Lambert G W, Kaye D M, Thompson J M, Turner A G, Cox H S, Vaz M, Jennings G L, Wallin B G, Esler M D
Human Autonomic Function Laboratory, Baker Medical Research Institute, Prahran Victoria, Australia.
Acta Physiol Scand. 1998 Jun;163(2):155-63. doi: 10.1046/j.1365-201X.1998.00348.x.
It is recognized that the brain plays a pivotal role in the maintenance of blood pressure and the control of myocardial function. By combining direct sampling of internal jugular venous blood with a noradrenaline isotope dilution method, for examining neuronal transmitter release, and microneurographic nerve recording, we were able to quantify the release of central nervous system noradrenaline and its metabolites and investigate their association with efferent sympathetic nervous outflow in healthy subjects and patients with pure autonomic failure. To further investigate the relationship between brain noradrenaline, sympathetic nervous activity and blood pressure regulation we examined brain catecholamine turnover, based on the internal jugular venous overflow of noradrenaline and its principal central nervous system metabolites, in response to a variety of pharmacological challenges. A substantial increase was seen in brain noradrenaline turnover following trimethaphan, presumably resulting from a compensatory response in sympathoexcitatory forebrain noradrenergic neurones in the face of interruption of sympathetic neural traffic and reduction in arterial blood pressure. In contrast, reduction in central nervous system noradrenaline turnover accompanied the blood pressure fall produced by intravenous clonidine administration, thus representing the blood pressure lowering action of the drug. Following vasodilatation elicited by intravenous adrenaline infusion, brain noradrenaline turnover increased in parallel with elevation in muscle sympathetic nervous activity. While it is difficult to assess the source of the noradrenaline and metabolites determined in our studies, available evidence implicates noradrenergic cell groups of the posterolateral hypothalamus, amygdala, the A5 region and the locus coeruleus as being involved in the regulation of sympathetic outflow and autonomic cardiovascular control.
人们认识到，大脑在维持血压和控制心肌功能方面起着关键作用。通过将颈内静脉血的直接采样与去甲肾上腺素同位素稀释法相结合，以检测神经元递质释放，并进行微神经图神经记录，我们能够量化中枢神经系统去甲肾上腺素及其代谢产物的释放，并研究它们与健康受试者和单纯自主神经功能衰竭患者的传出交感神经流出之间的关联。为了进一步研究脑内去甲肾上腺素、交感神经活动与血压调节之间的关系，我们基于颈内静脉去甲肾上腺素及其主要中枢神经系统代谢产物的溢出情况，检测了脑儿茶酚胺周转率，以应对各种药理学挑战。在使用三甲噻方后，脑内去甲肾上腺素周转率显著增加，这可能是由于面对交感神经传导中断和动脉血压降低，交感兴奋的前脑去甲肾上腺素能神经元产生了代偿反应。相比之下，静脉注射可乐定导致血压下降时，中枢神经系统去甲肾上腺素周转率降低，从而体现了该药物的降压作用。静脉注射肾上腺素引起血管扩张后，脑内去甲肾上腺素周转率与肌肉交感神经活动的升高平行增加。虽然很难评估我们研究中所测定的去甲肾上腺素和代谢产物的来源，但现有证据表明，下丘脑后外侧、杏仁核、A5区和蓝斑的去甲肾上腺素能细胞群参与了交感神经流出和自主心血管控制的调节。
