Baroreflex control of the circulation in patients with congestive heart failure.
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.
Kassis
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Cardiovascular Laboratory, Gentofte Hospital, University of Copenhagen.
D000328:Adult; D000368:Aged; D001775:Blood Circulation; D002346:Carotid Sinus / Q000294:innervation / Q000503:physiopathology*; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011311:Pressoreceptors / Q000503:physiopathology*