Kassis E
Cardiovascular Laboratory, Gentofte Hospital, University of Copenhagen.
Dan Med Bull. 1989 Jun;36(3):195-211.
Vagal and glossopharyngeal afferents from cardiopulmonary and arterial baroreceptors exert supraspinal tonic restraint on sympathetic efferent outflow. The baroreceptor inhibitory influence is directly related to physiological changes in cardiac filling and arterial pressures. Increased cardiac pressures and dimensions during CHF may provide chronic stimulation that reduces responsiveness of these receptors and thereby influence the neurohumoral control of the circulation. Patients with chronic and severe CHF of ischemic cause were compared with control subjects whose ischemic heart disease did not affect cardiac performance. Orthostatic pooling of blood with use of upright tilt (45 degree), provided an apparently sufficient stimulus to unload baroreceptors in patients like controls. In contrast to peripheral vasoconstriction in controls, the patients dilated their resistance vessels during upright tilt. This abnormal vasodilation was systemic and uniform in skeletal muscle and subcutaneous tissue of the forearm remaining at heart level. Such an inability to vasoconstrict in the patients, could not be attributed to depression of local vasoconstrictor reflex or autoregulatory responsiveness of forearm vascular beds. Neural blockade carried out separately or in combination with blockades of forearm vascular effector receptors revealed; increased neural efferent activity to the forearm during tilting the patients which mediated beta-adrenergic vasodilation in both vascular beds. The patients had augmented circulating catecholamine levels, those for epinephrine increased in venous effluents but were maintained in brachial arterial inflow, and those for norepinephrine increased in arterial rather than venous plasma in the forearm. Following the patients during a course of therapy with a selective vasodilator calcium antagonist, the beta-adrenergic reflex vasodilation became substantially attenuated but was preserved during a placebo course of therapy. The beta-adrenergic reflex effect evidenced in the studied patients is most probably a manifestation of reduced baroreceptor afferent restraint and it could subsequently relate to the severity of depression of baroreceptor sensitivity during the course of CHF.
来自心肺和动脉压力感受器的迷走神经和舌咽神经传入纤维对交感神经传出冲动施加脊髓上的紧张性抑制。压力感受器的抑制性影响与心脏充盈和动脉血压的生理变化直接相关。心力衰竭期间心脏压力和尺寸的增加可能提供慢性刺激，从而降低这些感受器的反应性，进而影响循环系统的神经体液控制。将患有慢性重度缺血性心力衰竭的患者与缺血性心脏病不影响心脏功能的对照受试者进行比较。使用直立倾斜（45度）使血液直立性积聚，为患者提供了与对照受试者类似的明显足以使压力感受器卸载的刺激。与对照组的外周血管收缩相反，患者在直立倾斜期间扩张了其阻力血管。这种异常的血管舒张是全身性的，并且在保持于心脏水平的前臂骨骼肌和皮下组织中是均匀的。患者无法进行血管收缩，这不能归因于局部血管收缩反射的抑制或前臂血管床的自身调节反应性。单独进行或与前臂血管效应器受体阻断联合进行的神经阻断显示；在患者倾斜期间，前臂的神经传出活动增加，这介导了两个血管床中的β-肾上腺素能血管舒张。患者的循环儿茶酚胺水平升高，静脉流出物中的肾上腺素水平升高，但在肱动脉流入中保持不变，而前臂动脉血浆中的去甲肾上腺素水平升高而非静脉血浆中的升高。在患者接受选择性血管扩张剂钙拮抗剂治疗的过程中，β-肾上腺素能反射性血管舒张明显减弱，但在安慰剂治疗过程中得以保留。在所研究的患者中证实的β-肾上腺素能反射效应很可能是压力感受器传入抑制降低的表现，并且它随后可能与心力衰竭过程中压力感受器敏感性降低的严重程度有关。
