Effect of dopamine on hypoxic ventilatory response of sedated piglets with intact and denervated carotid bodies

1994 ◽  
Vol 77 (1) ◽  
pp. 285-289 ◽  
Author(s):  
C. Suguihara ◽  
D. Hehre ◽  
E. Bancalari
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Initial Increase ◽  
Dopamine Antagonist ◽  
Drug Infusion ◽  
Endogenous Dopamine ◽  
Arterial Blood ◽  
Carotid Bodies

To determine whether the neonatal hypoxic ventilatory depression is in part produced by an increased endogenous dopamine release that can depress the activity of central and peripheral chemoreceptors, 31 sedated and spontaneously breathing newborn piglets [age 5 +/- 1 (SD) days; weight 1.7 +/- 0.4 kg] were randomly assigned to an intact carotid body or a chemodenervated group. Minute ventilation (VE), arterial blood pressure, and cardiac output (CO) were measured in room air before infusion of saline or the dopamine antagonist flupentixol (0.2 mg/kg i.v.) and 15 min after drug infusion and were repeated after 10 min of hypoxia (inspiratory O2 fraction = 0.10). VE increased significantly after 10 min of hypoxia in the piglets that received flupentixol independent of whether the carotid bodies were intact or denervated. However, the increase in VE was largest and sustained throughout the 10 min of hypoxia only in the intact carotid body flupentixol group. As expected, the initial increase in VE with hypoxia was abolished by carotid body denervation. Changes in arterial blood gases, CO, and mean arterial blood pressure with hypoxia were not different among groups. These results demonstrate that flupentixol reverses the late hypoxic decrease in VE, acting through peripheral and central dopamine receptors. This effect is not related to changes in cardiovascular function or acid-base status.

Relative latency of responses of chemoreceptor afferents from aortic and carotid bodies

1980 ◽  
Vol 48 (2) ◽  
pp. 362-369 ◽  
Author(s):  
S. Lahiri ◽  
T. Nishino ◽  
E. Mulligan ◽  
A. Mokashi
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Carotid Body ◽  
Blood Gases ◽  
Unexpected Result ◽  
Blood Gas ◽  
Arterial Blood Gases ◽  
Carotid Chemoreceptors ◽  
Arterial Blood ◽  
Carotid Bodies

Discharges from aortic and carotid body chemoreceptor afferents were simultaneously recorded in 18 anesthetized cats to test the hypothesis that aortic chemoreceptors, because of their proximity to the heart, respond to changes in arterial blood gases before carotid chemoreceptors. We found that carotid chemoreceptor responses to the onset of hypoxia and hypercapnia, and to the intravenously administered excitatory drugs (cyanide, nicotine, and doxapram), preceded those of aortic chemoreceptors. Postulating that this unexpected result was due to differences in microcirculation and mass transport, we also investigated their relative speed of responses to changes in arterial blood pressure. The aortic chemoreceptors responded to decreases in arterial blood pressure before the carotid chemoreceptors, supporting the idea that the aortic body has microcirculatory impediments not generally present in the carotid body. These findings strengthened the concept that carotid bodies are more suited for monitoring blood gas changes due to respiration, whereas aortic bodies are for monitoring circulation.

Interplay among carotid sinus, cardiopulmonary, and carotid body reflexes in dogs

1976 ◽  
Vol 230 (1) ◽  
pp. 19-24 ◽  
Author(s):  
G Mancia ◽  
JT Shepherd ◽  
DE Donald
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Dominant Role ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
Sinus Pressure

Interactions among vascular reflexes evoked from carotid sinuses, carotid bodies, and cardiopulmonary region were examined in anesthetized, atropinized, and respired dogs with aortic nerves cut. The carotid sinuses were perfused at 220, 150, and 40-50 mmHg; the chemoreceptors were stimulated by perfusion with hypoxic hypercapnic blood. Cardiopulmonary vasomotor inhibition was interrupted by vagal cold block. Measurements were made of arterial blood pressure and of kidney and hindlimb vascular resistance. At sinus pressures less than 170-160 mmHg, cardiopulmonary vasomotor inhibition increased with increase in blood volume. At high sinus pressure, interruption of this augmented cardiopulmonary inhibition was as ineffective in changing vascular resistance as interruption of the lesser inhibition present during normovolemia. Chemoreceptor stimulation increased the response to vagal block at intermediate but not at high or low sinus pressure. The studies demonstrate the dominant role of the carotid sinus reflex when the three systems interact and the ineffectiveness of chemoreceptor stimulation when carotid or cardiopulmonary inhibition is maximal.

Control of diving responses by carotid bodies and baroreceptors in ducks

1982 ◽  
Vol 242 (1) ◽  
pp. R105-R108 ◽  
Author(s):  
R. S. Lillo ◽  
D. R. Jones
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Carotid Body ◽  
Cardiovascular Responses ◽  
Pekin Ducks ◽  
Cardiac Responses ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
Carotid Body Chemoreceptors

The precise role of carotid body chemoreceptors and systemic baroreceptors in cardiovascular responses during experimental diving in ducks is controversial. The diving responses of chronically baroreceptor-denervated, chemoreceptor-denervated, and combined baroreceptor- and chemoreceptor-denervated White Pekin ducks, Anas platyrhynchos, were compared with those of intact and sham-operated birds. All three types of denervation elevated predive heart rates on average by 100-150 beats/min. During submergence, the cardiac rate of the barodenervates quickly dropped and after 60 s stabilized at levels similar to those of submerged intact ducks for the remainder of a 2-min dive. However, arterial blood pressure declined drastically in the barodenervates. Ducks without functional carotid bodies showed significant bradycardia during submergence, although heart rate only fell to the predive rate of intact animals. Birds with combined baroreceptor and chemoreceptor denervation exhibited the same degree of bradycardia as chemoreceptor denervates, and arterial blood pressure rose spectacularly during a dive. It is concluded that during experimental diving in ducks 1) cardiac responses are not baroreflexive in origin, 2) the major portion of bradycardia is due to stimulation of carotid body chemoreceptors, and 3) intact system baroreceptors appear essential for maintenance of blood pressure.

Augmentation of respiratory sinus arrhythmia in response to progressive hypercapnia in conscious dogs

2001 ◽  
Vol 280 (5) ◽  
pp. H2336-H2341 ◽  
Author(s):  
Fumihiko Yasuma ◽  
Jun-Ichiro Hayano
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Respiratory Sinus Arrhythmia ◽  
Physiological Response ◽  
Minute Ventilation ◽  
Control Level ◽  
Conscious Dogs ◽  
Sinus Arrhythmia ◽  
Arterial Blood

Respiratory sinus arrhythmia (RSA) may serve to enhance pulmonary gas exchange efficiency by matching pulmonary blood flow with lung volume within each respiratory cycle. We examined the hypothesis that RSA is augmented as an active physiological response to hypercapnia. We measured electrocardiograms and arterial blood pressure during progressive hypercapnia in conscious dogs that were prepared with a permanent tracheostomy and an implanted blood pressure telemetry unit. The intensity of RSA was assessed continuously as the amplitude of respiratory fluctuation of heart rate using complex demodulation. In a total of 39 runs of hypercapnia in 3 dogs, RSA increased by 38 and 43% of the control level when minute ventilation reached 10 and 15 l/min, respectively ( P < 0.0001 for both), and heart rate and mean arterial pressure showed no significant change. The increases in RSA were significant even after adjustment for the effects of increased tidal volume, respiratory rate, and respiratory fluctuation of arterial blood pressure ( P < 0.001). These observations indicate that increased RSA during hypercapnia is not the consequence of altered autonomic balance or respiratory patterns and support the hypothesis that RSA is augmented as an active physiological response to hypercapnia.

scholarly journals Multi-Model Adaptive Predictive Control System for Automated Regulation of Mean Blood Pressure

2019 ◽  
Vol 15 (11) ◽  
pp. 69 ◽  
Author(s):  
Humberto Silva ◽  
Celina Leão ◽  
Eurico Seabra
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Infusion Rate ◽  
Weighting Factor ◽  
Control Procedure ◽  
Drug Infusion ◽  
Arterial Blood ◽  
Simulation Results

After cardiac surgery operation, severe complications may occur in patients due to hypertension. To decrease the chances of complication it is necessary to reduce elevated mean arterial pressure (MAP) as soon as possible. Continuous infusion of vasodilator drugs, such as sodium nitroprusside (Nipride), it is used to reduce MAP quickly in most patients. For maintaining the desired blood pressure, a constant monitoring of arterial blood pressure is required and a frequently adjust on drug infusion rate. The manual control of arterial blood pressure by clinical professionals it is very demanding and time consuming, usually leading to a poor control quality of the hypertension. The objective of the study is to develop an automated control procedure of mean arterial pressure (MAP), during acute hypotension, for any patient, without changing the controller. So, a multi-model adaptive predictive methodology was developed and, for each model, a Predictive Controller can be a priori designed (MMSPGPC). In this paper, a sensitivity analysis was performed and the simulation results showed the importance of weighting factor (φ), which controls the initial drug infusion rate, to prevent hypotension and thus preserve patient's health. Simulation results, for 51 different patients, showed that the MMSPGPC provides a fast control with mean settling time of 04:46 min, undershoots less than 10 mmHg and steady-state error less than ± 5 %  from the MAP setpoint.

Ventilatory response to isocapnic hyperoxia

1995 ◽  
Vol 78 (2) ◽  
pp. 696-701 ◽  
Author(s):  
H. Becker ◽  
O. Polo ◽  
S. G. McNamara ◽  
M. Berthon-Jones ◽  
C. E. Sullivan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Minute Ventilation ◽  
Normobaric Hyperoxia ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Blood Gas Analyses ◽  
End Tidal ◽  
Arterial Po2

Breathing O2 for up to 1 h has been shown to either not influence or slightly increase (6–13%) minute ventilation. However, end-tidal PCO2 was not kept constant in these experiments. In nine healthy men, we studied the ventilatory, blood pressure, and heart rate responses to 30 min of normobaric hyperoxia (50% O2) at isocapnic conditions. Hyperoxia led to a 60% increase in mean minute ventilation (P = 0.002), largely due to an increase in mean tidal volume from 0.66 +/- 0.04 (SE) to 0.88 +/- 0.05 liter (P = 0.007). Fifteen minutes after the termination of hyperoxia, minute ventilation was still increased (P = 0.02) compared with baseline, although it was reduced compared with hyperoxia (P = 0.02). Arterial blood gas analyses in six subjects before and during hyperoxia showed an increase in arterial PO2 and O2 saturation but no change in arterial PCO2 or pH. Hyperoxia induced no changes in arterial blood pressure or heart rate. We conclude that 1) isocapnic hyperoxia stimulates respiration markedly, an effect that is approximately five times higher than previously measured; 2) the increase in ventilation induced by hyperoxia does not affect arterial blood pressure and heart rate; and 3) in experiments using hyperoxia, its effect on breathing and subsequently on PCO2 has to be taken into account.

Sympathetic nervous activity and arterial blood pressure control in conscious rat during rest and behavioral stress

1994 ◽  
Vol 267 (5) ◽  
pp. R1241-R1249 ◽  
Author(s):  
D. C. Randall ◽  
D. R. Brown ◽  
L. V. Brown ◽  
J. M. Kilgore
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Neural Control ◽  
Nervous Activity ◽  
Sympathetic Nervous Activity ◽  
Initial Increase ◽  
Conditional Response ◽  
Arterial Blood ◽  
Behavioral Stress ◽  
Sympathetic Nervous

The object of this experiment is to analyze the neural control of arterial blood pressure (BP) during rest and a sudden behavioral stress. Sprague-Dawley rats were classically conditioned by following a 15-s tone (CS+) with a 0.5-s tail shock. Bipolar renal nerve electrodes and a caudal artery catheter were implanted. Two days later BP and sympathetic nervous activity (SNA) were recorded in the behaviorally trained animals. The CS+ evoked a large initial increase in BP (peak, 14 +/- 5 mmHg, mean +/- SD; n = 12) that lasted 3.9 +/- 0.8 s. An abrupt (latency = 0.16 +/- 0.03 s), short (duration = 0.58 +/- 0.12 s), and intense (4.09 +/- 1.02 times average control) burst in sympathetic activity preceded this first component (C1) of the BP conditional response. The size of C1 was related to the magnitude of the SNA burst. SNA then fell below control; this quiet period preceded a fall in BP after the C1 peak. Pressure rose again (C2; peak = 6 +/- 3 mmHg, average increase = 3 +/- 3 mmHg) for the remainder of the CS+. SNA increased to 1.24 +/- 0.14 of control during this second component of the BP conditional response. Ganglionic blockade eliminated the BP and SNA conditional response (n = 3). The C1 pressure increase appears to result from an “open-loop” process in which a brief barrage of nerve activity governs BP changes lasting several seconds. The quite period probably results from a negative feedback (i.e., baroreflex) relationship between SNA and BP.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Resection of Carotid Body Tumors reduces arterial blood pressure. An underestimated neuroendocrine syndrome

2014 ◽  
Vol 12 ◽  
pp. S63-S67 ◽  
Author(s):  
Stefano de Franciscis ◽  
Raffaele Grande ◽  
Lucia Butrico ◽  
Gianluca Buffone ◽  
Luca Gallelli ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Carotid Body ◽  
Arterial Blood ◽  
Carotid Body Tumors
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