Cerebral blood flow, plasma catecholamines, and electroencephalogram during hypoglycemia and recovery after glucose...

Regional cerebral blood flow (rCBF) and plasma catecholamines were measured in separate experiments during the onset of insulin-induced hypoglycemia and during recovery. The purpose of these experiments was twofold: first, to study the relationship between plasma catecholamines and rCBF to determine if increased concentrations of plasma catecholamines were responsible for the increase in rCBF observed during insulin-induced hypoglycemia, and second, to study changes in rCBF after recovery from hypoglycemia. Male Long-Evans rats were fasted overnight, surgically prepared under isoflurane anesthesia, restrained, and allowed to awake from anesthesia. In the first series of experiments, plasma catecholamines, arterial blood pressure, arterial blood gases, and electroencephalogram (EEG) were measured during the onset of hypoglycemia produced by i.v. insulin and the recovery after i.v. glucose. The EEG showed a characteristic high-amplitude, slow-wave pattern during hypoglycemia (plasma glucose, 38 +/- 2 mg/dl; n = 3). Plasma epinephrine in the normoglycemic control rats was 529 +/- 122 pg/ml (n = 5) and increased 4.5 times as plasma glucose reached 50 +/- 3 mg/dl. After the initial increase, plasma epinephrine steadily decreased toward baseline over the next 90 min as the hypoglycemia became more severe. Plasma norepinephrine significantly increased by 60% when plasma glucose was 40 +/- 2 mg/dl and remained increased during much of the recovery period. In other studies, rCBF was measured in four groups of rats, one group with normoglycemia (control), one with hypoglycemia, one at 5 min of recovery, and one at 30 min of recovery. Regional CBF increased during hypoglycemia (plasma glucose, 39 +/- 1 mg/dl; n = 6) in most regions studied and ranged from 28 to 99% above control. After 5 min of the recovery (plasma glucose, 269 +/- 15 mg/dl), rCBF returned to or decreased below baseline. In a previous study, we determined that rCBF did not increase during hypoglycemia until plasma glucose decreased to 40 mg/dl. In the present study, the peak increase in plasma epinephrine occurred when plasma glucose was 50 mg/dl. At plasma glucose concentrations which rCBF began to increase, plasma epinephrine was decreasing from its peak level. Regional CBF and plasma norepinephrine increased in parallel during the onset of hypoglycemia; however, during the recovery period, plasma norepinephrine remained increased while rCBF decreased to or below baseline. The dissociation of rCBF and plasma catecholamines casts doubt on the hypothesis that plasma catecholamines are responsible for increases in rCBF.