Abstract
The permeability of the rat blood-brain barrier during different levels of hypothermia was examined using a new and more sensitive quantitative radiotracer technique. In contrast to the findings of previous studies, tracer permeation as measured here by the calculated cerebrovascular permeability-area product (PA), did not increase during hypothermia. Rather, rats maintained at specific temperatures between 30–16° C (1h) by contact surface cooling, displayed lowered permeation (PA) of i.v. injected14C-sucrose,125I-bovine serum albumin and3H-α-amino-isobutyric acid in all brain regions examined. This effect was temperature-dependent and reversible on rewarming to normothermic temperature. Elevated plasma tracer concentration vs. time was characteristic of hypothermic rats except those cooled to 30° C. That no elevation in plasma tracer accompanied alterations in tracer permeation at 30° C, indicates hypothermic induced reductions in PA are independent of altered plasma tracer levels. Furthermore, the nature of α-amino-isobutyric acid to rapidly distribute to intracellular vs. extracellular sites suggests the effects of hypothermia seen here are due primarily to the condition of cerebrovascular membranes.