Osmotic Opening Of Blood-brain Barrier Research Articles

Signs of myelin impairment in cerebrospinal fluid after osmotic opening of the blood-brain barrier in rats.

A number of clinical neurological pathologies are associated with increased permeability of the blood brain barrier (BBB). Induced changes of the homeostatic mechanisms in the brain microenvironment lead among others to cellular changes in the CNS. The question was whether some of these changes can be induced by osmotic opening of BBB in an in vivo experiment and whether they can be detected in cerebrospinal fluid (CSF). CSF was taken via the suboccipital puncture from 10 healthy rats and six rats after the osmotic opening of the BBB. In all 16 animals, concentration of myelin basic protein (MBP ng/ml), Neuron-specific enolase (NSE ng/ml) and Tau-protein (Tau pg/ml) were determined in CSF by ELISA. Values in both groups were statistically evaluated. Significant difference between the control and experimental group was revealed only for the concentration of myelin basic protein (p<0.01). The presented results indicate that osmotic opening of the BBB in vivo experiment without the presence of other pathological conditions of the brain leads to a damage of myelin, without impairment of neurons or their axons.

A possible role of calcium ion in osmotic opening of blood-brain barrier

A possible role of calcium ion in osmotic opening of blood-brain barrier

Hyperammonemia-induced cytotoxic brain edema under osmotic opening of blood-brain barrier in dogs.

Infusion of an ammonium acetate solution into dogs during mannitol-induced reversible opening of the blood-brain barrier (BBB) resulted in a marked rise in intracranial pressure with exclusion of Evans blue dye. This indicated cytotoxic brain edema. These findings suggest a role for hyperammonemia in cerebral edema during acute liver failure.

Testing of a hypothesis for osmotic opening of the blood-brain barrier.

Testing of a hypothesis for osmotic opening of the blood-brain barrier.