Catecholamine Metabolites in Internal Jugular Plasma: A Window into the Human Brain

Abstract

Publisher Summary From recent research it is clear that the old idea of brain noradrenergic neurons subserving a predominantly sympathoinhibitory role is no longer tenable. The substantial increase in brain norepinephrine (NE) turnover following trimethaphan presumably results from a compensatory response in sympathoexcitatory forebrain noradrenergic neurons in the face of interruption of sympathetic neural traffic and reduction in arterial blood pressure, while the reduction in central nervous system (CNS) NE turnover in response to intravenous clonidine administration underlies the blood pressure-lowering action of the drug. Following the characterization of NE as the sympathetic neurotransmitter and the subsequent finding of a direct relationship between rates of sympathetic nerve firing and neurotransmitter release, the potential to use NE washout, or spillover to plasma, as an index of sympathetic nervous function is well established. Recent research extends this reasoning to CNS neurons and suggests the utility of using direct internal jugular vein blood sampling techniques in the assessment of central nervous system neuronal activity, by demonstrating a reduction in 3-methoxy-4-hydroxyphenylglycol (MHPG) jugular venous overflow from the brain of stump-tailed monkeys following clonidine administration. The clinical application of such methodology, however, is in line with current advancement.