Taurine and Osmoregulation. III. Taurine Deficiency Protects against Cerebral Edema during Acute Hyponatremia

Trachtman, Howard; Pizzo, R.; Sturman, John A.

doi:10.1203/00006450-199001000-00022

Cited by 21 publications

(6 citation statements)

References 17 publications

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“…Taurine deficiency in experimental cats was protective against CE during acute hyponatremia [35], implicated as a risk factor in the pathogenesis of DKA associated CE [36]. Our demonstration of rapid, but incomplete, extrusion of taurine under such conditions supports these findings.…”

Section: Discussionsupporting

confidence: 81%

An In Vitro Paradigm for Diabetic Cerebral Oedema and its Therapy: A Critical Role for Taurine and Water Channels

et al. 2011

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The pathophysiology of cerebral oedema (CE) in diabetic ketoacidosis (DKA) remains enigmatic. We investigated the role of the idiogenic osmol taurine and aquaporin channels in an in vitro model, the SH-SY5Y neuroblastoma cell line, by sequentially mimicking DKA-like hyperglycemia/hypertonicity and hypotonic fluid therapy. Exposure to DKA-like hyperosmolarity led to shrinkage, while hypotonic fluid exposure led to cell swelling and impaired viability. Low sodium compensated in part for elevated glucose, pointing to a critical role for overall osmolality. Taurine, was synthesized and retained intracellularly during DKA-like hypertonicity, and released during hypotonicity, in part mitigating neuronal swelling. Metabolic labeling showed that the rate of taurine release was inadequate to fully prevent neuronal swelling during hypotonic fluid therapy following DKA-like hypertonicity. Under these conditions, Aquaporin4 & 9 channels were respectively down and up-regulated. Our study provides further novel insights into molecular mechanisms contributing to CE in DKA and its therapy.

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Section: Discussionsupporting

confidence: 81%

An In Vitro Paradigm for Diabetic Cerebral Oedema and its Therapy: A Critical Role for Taurine and Water Channels

et al. 2011

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“…However, changes in the number of osmotically active particles do not necessarily reflect the volume regulating capacity of the brain. For instance, Trachtman et al (1990) reported that an average decrease in taurine by as little as 1.5 m M in the brains of taurinedeficient kittens significantly protects against hypoos-motic cerebral edema. The fact that brain electrolytes, the quantitatively most important osmolytes, are not different between hypoosmotic taurine-supplemented and -deficient kittens (Trachtman et al, 1990) supports the contention above.…”

Section: Discussionmentioning

confidence: 99%

Elevation of Taurine in Hippocampal Extracellular Fluid and Cerebrospinal Fluid of Acutely Hypoosmotic Rats: Contribution by Influx from Blood?

Lehmann¹,

Carlström²,

Nagelhus³

et al. 1991

Journal of Neurochemistry

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Previous work has demonstrated that there is a selective increase in extracellular taurine in the brain during acute water intoxication. One aim of the present study was to investigate whether plasma taurine contributes to this increase. To this end, the concentrations of taurine, other amino acids, and ethanolamine (EA) were measured in plasma and CSF of urethane-anesthetized rats injected with 150 ml/kg body weight of distilled water. Blood pressure, blood gases, and pH, as well as plasma and CSF osmolality, were also measured. The CSF level of albumin was quantitated to study the function of the blood-CSF barrier. In separate experiments, hippocampal microdialysis was performed to determine the effects of acute plasma hypoosmolality on extracellular amino acids. Finally, the effect of water injection on hippocampal specific gravity and tissue amino acids was assessed. Blood gases and pH were essentially unchanged after water administration. Mean arterial blood pressure increased to peak levels approximately 50 mm Hg above control. Plasma osmolality decreased rapidly, whereas the depression of CSF osmolality was slower and less pronounced. The average volume of the hippocampus increased by 8%. Water injection was accompanied by a 25-fold elevation of taurine in plasma, whereas phosphoethanolamine (PEA) and EA increased moderately. A small fraction of the increase in plasma taurine might derive from blood cells because dilution of blood in vitro led to doubled plasma levels of the amino acid. Taurine, PEA, and EA increased consistently in CSF and hippocampal microdialysates. Plasma hypoosmolality transiently opened the blood-CSF barrier is reflected by augmented CSF concentrations of albumin.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Indeed, intravenous administration of mannitol has been found to reduce cellular edema, minimize swelling-induced disruption of the cell membrane and eliminate the no-reflow phenomenon in the ischemic myocardium. Similarly, a reduction in the intracellular osmotic load through taurine depletion reduces cerebral edema during acute hyponatremia 4 and protects the heart against ischemia 5 • Thus, the acute effects of taurine loss can significantly benefit the osmotically stressed cell.…”

Section: Osmoregulation As a Cytoprotective Mechanismmentioning

confidence: 99%

Why Is Taurine Cytoprotective?

Schaffer

Azuma

Takahashi

et al. 2003

Advances in Experimental Medicine and Biology

136

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Taurine and Osmoregulation. III. Taurine Deficiency Protects against Cerebral Edema during Acute Hyponatremia

Cited by 21 publications

References 17 publications

An In Vitro Paradigm for Diabetic Cerebral Oedema and its Therapy: A Critical Role for Taurine and Water Channels

An In Vitro Paradigm for Diabetic Cerebral Oedema and its Therapy: A Critical Role for Taurine and Water Channels

Elevation of Taurine in Hippocampal Extracellular Fluid and Cerebrospinal Fluid of Acutely Hypoosmotic Rats: Contribution by Influx from Blood?

Why Is Taurine Cytoprotective?

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