultaneous synthetic human ANP (0.05 micrograms.kg-1.min-1). Hypertonic saline alone produced a progressive rise in plasma vasopressin with increasing serum sodium. During hypertonic saline alone, vasopressin levels began to rise at an increment in serum sodium of 1.67 +/- 0.35 mM in the young and 1.43 +/- 0.32 mM in the elderly and rose linearly with increasing serum sodium. When ANP was infused with hypertonic saline (with peak ANP levels of approximately 1,000 pM), vasopressin levels began to rise at an increment in serum sodium of 4.43 +/- 0.67 mM in the young and 4.57 +/- 0.43 mM in the elderly (P less than 0.01 vs. saline alone). Furthermore, the vasopressin response for any given serum sodium was significantly reduced in both young and elderly subjects, resulting in a rightward displacement of the curve relating vasopressin response to sodium concentration (P less than 0.001). In conclusion, ANP not only suppresses vasopressin but raises the threshold for release of vasopressin in response to osmotic stimulation in both young and elderly individuals. High circulating ANP levels may be responsible in part for the suppression of vasopressin levels and water diuresis seen during states of volume expansion.


2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.


1980 ◽  
Vol 8 (3) ◽  
pp. 349-352 ◽  
Author(s):  
Luen Bik To ◽  
P. J. Phillips

Eighteen patients with hyperosmolar non-ketotic diabetic coma were studied retrospectively to identify factors affecting prognosis and to review treatment. This condition affected older women two-thirds of whom were unrecognised diabetics. Eight (44%) died. Mortality correlated with age above 60, uraemia and hyperosmolarity, but not with the degree or rate of fall of hyperglycaemia. Hyperglycaemia responded to rehydration and insulin, but in all patients serum osmolarity remained high for several days. In 14 patients (78%) the serum sodium concentration initially increased and in four (22 %) serum osmolarity increased. This persistence or worsening of the hyperosmolar state can be avoided without the risk of cerebal oedema by replacing the fluid and electrolyte deficits over 48 hours and using 5% dextrose for the water deficit.


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