The Influence of Blood Pressure and Blood Flow on the Local Tissue Po2 of the Carotid Body

1973 ◽  
pp. 463-472 ◽  
Author(s):  
D. W. Lübbers ◽  
H. Acker ◽  
H. P. Keller ◽  
E. Seidl
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Body ◽  
Local Tissue ◽  
Tissue Po2

Chronic CO inhalation and carotid body catecholamines: testing of hypotheses

1989 ◽  
Vol 67 (1) ◽  
pp. 239-242 ◽  
Author(s):  
S. Lahiri ◽  
D. G. Penney ◽  
A. Mokashi ◽  
K. H. Albertine
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Direct Action ◽  
Systemic Effect ◽  
Hypoxic Hypoxia ◽  
Tissue Blood Flow ◽  
Catecholamine Content ◽  
Carotid Bodies ◽  
Significant Stimulation ◽  
Tissue Po2

The purpose of this study was twofold: one concerns carotid blood flow and tissue PO2 and the other the effect of chronic hypoxic hypoxia on enhanced catecholamine content. The rationale was that chronic CO inhalation would not mimic the effect of hypoxia on the carotid body if its tissue blood flow is sufficiently high to counteract the effect of CO on O2 delivery and, hence, on tissue PO2. The differential effects of CO on the carotid body and erythropoietin-producing tissue would also indicate that the effect of hypoxic hypoxia on the carotid body is the result of a direct action of a local low O2 stimulus rather than secondary to a systemic effect initiated by other O2-sensing tissues. To test these alternatives we studied the effects of chronic CO inhalation on carotid body catecholamine content and hematocrit in the rats, which were exposed to an inspired PCO of 0.4–0.5 Torr at an inspired PO2 of approximately 150 Torr for 22 days. The hematocrit of CO-exposed rats was 75 +/- 1.1% compared with 48 +/- 0.7% in controls. Dopamine and norepinephrine content of the carotid bodies (per pair) was 5.88 +/- 0.91 and 3.02 +/- 0.19 ng, respectively, in the CO-exposed rats compared with 6.20 +/- 1.0 and 3.29 +/- 0.6 ng, respectively, in the controls. Protein content of the carotid bodies (per pair) was 18.4 +/- 1.6 and 20.5 +/- 0.9 micrograms, respectively. Thus, despite a vigorous erythropoietic response, the CO-exposed rats failed to show any significant stimulation of carotid body in terms of the content of either catecholamine or protein. The results suggest that carotid body tissue PO2 is not compromised by moderate carboxyhemoglobinemia because of its high tissue blood flow and that the chronic effect of hypoxic hypoxia on carotid body is direct.

Some factors affecting tissue Po2 in the carotid body

1975 ◽  
Vol 39 (4) ◽  
pp. 562-566 ◽  
Author(s):  
W. J. Whalen ◽  
P. Nair
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Carotid Body ◽  
Discharge Rate ◽  
Reduced Pressure ◽  
Factors Affecting ◽  
Arterial Blood ◽  
Nervous System Activity ◽  
Tissue Po2 ◽  
Anesthetized Cat

In the carotid body (CB) of the anesthetized cat tissue Po2 (Pto2) measured with a micro O2 electrode averaged about 65 mmHg at normal arterial pressure (mean = 96 mmHg). Pto2 correlated significantly with the hematocrit of the arterial blood but not with % saturation. When arterial pressure was reduced (mean = 58 mmHg) by bleeding Pto2 fell significantly. Phentolamine injection (1 mg/kg iv) at the reduced pressure caused Pto2 to rise significantly. At normal arterial pressure blowing moistened O2 over the CB did not affect Pto2 if the electrode tip was about 90 mum into the CB. At a reduced pressure (and blood flow) the sensitive depth increased to about 301 mum, and to about 600 mum when flow was stopped. We concluded that a) the increased chemoceptor discharge usually seen with hemorrhage is due to reduced Pto2; b) the reduction in Pto2 is probably due to reduced blood flow which is, in turn, caused partly, at least, by sympathetic nervous system activity; c) O2 content, rather than Po2, may determine chemoreceptor discharge rate; and d) there are no barriers in the CB which are impermeable to O2.

PO2 in the carotid body perfused and/or superfused with cell-free media

1976 ◽  
Vol 41 (2) ◽  
pp. 180-184 ◽  
Author(s):  
W. J. Whalen ◽  
P. Nair
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Marked Reduction ◽  
Blood Perfusion ◽  
Normal Blood ◽  
O2 Consumption ◽  
Relative Measure ◽  
Artificial Cell ◽  
Tissue Po2 ◽  
Free Media

We measured with a micro-O2 electrode the tissue PO2 (PtO2) in the cat carotid body (CB) to see whether it was adequately oxygenated when perfused or superfused with artificial, cell-free (c-f) solutions (pH = 7.4; temp = 35–38 degrees C). To obtain a relative measure of O2 consumption (VO2), we also measured the rate of disappearance of O2 following stoppage of the blood flow, and compared these disappearance curves with those during stoppage of the c-f perfusion solutions. In 14 cats normal (blood perfusion) PtO2 values ranged from 10 to 104 mmHG; chi = 72 +/- 4 (SE--as used throughout). During 3 h of c-f perfusion with air-equilibrated Locke's solution, PtO2 ranged from 62 to about 160 mmHg; chi = 133 +/- 4. When perfused with Fay's equilibrated with 98% O2–2% CO2 no PtO2 values in the CB were below 300 mmHg (4 cats). In eight additional cats the CB was cleared of blood then superfused with saline equilibrated with 50% O2 underneath and air-equilibrated saline over. Less than 5% of the PtO2 values found were below 5 mmHg. We conclude that most studies on the artificially perfused or superfused CB cannot be invalidated on the basis that the preparations were hypoxic. O2 disappearance curves taken during blood perfusion were significantly faster than during c-f perfusion indicating a marked reduction in VO2 with c-f perfusion.

Carotid chemoreceptor reflex parasympathetic coronary vasodilation in the dog

1985 ◽  
Vol 249 (6) ◽  
pp. H1167-H1175 ◽  
Author(s):  
B. R. Ito ◽  
E. O. Feigl
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Body ◽  
Cardiac Metabolism ◽  
Transient Increase ◽  
Coronary Vasodilation ◽  
Arterial Blood ◽  
Body Regions ◽  
Aortic Blood ◽  
Aortic Blood Pressure

The hypothesis that carotid body chemoreceptor activation with hypoxic-hypercapnic blood elicits reflex coronary vasodilation was investigated. Circumflex or anterior descending coronary artery blood flow was measured in alpha-chloralose-anesthetized, closed-chest dogs. To minimize changes in cardiac metabolism, the heart was paced at a constant rate after atrioventricular heart block, propranolol (1 mg/kg) was given to prevent beta-receptor-mediated alterations in cardiac contractility, and aortic blood pressure was stabilized by means of a blood reservoir. The carotid body regions were vascularly isolated and perfused at constant pressure with arterial blood or hypoxic-hypercapnic blood. Under these conditions, carotid body chemoreceptor stimulation with hypoxic or hypoxic-hypercapnic blood for 90 s produced atrial bradycardia and a transient increase in coronary blood flow of 36–53% above prestimulation values. The augmented coronary flow was accompanied by a transient increase in coronary sinus O2 tension of 4.6–5.7 mmHg. Aortic blood pressure varied less than 10 mmHg. Intracarotid injections of nicotine (0.1 microgram/kg) or cyanide (150 micrograms) produced similar results. The coronary response to chemoreceptor stimulation with hypoxic blood or drugs was abolished when the reflex arc was interrupted with atropine (0.5 mg/kg). It is concluded that transient reflex parasympathetic coronary vasodilation is elicited by hypoxic or hypoxic-hypercapnic stimulation of carotid body chemoreceptors.

Two-cytochrome metabolic model for carotid body PtiO2 and chemosensitivity changes after hemorrhage

1989 ◽  
Vol 67 (1) ◽  
pp. 60-68 ◽  
Author(s):  
D. G. Buerk ◽  
P. K. Nair ◽  
W. J. Whalen
Keyword(s):  
Blood Pressure ◽  
Carotid Body ◽  
Metabolic Model ◽  
Arterial Blood ◽  
Blood Ph ◽  
Tissue Po2 ◽  
Blood Pressures ◽  
Microelectrode Measurements ◽  
Made In ◽  
Nerve Discharge

O2 microelectrode measurements were made in the cat carotid body (CB) at normal control blood pressures (C) and after hemorrhage (H) to reduce mean arterial blood pressure [C, 98.7 +/- 4.6 (SE) mmHg; H, 58.1 +/- 1.8; P less than 0.001; paired t test; n = 9 cats]. Mean tissue PO2 (PtiO2) was significantly lower (C, 78.4 +/- 3.0 Torr; H, 65.3 +/- 4.8; P less than 0.01). Except for two experiments with good autoregulation, the decrease in PtiO2 correlated with the reduction in blood pressure (r = 0.791, P less than 0.005). Measurements of O2 disappearance curves (DCs) and sinus nerve discharge (ND) were obtained after blood supply was occluded for 30–45 s (56 C DCs, 44 H DCs). Disappearance rates (dPO2/dt) were significantly slower after hemorrhage (C, -7.52 +/- 0.47 Torr/s; H, -6.60 +/- 0.44; P less than 0.01), decreasing by 0.656 Torr/s for each 10 Torr fall in PtiO2 (r = 0.626, P less than 0.05). Resting ND before occlusion increased during hypotension (11.6 +/- 2.9% of control, P less than 0.01) and correlated with the decrease in PtiO2 (r = -0.792, P less than 0.005). A computer simulation was performed for a two-cytochrome metabolic model with a second, low-O2-affinity oxidase in addition to normal oxidative metabolism. The effects of cat oxyhemoglobin and blood pH on the O2 DC measurement were also taken into account. The simulation for the two-cytochrome model was consistent with our experimental data and predicts reductions in blood flow and O2 metabolism with hypotension after hemorrhage that have similarities, as well as aspects that disagree, with previous reports in the literature.

Chronic CO exposure stimulates erythropoiesis but not glomus cell growth

1989 ◽  
Vol 67 (4) ◽  
pp. 1383-1387 ◽  
Author(s):  
A. K. Sherpa ◽  
K. H. Albertine ◽  
D. G. Penney ◽  
B. Thompkins ◽  
S. Lahiri
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Local Effect ◽  
Male Rats ◽  
Capillary Endothelium ◽  
Tissue Blood Flow ◽  
Type I ◽  
Carotid Bodies ◽  
Tissue Po2 ◽  
Significant Difference

The effect of chronic CO exposure, which stimulates erythropoietin production and erythropoiesis, was studied on carotid body cells in the rat. The hypothesis to be tested was that chronic CO inhalation would stimulate cellular hypertrophy and hyperplasia of carotid body if it caused local tissue hypoxia as in chronic hypoxia. The failure of an appropriate response would indicate a lack of a specific local effect on carotid body tissue PO2 presumably because of its unusually high tissue blood flow. Six young male rats were exposed to 0.4–0.5 Torr (0.05–0.07%) inspired PCO in air for 22 days. Control rats (n = 6) were maintained under similar conditions except for CO exposure. After the exposure period the rats were anesthetized, blood was collected for hematocrit, and the carotid bodies were surgically exposed and fixed for electron microscopy and morphometry of type I and type II cells and capillary endothelium. Hematocrit was significantly greater in the CO-exposed group (75 vs. 48%), whereas no significant difference was found in the carotid body parenchyma between the control and CO-exposed groups. We conclude that the lack of an effect of chronic CO exposure on the carotid bodies in contrast to the strong erythropoietic response indicates a relatively high tissue blood flow rate in the carotid body and that CO did not exert a direct cellular effect. The results also suggest that the hypertrophic response of carotid body glomus cells to chronic hypoxic hypoxia is the result of a local direct effect of low PO2 rather than secondary to systemic effects.

Decreased exercise hyperpnea in patients with bilateral carotid chemoreceptor resection

1979 ◽  
Vol 46 (5) ◽  
pp. 908-912 ◽  
Author(s):  
Y. Honda ◽  
S. Myojo ◽  
S. Hasegawa ◽  
T. Hasegawa ◽  
J. W. Severinghaus
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Carotid Body ◽  
Flow Limitation ◽  
Pulmonary Flow ◽  
Bilateral Carotid ◽  
Exercise Hyperpnea ◽  
Ventilatory Effects ◽  
End Tidal

Exercise hyperpnea was compared in 5 asthmatics 25 yr after bilateral carotid body resection (BR), 4 others 19 yr after unilateral resection (UR), and 12 controls (C) matched for age and pulmonary flow limitation. In the BR group, ventilation rose less with exercise, mostly because BR experienced less tachypnea. End-tidal PCO2 rose 5.8 +/- 3.2 (P less than 0.05) to 46 Torr at 50 W. In UR and C the same load did not increase PETCO2 significantly (+2.1 and +1.4 Torr, respectively). Arterial-end-tidal PCO2 differences before and 15--45 s postexercise were insignificant in all three groups. Heart rate and blood pressure rose equally in the three groups, suggesting that the ventilatory effects were not secondary to blood flow differences and disclosing no evidence of baroreceptor denervation during glomectomy.

Lutein Complex Supplementation Increases Ocular Blood Flow Biomarkers in Healthy Subjects

2019 ◽  
Vol 89 (1-2) ◽  
pp. 5-12
Author(s):  
Alon Harris ◽  
Brent Siesky ◽  
Amelia Huang ◽  
Thai Do ◽  
Sunu Mathew ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Diastolic Blood Pressure ◽  
Healthy Subjects ◽  
Ocular Blood Flow ◽  
Capillary Blood ◽  
Post Treatment ◽  
Capillary Blood Flow ◽  
Doppler Imaging ◽  
Retinal Capillary

Abstract. Introduction: To investigate the effects of a lutein complex supplementation on ocular blood flow in healthy subjects. Materials and Methods: Sixteen healthy female patients (mean age 36.8 ± 12.1 years) were enrolled in this randomized, placebo-controlled, double-blinded, two-period crossover study. Subjects received daily an oral dose of the lutein with synergistic phytochemicals complex (lutein (10 mg), ascorbic acid (500 mg), tocopherols (364 mg), carnosic acid (2.5 mg), zeaxanthin (2 mg), copper (2 mg), with synergistic effects in reducing pro-inflammatory mediators and cytokines when administered together in combination) and placebo during administration periods. Measurements were taken before and after three-week supplementation periods, with crossover visits separated by a three-week washout period. Data analysis included blood pressure, heart rate, intraocular pressure, visual acuity, contrast sensitivity detection, ocular perfusion pressure, confocal scanning laser Doppler imaging of retinal capillary blood flow, and Doppler imaging of the retrobulbar blood vessels. Results: Lutein complex supplementation produced a statistically significant increase in mean superior retinal capillary blood flow, measured in arbitrary units (60, p = 0.0466) and a decrease in the percentage of avascular area in the superior (−0.029, p = 0.0491) and inferior (−0.023, p = 0.0477) retina, as well as reduced systolic (−4.06, p = 0.0295) and diastolic (−3.69, p = 0.0441) blood pressure measured in mmHg from baseline. Data comparison between the two supplement groups revealed a significant decrease in systemic diastolic blood pressure (change from pre- to post-treatment with lutein supplement (mean (SE)): −3.69 (1.68); change from pre- to post-treatment with placebo: 0.31 (2.57); p = 0.0357) and a significant increase in the peak systolic velocity (measured in cm/sec) in the central retinal artery (change from pre- to post-treatment with lutein supplement: 0.36 (0.19); change from pre- to post-treatment with placebo: −0.33 (0.21); p = 0.0384) with lutein complex supplement; data analyses from the placebo group were all non-significant. Discussion: In healthy participants, oral administration of a lutein phytochemicals complex for three weeks produced increased ocular blood flow biomarkers within retinal vascular beds and reduced diastolic blood pressure compared to placebo.

Patterns of Cerebral Blood Flow and Systemic Hemodynamics During Arithmetic Processing

2008 ◽  
Vol 22 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Natalie Werner ◽  
Neval Kapan ◽  
Gustavo A. Reyes del Paso
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Doppler Sonography ◽  
Transcranial Doppler Sonography ◽  
Systemic Hemodynamics ◽  
Heart Period ◽  
Blood Flow Velocities ◽  
Flow Velocities

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.

COMPARISON OF ANTIHYPERTENSIVE EFFECT OF MOXONIDINE VERSUS CLONIDINE IN RENAL FAILURE PATIENTS.

2018 ◽  
Vol 6 (9) ◽  
Author(s):  
DR.MATHEW GEORGE ◽  
DR.LINCY JOSEPH ◽  
MRS.DEEPTHI MATHEW ◽  
ALISHA MARIA SHAJI ◽  
BIJI JOSEPH ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Blood Flow ◽  
Blood Vessel ◽  
Blood Vessels ◽  
High Blood Pressure ◽  
Antihypertensive Effect ◽  
The Body ◽  
Ability To Work ◽  
Blood Flows

Blood pressure is the force of blood pushing against blood vessel walls as the heart pumps out blood, and high blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the body. Factors that can increase this force include higher blood volume due to extra fluid in the blood and blood vessels that are narrow, stiff, or clogged(1). High blood pressure can damage blood vessels in the kidneys, reducing their ability to work properly. When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys.

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