Carotid baroreflex resetting during drug-induced arterial pressure changes in humans

1989 ◽  
Vol 256 (2) ◽  
pp. R549-R553 ◽  
Author(s):  
J. M. Fritsch ◽  
R. F. Rea ◽  
D. L. Eckberg
Keyword(s):  
Arterial Pressure ◽  
Systolic Pressure ◽  
Chamber Pressure ◽  
Base Line ◽  
Drug Induced ◽  
Maximum Slope ◽  
Reflex Responses ◽  
Cardiac Responses ◽  
Carotid Baroreflex ◽  
Pressure Changes

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.

Head-down bed rest impairs vagal baroreflex responses and provokes orthostatic hypotension

1990 ◽  
Vol 68 (4) ◽  
pp. 1458-1464 ◽  
Author(s):  
V. A. Convertino ◽  
D. F. Doerr ◽  
D. L. Eckberg ◽  
J. M. Fritsch ◽  
J. Vernikos-Danellis
Keyword(s):  
Orthostatic Hypotension ◽  
Plasma Volume ◽  
Systolic Pressure ◽  
Bed Rest ◽  
Chamber Pressure ◽  
Plasma Norepinephrine ◽  
Base Line ◽  
Maximum Slope ◽  
Before And After ◽  
Neck Pressure

We studied vagally mediated carotid baroreceptor-cardiac reflexes in 11 healthy men before, during, and after 30 days of 6 degrees head-down bed rest to test the hypothesis that baroreflex malfunction contributes to orthostatic hypotension in this model of simulated microgravity. Sigmoidal baroreflex response relationships were provoked with ramped neck pressure-suction sequences comprising pressure elevations to 40 mmHg followed by serial R-wave-triggered 15-mmHg reductions to -65 mmHg. Each R-R interval was plotted as a function of systolic pressure minus the neck chamber pressure applied during the interval. Compared with control measurements, base-line R-R intervals and the minimum, maximum, range, and maximum slope of the R-R interval-carotid pressure relationships were reduced (P less than 0.05) from bed rest day 12 through recovery day 5. Baroreflex slopes were reduced more in four subjects who fainted during standing after bed rest than in six subjects who did not faint (-1.8 +/- 0.7 vs. -0.3 +/- 0.3 ms/mmHg, P less than 0.05). There was a significant linear correlation (r = 0.70, P less than 0.05) between changes of baroreflex slopes from before bed rest to bed rest day 25 and changes of systolic blood pressure during standing after bed rest. Although plasma volume declined by approximately 15% (P less than 0.05), there was no significant correlation between reductions of plasma volume and changes of baroreflex responses. There were no significant changes of before and after plasma norepinephrine or epinephrine levels before and after bed rest during supine rest or sitting.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympathetic transients caused by abrupt alterations of carotid baroreceptor activity in humans

1982 ◽  
Vol 242 (2) ◽  
pp. H185-H190 ◽  
Author(s):  
B. G. Wallin ◽  
D. L. Eckberg
Keyword(s):  
Sympathetic Activity ◽  
Chamber Pressure ◽  
Reduced Pressure ◽  
Cardiac Responses ◽  
Carotid Baroreceptor ◽  
Sympathetic Responses ◽  
Nerve Muscle ◽  
Neck Pressure ◽  
Pressure Changes ◽  
Neck Chamber

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.

scholarly journals Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure

1997 ◽  
Vol 83 (2) ◽  
pp. 371-375 ◽  
Author(s):  
Oommen P. Mathew
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Systolic Blood Pressure ◽  
Cardiac Cycle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Intrathoracic Pressure ◽  
Systemic Arterial Pressure ◽  
Pressure Changes

Mathew, Oommen P. Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure. J. Appl. Physiol. 83(2): 371–375, 1997.—The purpose of the study was to determine the effect of transient changes in intrathoracic pressure on systemic arterial pressure by utilizing hiccups as a tool. Values of systolic and diastolic pressures before, during, and after hiccups were determined in 10 intubated preterm infants. Early-systolic hiccups decreased systolic blood pressure significantly ( P < 0.05) compared with control (39.38 ± 2.72 vs. 46.46 ± 3.41 mmHg) and posthiccups values, whereas no significant change in systolic blood pressure occurred during late-systolic hiccups. Diastolic pressure immediately after the hiccups remained unchanged during both early- and late-systolic hiccups. In contrast, diastolic pressure decreased significantly ( P < 0.05) when hiccups occurred during diastole (both early and late). Systolic pressures of the succeeding cardiac cycle remained unchanged after early-diastolic hiccups, whereas they decreased after late-diastolic hiccups. These results indicate that transient decreases in intrathoracic pressure reduce systemic arterial pressure primarily through an increase in the volume of the thoracic aorta. A reduction in stroke volume appears to contribute to the reduction in systolic pressure.

Enhanced vagal baroreflex response during 24 h after acute exercise

1991 ◽  
Vol 260 (3) ◽  
pp. R570-R575 ◽  
Author(s):  
V. A. Convertino ◽  
W. C. Adams
Keyword(s):  
Acute Exercise ◽  
Systolic Pressure ◽  
Underlying Mechanism ◽  
Chamber Pressure ◽  
External Application ◽  
Maximum Slope ◽  
Acute Bout ◽  
Graded Exercise ◽  
Pressure Stability ◽  
Neck Chamber

We evaluated carotid-cardiac baroreflex responses in eight normotensive men (25-41 yr) on two different test days, each separated by at least 1 wk. On one day, baroreflex response was tested before and at 3, 6, 12, 18, and 24 h after graded supine cycle exercise to volitional exhaustion. On another day, this 24-h protocol was repeated with no exercise (control). Beat-to-beat R-R intervals were measured during external application of graded pressures to the carotid sinuses from 40 to -65 mmHg; changes of R-R intervals were plotted against carotid pressure (systolic pressure minus neck chamber pressure). The maximum slope of the response relationship increased (P less than 0.05) from preexercise to 12 h (3.7 +/- 0.4 to 7.1 +/- 0.7 ms/mmHg) and remained significantly elevated through 24 h. The range of the R-R response was also increased from 217 +/- 24 to 274 +/- 32 ms (P less than 0.05). No significant differences were observed during the control 24-h period. An acute bout of graded exercise designed to elicit exhaustion increases the sensitivity and range of the carotid-cardiac baroreflex response for 24 h and enhances its capacity to buffer against hypotension by increasing heart rate. These results may represent an underlying mechanism that contributes to blood pressure stability after intense exercise.

Regional vascular influences on tail-cuff measurements of drug-induced changes in systolic pressure

1975 ◽  
Vol 39 (5) ◽  
pp. 724-727 ◽  
Author(s):  
R. D. Bunag ◽  
N. Mueting ◽  
E. Riley
Keyword(s):  
Arterial Pressure ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Drug Effects ◽  
Indirect Measurement ◽  
Systemic Arterial Pressure ◽  
Drug Induced ◽  
Caudal Artery ◽  
Induced Changes ◽  
Tail Cuff

When drug effects are quantified using the tail-cuff method, changes in systemic arterial pressure are extrapolated from those occurring in the caudal artery. The validity of this extrapolation was tested in anesthetized rats by recording drug-induced changes in phasic arterial pressure simultaneously from catheters inserted into the lower abdominal aorta, carotid, and caudal arteries. Pressor responses to norepinephrine or angiotensin were of equal magnitude at all three sites, but phentolamine reduced systolic pressure in the aorta or caudal artery more than that in the carotid artery. Unlike previous discrepancies between carotid and tail-cuff systolic pressures, aortic hypotension caused by injections of phentolamine or pentolinium in awake normotensive or spontaneously hypertensive rats was accurately predicted by the tail-cuff method. Because drug-induced changes in diastolic pressure always varied much less than those in systolic pressure, should indirect measurement of diastolic pressure become technically feasible, it might be preferable for assessing drug effects on blood pressure.

scholarly journals Carotid baroreflex control of heart rate is enhanced, while control of mean arterial pressure is preserved during whole body heat stress in young healthy men

2016 ◽  
Vol 311 (4) ◽  
pp. R735-R741 ◽  
Author(s):  
Davor Krnjajic ◽  
Dustin R. Allen ◽  
Cory L. Butts ◽  
David M. Keller
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Whole Body ◽  
Chamber Pressure ◽  
Carotid Baroreflex ◽  
Whole Body Heat Stress ◽  
Neck Pressure ◽  
Body Heat

Whole body heat stress (WBH) results in numerous cardiovascular alterations that ultimately reduce orthostatic tolerance. While impaired carotid baroreflex (CBR) function during WBH has been reported as a potential reason for this decrement, study design considerations may limit interpretation of previous findings. We sought to test the hypothesis that CBR function is unaltered during WBH. CBR function was assessed in 10 healthy male subjects (age: 26 ± 3; height: 185 ± 7 cm; weight: 82 ± 10 kg; BMI: 24 ± 3 kg/m2; means ± SD) using 5-s trials of neck pressure (+45, +30, and +15 Torr) and neck suction (−20, −40, −60, and −80 Torr) during normothermia (NT) and passive WBH (Δ core temp ∼1°C). Analyses of stimulus response curves (four-parameter logistic model) for CBR control of heart rate (CBR-HR) and mean arterial pressure (CBR-MAP), as well as separate two-way ANOVA of the hypotensive and hypertensive stimuli (factor 1: thermal condition, factor 2: chamber pressure), were performed. For CBR-HR, maximal gain was increased during WBH (−0.73 ± 0.11) compared with NT (−0.39 ± 0.04, mean ± SE, P = 0.03). In addition, the CBR-HR responding range was increased during WBH (33 ± 5) compared with NT (19 ± 2 bpm, P = 0.03). Separate analysis of hypertensive stimulation revealed enhanced HR responses during WBH at −40, −60, and −80 Torr (condition × chamber pressure interaction, P = 0.049) compared with NT. For CBR-MAP, both logistic analysis and separate two-way ANOVA revealed no differences during WBH. Therefore, in response to passive WBH, CBR control of heart rate (enhanced) and arterial pressure (no change) is well preserved.

Pulsatile sinus pressure changes evoke sustained baroreflex responses in awake dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H673-H678 ◽  
Author(s):  
D. Mendelowitz ◽  
A. M. Scher
Keyword(s):  
Arterial Pressure ◽  
Pulse Pressure ◽  
Carotid Sinus ◽  
Pressure Change ◽  
Conscious Dogs ◽  
Reflex Responses ◽  
Depressor Response ◽  
Pulsatile Pressure ◽  
Pressure Changes ◽  
Sinus Pressure

A modified Stephenson-Donald preparation was used to control pressure in an isolated carotid sinus in conscious dogs with all other arterial baroreceptors denervated. Sinus pressure was changed from preisolation control levels to either an elevated static or an elevated pulsatile pressure for 5 min. These sinus pressure changes evoked similar initial decreases in arterial pressure. The elevated static sinus pressure (150 or 175 mmHg) caused an initial depressor response of -32.7 +/- 5.5 mmHg, which then decayed rapidly. Five minutes after the change in sinus pressure, the depressor response was abolished, as arterial pressure returned to control pressure. This decay of the response would be expected if resetting occurred. In contrast, when the sinus was exposed to elevated pulsatile pressures (125 or 150 mmHg mean, 50 mmHg pulse pressure) depressor responses were sustained throughout the sinus pressure change (-23.2 +/- 5.3 mmHg initial, -29.0 +/- 4.8 mmHg at 5 min; P greater than 0.4). These results demonstrate that while the reflex responses rapidly reset to elevated static sinus pressures, elevated pulsatile pressures elicit sustained reflex responses.

Reproducibility of human vagal carotid baroreceptor-cardiac reflex responses

1992 ◽  
Vol 263 (1) ◽  
pp. R215-R220 ◽  
Author(s):  
D. L. Eckberg ◽  
V. A. Convertino ◽  
J. M. Fritsch ◽  
D. F. Doerr
Keyword(s):  
Correlation Coefficients ◽  
Experimental Session ◽  
Experimental Conditions ◽  
Reduced Pressure ◽  
Maximum Slope ◽  
Reflex Responses ◽  
Stimulus Response ◽  
Carotid Baroreceptor ◽  
Neck Pressure ◽  
Pressure Changes

Published information on the reproducibility of human baroreflex responses in the absence of interventions is limited. Therefore, we analyzed retrospectively vagally mediated carotid baroreceptor-cardiac reflex responses of 34 healthy young adult volunteers whom we studied twice, 7-10 days apart (all 34 subjects) or 10 wk apart (8 subjects). We delivered a sequence of neck pressure changes during held expiration: A computer-driven bellows initially raised pressure to approximately 40 mmHg for five heart beats, and then reduced pressure in a stepwise series of R-wave-triggered 15-mmHg decrements to about -65 mmHg. R-R interval changes were plotted as functions of the carotid distending (systolic less neck) pressure occurring within each interval. Each experimental session yielded one stimulus-response relation, which comprised the average of seven separate trials. Six measures were derived from these relations: minimum, maximum, and range of R-R intervals; maximum slope; and operational point [(R-R interval shortening/R-R interval range) x 100%]. Linear regression correlation coefficients for measurements made on two occasions were all highly significant (range: 0.64-0.99). Our results indicate that human vagally mediated carotid baroreceptor-cardiac reflex responses, studied serially under exacting experimental conditions, are highly reproducible.

scholarly journals Blood pressure changes in dogs with babesiosis

2000 ◽  
Vol 71 (1) ◽  
Author(s):  
L.S. Jacobson ◽  
R.G. Lobetti ◽  
T. Vaughan-Scott
Keyword(s):  
Arterial Pressure ◽  
Systolic Pressure ◽  
Systolic Arterial Pressure ◽  
Significant Negative Correlation ◽  
Arterial Blood ◽  
Significant Relationships ◽  
Normal Mean ◽  
Blood Pressures ◽  
Pressure Changes ◽  
And Control

Systemic arterial blood pressures were measured in 30 dogs with acute babesiosis, 10 each with mild uncomplicated, severe uncomplicated and complicated disease. Ten healthy dogs were used as controls. Hypotension was defined as more than 3 standard deviations below the control mean. Normal mean pressures (±SD) were: systolic arterial pressure 151 (±11) mm Hg, diastolic arterial pressure 89 (±8) mm Hg and mean arterial pressure 107 (±10) mmHg. Hypotension was the most frequent abnormality, and increased strikingly in incidence as disease severity increased, with 5/10 dogs in the complicated group being hypotensive for systolic, diastolic and mean arterial pressures, compared with 2/10 in the severe uncomplicated group and 0/10 in the mild uncomplicated group. Systolic, diastolic and mean arterial pressures in the complicated group and severe uncomplicated group, and systolic pressure in the mild uncomplicated group, were significantly lower than in the controls. There were no significant relationships between arterial pressures and age, pulse rate, respiratory rate, temperature, mucous membrane colour or haematocrit. There was a significant negative correlation between arterial pressures and white cell and immature neutrophil counts. Arterial pressures differed significantly between dogs that were clinically collapsed and those that were not, but not between survivors and non-survivors. Pulse pressure (systolic - diastolic) was low in 7/10 complicated, 1/10 mild uncomplicated, and 1/10 severe uncomplicated cases, and differed significantly between the complicated and control groups. The high incidence of hypotension in clinically severe babesiosis has important implications for therapy.

Hemodynamic effects of anti-G suit inflation in a 1-G environment

1985 ◽  
Vol 59 (4) ◽  
pp. 1145-1151 ◽  
Author(s):  
J. F. Seaworth ◽  
T. J. Jennings ◽  
L. L. Howell ◽  
J. W. Frazier ◽  
C. D. Goodyear ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Cardiac Preload ◽  
Base Line ◽  
End Diastolic Volume ◽  
Dimensional Echocardiography ◽  
Pressure Changes ◽  
Relationship Of

This study evaluated effects of various anti-G inflation pressures on cardiac volumes and the relationship of these volume changes to mean arterial pressure changes. Ventricular volumes were calculated using two-dimensional echocardiography. An anti-G suit was inflated to 2, 4, and 6 psi in the standing and supine positions for 10 male subjects. In the supine position, mean arterial pressure increased from base line for all three inflation pressures (P = 0.05). The end-diastolic volume increased after 2-psi inflation (P = 0.03). Cardiac output or stroke volume did not change. After standing, mean arterial pressure (P = 0.002), end-diastolic volume (P = 0.002), and stroke volume (P = 0.05) fell after suit deflation. Peripheral vascular resistance fell in the 2- and 4-psi inflation profiles. In the standing protocol, mean arterial pressure, end-diastolic volume, stroke volume, and cardiac output rose with all three inflation pressures (P less than 0.05). After reclining, heart rate increased (P = 0.02) and mean arterial pressure fell (P less than 0.05) in the 4- and 6-psi inflation profiles after suit deflation. Increases in mean arterial pressure are caused by increases in cardiac preload and cardiac output after inflation of the anti-G suit while subjects were standing. Increased cardiac preload was not consistently seen after inflation while subjects were supine. Changes in end-diastolic volume and mean arterial pressure were dependent on the pressure used to inflate the anti-G suit.

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