Singewald N, Schneider C, Philippu A
Institut für Pharmakologie und Toxikologie, Universität Innsbruck, Austria.
Naunyn Schmiedebergs Arch Pharmacol. 1993 Sep;348(3):242-8. doi: 10.1007/BF00169151.
Effects of carotid occlusion and drugs applied intravenously on the release of endogenous catecholamines in the locus coeruleus of cats anaesthetized with pentobarbital or chloralose were investigated. The locus coeruleus was superfused bilaterally with artificial cerebrospinal fluid through push-pull cannulae inserted stereotaxically. Dopamine, noradrenaline and in some experiments also adrenaline were determined radioenzymatically in the superfusate. Under pentobarbital anaesthesia, a bilateral carotid occlusion increased the release rate of noradrenaline in the locus coeruleus, while the release of dopamine was decreased. These changes were due to the fall of blood pressure in the carotid sinus caused by the occlusion. Loading of baroreceptors by elevating blood pressure with phenylephrine (10 micrograms.kg-1 x min-1, i.v. infusion) was accompanied by a decreased release of noradrenaline in the locus coeruleus. This decrease in noradrenaline release was not detected in the caudal aspect of the locus coeruleus. Under chloralose anaesthesia, phenylephrine diminished the release rate of noradrenaline to about the same extent as under pentobarbital anaesthesia. The release rate of adrenaline was also decreased. A prolonged infusion of phenylephrine led to a prolonged pressor response associated with a sustained decrease in the noradrenaline release rate. Intravenous injection of chlorisondamine (3 mg.kg-1) did not change the release of noradrenaline, while dopamine release was reduced. It is concluded that the release of catecholamines in the locus coeruleus is influenced by signals originating from peripheral baroreceptors. The influences are similar under pentobarbital and chloralose anaesthesia. Noradrenergic neurons responding to haemodynamic signals are not uniformly distributed within the locus coeruleus.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了颈总动脉闭塞和静脉注射药物对戊巴比妥或氯醛糖麻醉猫蓝斑内源性儿茶酚胺释放的影响。通过立体定位插入的推挽式套管，用人工脑脊液对双侧蓝斑进行灌流。用放射酶法测定灌流液中的多巴胺、去甲肾上腺素，在某些实验中还测定肾上腺素。在戊巴比妥麻醉下，双侧颈总动脉闭塞增加了蓝斑中去甲肾上腺素的释放率，而多巴胺的释放减少。这些变化是由于闭塞导致颈静脉窦血压下降所致。用去氧肾上腺素（10微克·千克⁻¹·分钟⁻¹，静脉输注）升高血压使压力感受器负荷增加，同时蓝斑中去甲肾上腺素的释放减少。在蓝斑尾侧未检测到去甲肾上腺素释放的这种减少。在氯醛糖麻醉下，去氧肾上腺素使去甲肾上腺素的释放率降低程度与戊巴比妥麻醉下大致相同。肾上腺素的释放率也降低。长时间输注去氧肾上腺素导致长时间的升压反应，伴有去甲肾上腺素释放率持续下降。静脉注射氯异吲哚铵（3毫克·千克⁻¹）不改变去甲肾上腺素的释放，而多巴胺释放减少。结论是，蓝斑中儿茶酚胺的释放受外周压力感受器发出的信号影响。在戊巴比妥和氯醛糖麻醉下影响相似。对血流动力学信号有反应的去甲肾上腺素能神经元在蓝斑内分布不均。（摘要截短于250字）
