Continuous resetting of the human carotid baroreceptor-cardiac reflex

1987 ◽  
Vol 252 (4) ◽  
pp. R732-R736 ◽  
Author(s):  
G. A. Kasting ◽  
D. L. Eckberg ◽  
J. M. Fritsch ◽  
C. L. Birkett

Although human baroreflex responses have been studied during night as well as day, there has been no attempt to distinguish circadian changes of baroreflex function from those related to sleep. We measured carotid baroreceptor-cardiac reflex responses serially during a 24-h period in 11 normotensive volunteers who were awake and cooperative during testing. We applied sequences of ramped R-wave-triggered neck chamber pressure changes from +40 to -65 mmHg, during held expiration, at 3-h intervals. Subjects maintained their usual sleep-wake cycles but were awakened for three 30-min periods for night testing. There was no systematic change of baroreflex slope during the 24-h period. There were, however, parallel shifts of the entire sigmoid baroreceptor-cardiac reflex response relation along its R-R interval and arterial pressure axes associated with small, but significant, circadian changes of baseline R-R intervals and arterial pressures. Thus, although our data do not point toward major circadian variability of baro-reflex responsiveness, they provide evidence for an ongoing process of human baroreflex resetting.

1986 ◽  
Vol 60 (2) ◽  
pp. 727-732 ◽  
Author(s):  
J. M. Sprenkle ◽  
D. L. Eckberg ◽  
R. L. Goble ◽  
J. J. Schelhorn ◽  
H. C. Halliday

We designed, constructed, and evaluated a new device to characterize the human carotid baroreceptor-cardiac reflex response relation rapidly. We designed this system for study of reflex responses of astronauts before, during, and after space travel. The system comprises a new tightly sealing silicone rubber neck chamber, a stepping motor-driven electro-deposited nickel bellows pressure system, capable of delivering sequential R-wave-triggered neck chamber pressure changes between +40 and -65 mmHg, and a microprocessor-based electronics system for control of pressure steps and analysis and display of responses. This new system provokes classic sigmoid baroreceptor-cardiac reflex responses with threshold, linear, and saturation ranges in most human volunteers during one held expiration.


1982 ◽  
Vol 242 (2) ◽  
pp. H185-H190 ◽  
Author(s):  
B. G. Wallin ◽  
D. L. Eckberg

We examined the role of carotid baroreceptors in the short-term modulation of sympathetic outflow to the muscle vascular bed and parasympathetic outflow to the heart in 10 healthy adults. Afferent carotid baroreceptor activity was modified with 30-mmHg neck suction or pressure applied during held expiration, and efferent sympathetic activity was measured with microelectrodes inserted percutaneously into peroneal nerve muscle fascicles. Sympathetic responses were conditioned importantly by directional changes of carotid transmural pressure: increased pressure (onset of neck suction or offset of neck pressure) inhibited (totally) sympathetic activity, and reduced pressure (offset of neck suction or onset of neck pressure) augmented sympathetic activity. Responses occurred after a latency of about 2 s and did not persist as long as changes of neck-chamber pressure. Cardiac intervals were prolonged by increased carotid transmural pressures and shortened by decreased carotid transmural pressures, but, in contrast to sympathetic responses, cardiac responses adapted only slightly during neck-chamber pressure changes. Our results suggest that in the human a common baroreceptor input is processed differently in central vagal and sympathetic networks. Muscle sympathetic responses to changing levels of afferent baroreceptor traffic are profound but transitory. They appear to be conditioned more by changes of arterial pressure than by its absolute levels.


1976 ◽  
Vol 51 (s3) ◽  
pp. 347s-349s ◽  
Author(s):  
J. Ludbrook ◽  
G. Mancia ◽  
A. Ferrari ◽  
A. Zanchetti

1. Transmission of pneumatic pressure from a neck chamber to the region of the carotid sinus is imperfect and asymmetric (86% of positive pressure, 64% of negative pressure). This has to be taken into account in the correct analysis of the carotid baroreceptor reflex. 2. There is no evidence for a reduction in cerebral blood flow nor of carotid chemoreceptor stimulation in response to an increase in neck chamber pressure of about 45 mmHg. Thus it is likely that the pressor response to this manoeuvre is in fact due to reduction in carotid baroreceptor activity.


1982 ◽  
Vol 62 (6) ◽  
pp. 581-588 ◽  
Author(s):  
Massimo Volpe ◽  
Bruno Trimarcoy ◽  
Bruno Ricciardelli ◽  
Carlo Vigorito ◽  
Nicola De Luca ◽  
...  

1. The effects of intravenous administration of neostigmine and propranolol, individually or in combination, on baroreflex responsiveness have been evaluated in 18 borderline hypertensive subjects and in 14 age-matched control subjects. 2. Baroreceptor sensitivity was tested by evaluating both heart rate response to phenylephrine-induced increase in arterial pressure, and heart rate and blood pressure changes induced by increasing neck-tissue pressure by means of a neck-chamber. 3. In borderline hypertensive subjects a reduced baroreflex responsiveness was demonstrated with both stimuli as compared with normal subjects. Neostigmine administration improved consistently both reflex responses. Similarly, after propranolol treatment, borderline hypertensive subjects showed a significant enhancement of the baroreflex sensitivity. Finally, the combined administration of neostigmine and propranolol restored the baroreflex responses. In fact, both the mean slopes of the regression lines between blood pressure and R-R interval after phenylephrine and the increase in mean arterial pressure and heart rate induced by the reduction in carotid transmural pressure in borderline hypertensive subjects were similar to those observed in normals. 4. These findings indicate that in borderline hypertensive subjects the impairment of baroreflex responsiveness is mainly due to abnormalities of autonomic regulation.


1979 ◽  
Vol 57 (s5) ◽  
pp. 165s-167s ◽  
Author(s):  
G. Mancia ◽  
G. Leonetti ◽  
G. B. Picotti ◽  
A. Ferrari ◽  
M. D. Galva ◽  
...  

1. Slight decreases and increases in carotid baroreceptor activity were induced in subjects with essential hypertension by slight alterations in carotid transmural pressure (variable pressure neck-chamber technique) in order to obtain limited increases and reductions in sympathetic adrenergic activity. 2. When sympathetic activity was reflexly increased there was a rise in arterial pressure but no significant increase in plasma catecholamines. Likewise when sympathetic activity was reflexly reduced there was a fall in arterial pressure but no significant reduction in plasma catecholamines. 3. Plasma noradrenaline and adrenaline significantly and markedly increased in the same subjects when sympathetic activity was increased by activation of both arterial and low pressure baroreceptor reflexes with tilting. 4. It is suggested that measurements of catecholamines in systemic plasma may reveal marked degrees of sympathetic activation but may not be a sensitive index of more moderate changes in sympathetic tone.


1976 ◽  
Vol 230 (4) ◽  
pp. 1026-1030 ◽  
Author(s):  
CP Bolter ◽  
Ledsome

In the chloralose-anesthetized dog the carotid sinus on one side of the neck was isolated vascularly. Pressure in the isolated sinus [carotid sinus pressure (CSP)], electrocardiogram, and systemic arterial pressure were recorded. Both vagosympathetic trunks were cut and the contralateral common carotid artery was occluded or the contralateral sinus nerve was cut to reduce reflex buffering of arterial pressure changes. By varying CSP from 50 to 250 mmHg the full range of the reflex response was examined. Electrical stimulation of the peripheral end of the cut ipsilateral cervical sympathetic nerve brought about a rapid decrease in mean arterial pressure (MAP) and heart rate (HR) at lower CSPs, no change in these variables at midrange CSPs, and a gradual increase at higher CSPs, such that the gain of the reflex was reduced (1.89 +/- 0.19 to 1.33 +/- 0.15 mmHg/mmHg). The decrease in MAP and HR at lower CSPs implies an increase in baroreceptor activity whereas the converse would appear to occur at higher CSPs. These responses attained a maximum value at low stimulus frequencies (less than 10 Hz).


1982 ◽  
Vol 62 (3) ◽  
pp. 307-309 ◽  
Author(s):  
D. H. Suarez ◽  
F. H. Messerli ◽  
H. O. Ventura ◽  
G. Aristimuno ◽  
G. R. Dreslinski ◽  
...  

1. The effects of carotid baroreceptor stimulation (neck chamber) on systemic haemodynamics were determined for normotensive and borderline hypertensive subjects during periods of resting and isometric exercise. 2. Both groups reacted to baroreceptor stimulation with a similar decrease in mean arterial pressure and cardiac index at rest and during isometric exercise, but baseline heart rate decreased more in borderline hypertensive patients. 3. Baroreceptor stimulation elicited the same haemodynamic response at rest and during exercise-induced arterial pressure increase. Since the magnitude of arterial pressure had no bearing on the subsequent response, these data suggest resetting of baroreceptors during this short-term blood pressure increase.


1989 ◽  
Vol 256 (2) ◽  
pp. R549-R553 ◽  
Author(s):  
J. M. Fritsch ◽  
R. F. Rea ◽  
D. L. Eckberg

We studied human baroreflex resetting during 25 min of drug-induced arterial pressure changes in 10 healthy volunteers. Average (+/- SE) base-line systolic pressure of 113 +/- 4 fell to 102 +/- 3 during nitroprusside infusions and rose to 135 +/- 6 mmHg during phenylephrine infusions. Average base-line R-R intervals of 932 +/- 37 shortened to 820 +/- 39 during nitroprusside infusions and lengthened to 1,251 +/- 61 ms during phenylephrine infusions. Carotid baroreceptor-cardiac reflex responses were evaluated with a complex series of neck chamber pressure changes, and R-R intervals were plotted as functions of carotid distending pressure. Baroreceptor-cardiac reflex relations shifted on both R-R interval and arterial pressure axes during drug infusions, but there was no significant change of the maximum slope or range of R-R interval responses. The position of baseline R-R intervals on the reflex relation (operational point) changed significantly. Resting R-R intervals were closer to threshold during pressure reductions and closer to saturation for baroreceptor-cardiac responses during pressure elevations. These results document short-term partial resetting of human baroreceptor-cardiac reflex responses as early as 25 min after the onset of arterial pressure changes.


1994 ◽  
Vol 77 (4) ◽  
pp. 1776-1783 ◽  
Author(s):  
J. M. Fritsch-Yelle ◽  
J. B. Charles ◽  
M. M. Jones ◽  
L. A. Beightol ◽  
D. L. Eckberg

Spaceflight is associated with decreased orthostatic tolerance after landing. Short-duration spaceflight (4–5 days) impairs one neural mechanism: the carotid baroreceptor-cardiac reflex. To understand the effects of longer-duration spaceflight on baroreflex function, we measured R-R interval power spectra, antecubital vein plasma catecholamine levels, carotid baroreceptor-cardiac reflex responses, responses to Valsalva maneuvers, and orthostatic tolerance in 16 astronauts before and after shuttle missions lasting 8–14 days. We found the following changes between preflight and landing day: 1) orthostatic tolerance decreased; 2) R-R interval spectral power in the 0.05 to 0.15-Hz band increased; 3) plasma norepinephrine and epinephrine levels increased; 4) the slope, range, and operational point of the carotid baroreceptor cardiac reflex response decreased; and 5) blood pressure and heart rate responses to Valsalva maneuvers were altered. Autonomic changes persisted for several days after landing. These results provide further evidence of functionally relevant reductions in parasympathetic and increases in sympathetic influences on arterial pressure control after spaceflight.


1998 ◽  
Vol 275 (3) ◽  
pp. H940-H945 ◽  
Author(s):  
Jonas Spaak ◽  
Patrik Sundblad ◽  
Dag Linnarsson

Our aim was to determine the roles of somatomotor activation and muscle ischemia for the tachycardia and hypertension of isometric arm contraction. Carotid-cardiac and carotid-mean arterial pressure (MAP) baroreflex response curves were determined in 10 men during rest, during isometric arm contraction at 30% of maximum, and during postcontraction ischemia. Carotid distending pressure (CDP) was changed by applying pressure and suction in a neck chamber. Pressures ranged from +40 to −80 mmHg and were applied repeatedly for 15 s during the three conditions. Maximum slopes and ranges of the response curves did not differ among conditions. The heart rate (HR) curve was shifted to a 14 ± 1.8 (mean ± SE) beats/min higher HR and a 9 ± 5.7 mmHg higher CDP during contraction and to a 14 ± 5.9 mmHg higher CDP during postcontraction ischemia with no change of HR compared with rest. The MAP curve was shifted to a 20 ± 2.8 mmHg higher MAP and to a 18 ± 5.4 mmHg higher CDP during contraction, and the same shifts were recorded during postcontraction ischemia. We conclude that neither somatomotor activation nor muscle ischemia changes the sensitivity of arterial baroreflexes. The upward shift of the MAP response curve, with no shift of the HR response curve during postexercise ischemia, supports the notion of parallel pathways for MAP and HR regulation in which HR responses are entirely caused by somatomotor activation and the pressor response is mainly caused by muscle ischemia.


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