THE EFFECT OF INTRAVENOUS LACTATE ON CEREBRAL FUNCTION DURING HYPOGLYCEMIA

Any factor which protects the brain against hypoglycaemia induced cere bral dysfunction could have important therapeutic implications for int ensive insulin therapy. This study tested the hypothesis that intraven ous lactate protects cerebral function during hypoglycaemia. Four choi ce reaction time, Auditory Brain Stem Response (ABR), and P-300 latenc y were used as measures of cerebral function. Nine healthy volunteers (six female) underwent two stepped hyperinsulinaemic clamps at least 4 weeks apart, achieving blood glucose levels of 4.5, 3.3, and 2.5 mmol l(-1). On one occasion 40 mu mol kg(-1) min(-1) sodium lactate was in fused, and on the other, normal saline. Cerebral function tests were m easured at each glucose level. At 3.3 mmol l(-1), there was a signific ant slowing of four choice reaction time with saline (p < 0.02) but no t with lactate; no changes in P-300 latency or ABR occurred on either occasion. At 2.5 mmol l(-1) results from all three tests deteriorated significantly during saline infusion (p < 0.001 reaction time, p < 0.0 2 ABR and p < 0.05 P-300), but not lactate. Lactate infusion was assoc iated with a reduction in noradrenaline (p < 0.05), adrenaline (p < 0. 05), and growth hormone (p < 0.02) responses at a glucose of 2.5 mmol l(-1). These results support the hypothesis that intravenous lactate p rotects cerebral function during hypoglycaemia.