INTERACTION OF BARORECEPTOR AND CHEMORECEPTOR REFLEXES - MODULATION OF CHEMORECEPTOR REFLEX BY CHANGES IN BARORECEPTOR ACTIVITY
INTERACTION OF BARORECEPTOR AND CHEMORECEPTOR REFLEXES - MODULATION OF CHEMORECEPTOR REFLEX BY CHANGES IN BARORECEPTOR ACTIVITY
复制标题
DOI：
10.1172/jci107669
复制
发表时间：
1974-01-01
影响因子：
15.9
通讯作者：
SCHMID, PG
中科院分区：
文献类型：
--
作者：
HEISTAD, DD;ABBOUD, FM;SCHMID, PG
本研究的目的是确定动脉压水平和压力感受器激活程度是否影响对化学感受器刺激的反应。麻醉和麻痹犬颈总动脉注射尼古丁刺激化学感受器。在神经支配的股薄肌中观察反应，以恒定流量灌注，同时测量灌注压力。动脉压通过给动物放血而降低，通过暂时阻断降主动脉而升高。血管收缩对化学感受器刺激的反应在低血压时增强，在动脉压升高时被抑制。出血性低血压引起的化学感受器反射增强不是股薄肌血管阻力改变、儿茶酚胺或酸中毒使化学感受器致敏或脑灌注压改变的结果。在其他研究中，我们排除了动脉压力变化对化学感受器的直接影响所导致的变化的可能性。分离并灌注两条颈动脉分叉。在一侧，升高压力刺激颈动脉窦压力感受器。另一方面，颈动脉体化学感受器受到尼古丁或低氧和高碳酸血症的刺激。一侧压力感受器的激活减弱了另一侧对化学感受器刺激的血管收缩反应。这排除了动脉压力变化对化学感受器的直接影响，并表明这些反射的中心相互作用。我们得出结论，血管收缩对化学感受器刺激的反应在低血压时增强，在短暂性高血压时被抑制。这些影响似乎至少部分是由化学感受器和压力感受器反射的中枢相互作用造成的。
The purpose of this study was to determine whether the level of arterial pressure and degree of baroreceptor activation affect responses to stimulation of chemoreceptors. Chemoreceptors were stimulated by injecting nicotine into the common carotid artery of anesthetized and paralyzed dogs. Responses were observed in the innervated gracilis muscle, perfused at constant flow while perfusion pressure was measured. Arterial pressure was lowered by bleeding the animals and raised by transient occlusion of the descending aorta. Vasoconstrictor responses to stimulation of chemoreceptors were enhanced by hypotension and inhibited by elevation of arterial pressure. Potentiation of the chemoreceptor reflex by hemorrhagic hypotension was not the result of altered vascular resistance in the gracilis muscle, sensitization of chemoreceptors by catecholamines or acidosis, or changes in cerebral perfusion pressure.Additional studies were done in which we excluded the possibility that the changes resulted from direct effects of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were isolated and perfused. On one side, pressure was raised to stimulate the carotid sinus baroreceptors. On the other side, the carotid body chemoreceptors were stimulated by nicotine or by hypoxic and hypercapnic blood. Activation of baroreceptors on one side attenuated the vasoconstrictor response to chemoreceptor stimulation on the other side. This excludes a direct effect of changes in arterial pressure on the chemoreceptors and suggests a central interaction of these reflexes.We conclude that vasoconstrictor responses to stimulation of chemoreceptors are potentiated by hypotension and inhibited by transient hypertension. These effects appear to result at least in part from a central interaction of chemoreceptor and baroreceptor reflexes.