Magnesium sulfate attenuates increased blood-brain barrier permeability during insulin-induced hypoglycemia in rats.

Magnesium probably protects brain tissue against the effects of cerebral ischemia, brain injury and stroke through its actions as a calcium antagonist and inhibitor of excitatory amino acids. The effects of magnesium sulfate on cerebrovascular permeability to a dye, Evans blue, were studied during insulin-induced hypoglycemia with hypothermia in rats. Hypoglycemia was induced by an intramuscular injection of insulin. After giving insulin, each animal received MgSO4 (270 mg/kg) ip, followed by a 27 mg/kg dose every 20 min for 2.5 h. Plasma glucose and Mg2+ levels of animals were measured. Magnesium concentrations increased in the serum following MgSO4 administration (6.05+/-0.57 vs. 2.58+/-0.14 mg/dL in the Mg2+ group, and 7.14+/-0.42 vs. 2.78+/-0.06 mg/dL in the insulin + Mg2+ group, P < 0.01). Plasma glucose levels decreased following hypoglycemia (4+/-0.66 vs. 118+/-2.23 mg/dL in the insulin group, and 7+/-1.59 vs. 118+/-4.84 mg/dL in the insulin + Mg2+ group, P < 0.01). Blood-brain barrier permeability to Evans blue considerably increased in hypoglycemic rats (P < 0.01). In contrast, blood-brain barrier permeability to Evans blue was significantly reduced in treatment of hypoglycemic rats with MgSO4 (P < 0.01). These results indicate that Mg2+ greatly reduced the passage of exogenous vascular tracer bound to albumin into the brain during hypoglycemia with hypothermia. Mg2+ could have protective effects on blood-brain barrier permeability against insulin-induced hypoglycemia.

Effect of aluminum on the blood-brain barrier permeability in acute and chronically hyperglycemic rats.

This study examined the changes in blood-brain barrier (BBB) permeability following acute aluminum (Al) exposure during acute and chronic hyperglycemia in rats. Acute hyperglycemia was induced by intraperitoneal injection of glucose solution at 30 min after giving Al. Chronic hyperglycemia was made by an injection of alloxan monohydrate. BBB permeability was measured in the four regions of the brain at 1 h after administrating Al by spectrophotometric quantification of Evans blue (EB) dye. The extravasation of EB dye was significantly more extensive in the two regions of brain in the groups treated with Al, Al plus glucose, and alloxan plus Al than in the groups treated with saline, glucose, and alloxan alone (p < 0.05). Under acute and chronic hyperglycemia plus Al treatment, the BBB permeability to EB was significantly higher than that observed solely in Al-treated rats (p < 0.05). These data indicate that Al toxicity leads to an additional increase in BBB permeability, in which acute and chronic hyperglycemia potentiates the effects of Al to enhance BBB permeability to EB.

Effects of profound hypothermia on the blood-brain barrier permeability in acute and chronically ethanol treated rats.

This study examines the effects of profound hypothermia on the blood-brain barrier (BBB) permeability in ethanol administrated rats. Vascular permeability to intravenously injected Evans blue (EB) was quantitatively examined in the brain regions of rats. Rats were treated with ethanol acute and chronically. Rectal temperature of rats was dropped into 20+/-1 degrees C during profound hypothermia. Mean arterial blood pressure in both acute and chronic ethanol treatments plus hypothermia significantly dropped into low levels as well as in hypothermia alone (P<0.01). Hypothermia led to a significant increase in the content of EB dye in the brain regions of rats (P<0.05). Both acute and chronic ethanol treatments plus hypothermia did not lead to a significant increase in the BBB permeability against intravenously injected EB dye. We conclude that ethanol intake protects the BBB against the effects of hypothermia.