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.

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.

Measurement of carotid body blood flow in cats by use of radioactive microspheres

1988 ◽  
Vol 65 (6) ◽  
pp. 2484-2489 ◽  
Author(s):  
S. Barnett ◽  
E. Mulligan ◽  
L. C. Wagerle ◽  
S. Lahiri
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Left Kidney ◽  
Tissue Blood Flow ◽  
Mechanically Ventilated ◽  
Carotid Bodies ◽  
Cervical Ganglia ◽  
New Evidence ◽  
Flow Experiments

To resolve the controversy regarding carotid body blood flow, we used the radioactive microsphere technique for determination of tissue blood flow. We also measured the blood flow to several other tissues in the cat. Blood flow experiments were performed on 13 cats that were anesthetized, paralyzed, and mechanically ventilated with air. Different numbers of differently labeled 9-, 15-, and 25-micron microspheres were injected via a catheter into the left atrium. It was determined that one injection of 5 x 10(6) 15-micron microspheres was appropriate for the determination of carotid body blood flow. Flows to the carotid bodies and other organs by use of this protocol were as follows (ml.min-1.100 g-1, means +/- SE): carotid bodies, 1,417 +/- 143; adrenal glands, 406 +/- 89; left kidney, 355 +/- 69; right kidney, 375 +/- 74; heart, 201 +/- 39; liver 81 +/- 14; pancreas, 80 +/- 21; superior cervical ganglia, 62 +/- 9; carotid artery wall, 2.4 +/- 1.1. The blood flow to the carotid bodies was the highest for any organ. This measurement provides new evidence that tissue blood flow to the carotid body is very high. This high flow is consistent with the prompt physiological reflex functions of the carotid body.

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.

Chemoreceptor involvement in cortisol responses to hypoxia in ventilated dogs

1982 ◽  
Vol 52 (4) ◽  
pp. 1092-1096 ◽  
Author(s):  
H. Raff ◽  
S. P. Tzankoff ◽  
R. S. Fitzgerald
Keyword(s):  
Carbon Monoxide ◽  
Carotid Body ◽  
Secretion Rate ◽  
Hypoxic Hypoxia ◽  
Cortisol Secretion ◽  
Carotid Bodies ◽  
Cortisol Responses

Changes in cortisol secretion rate (CSR) in response to hypoxic hypoxia (HH) and to carbon monoxide hypoxia (COH) were assessed in mongrel dogs that had intact chemoreceptors (INT); surgically deafferented carotid bodies (CBD) or aortic bodies (ABD); or both carotid and aortic chemoreceptors denervated (SAD). All dogs were anesthetized, paralyzed, ventilated, and maintained normocapnic. In the INT and ABD groups, CSR responded “maximally” to HH, whereas in CBD and SAD animals, the CSR was attenuated but not eliminated. COH, which does not stimulate the carotid body, caused a submaximal increase in CSR regardless of chemoreceptor status. It is concluded that 1) the carotid bodies are the principal chemoreceptor influence on CSR during HH and 2) there is a nonchemoreceptor-mediated increase in CSR during hypoxia.

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.

Analysis of inhibitory effect of dopamine on carotid body chemoreceptors in cats

1976 ◽  
Vol 230 (6) ◽  
pp. 1494-1498 ◽  
Author(s):  
SR Sampson ◽  
MJ Aminoff ◽  
RA Jaffe ◽  
EH Vidruk
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Carotid Sinus ◽  
Direct Action ◽  
Inhibitory Effect ◽  
Gas Mixture ◽  
Carotid Sinus Nerve ◽  
Perfusion Pump ◽  
Flow Through ◽  
Carotid Body Chemoreceptors

The inhibitory effect of dopamine on carotid body chemoreceptors was studied in anesthetized cats to determine whether it was dependent on changes in blood flow in the vicinity of the receptors. The blood supply to the carotid body was isolated, and flow was controlled with a perfusion pump. Single- or few-fiber recordings were made from the peripheral end of the cut carotid sinus nerve in seven cats. The rate of discharge of 68 chemoreceptor strands increased when flow through the carotid body was stopped. This response was reduced or abolished by dopamine in animals ventilated with either room air (15 strands) or a gas mixture of 95% O2 and 5% CO2 (53 strands). These results suggest that dopamine exerts its inhibitory effect primarily through a direct action on the chemoreceptors rather than by a vasomotor effect in the carotid body.

scholarly journals Autonomic innervation of the carotid body as a determinant of its sensitivity: implications for cardiovascular physiology and pathology

2020 ◽  
Author(s):  
Fernanda Brognara ◽  
Igor S A Felippe ◽  
Helio C Salgado ◽  
Julian F R Paton
Keyword(s):  
Blood Flow ◽  
Carotid Body ◽  
Neural Control ◽  
Metabolic Diseases ◽  
Cell Activity ◽  
Autonomic Innervation ◽  
Autonomic Nerves ◽  
Parasympathetic Nerves ◽  
Arterial Blood ◽  
Carotid Bodies

Abstract The motivation for this review comes from the emerging complexity of the autonomic innervation of the carotid body (CB) and its putative role in regulating chemoreceptor sensitivity. With the carotid bodies as a potential therapeutic target for numerous cardiorespiratory and metabolic diseases, an understanding of the neural control of its circulation is most relevant. Since nerve fibres track blood vessels and receive autonomic innervation, we initiate our review by describing the origins of arterial feed to the CB and its unique vascular architecture and blood flow. Arterial feed(s) vary amongst species and, unequivocally, the arterial blood supply is relatively high to this organ. The vasculature appears to form separate circuits inside the CB with one having arterial venous anastomoses. Both sympathetic and parasympathetic nerves are present with postganglionic neurons located within the CB or close to it in the form of paraganglia. Their role in arterial vascular resistance control is described as is how CB blood flow relates to carotid sinus afferent activity. We discuss non-vascular targets of autonomic nerves, their possible role in controlling glomus cell activity, and how certain transmitters may relate to function. We propose that the autonomic nerves sub-serving the CB provide a rapid mechanism to tune the gain of peripheral chemoreflex sensitivity based on alterations in blood flow and oxygen delivery, and might provide future therapeutic targets. However, there remain a number of unknowns regarding these mechanisms that require further research that is discussed.

Relative responses of aortic body and carotid body chemoreceptors to carboxyhemoglobinemia

1981 ◽  
Vol 50 (3) ◽  
pp. 580-586 ◽  
Author(s):  
S. Lahiri ◽  
E. Mulligan ◽  
T. Nishino ◽  
A. Mokashi ◽  
R. O. Davies
Keyword(s):  
Carbon Monoxide ◽  
Carotid Body ◽  
Carotid Chemoreceptors ◽  
State Response ◽  
Discharge Rates ◽  
Carotid Bodies ◽  
Tissue Po2 ◽  
Stimulus Source ◽  
Carotid Body Chemoreceptors ◽  
O2 Delivery

The effects of carbon monoxide inhalation and of consequent carboxyhemoglobinemia (HbCO) on the discharge rates of aortic body and carotid body chemoreceptor afferents were investigated in 18 anesthetized cats. In 10 experiments both aortic and carotid chemoreceptor activities were monitored simultaneously. Carbon monoxide inhalation during normoxia always stimulated aortic chemoreceptors before carotid chemoreceptors, and the steady-state response of aortic chemoreceptors to HbCO was greater than that of most carotid chemoreceptors. Only 2 of the 18 carotid chemoreceptor fibers tested showed a distinct increase in activity in response to moderate increases in HbCO%. Thus, oxyhemoglobin contributed substantially to maintain tissue PO2 of all aortic chemoreceptors and of a few carotid chemoreceptors. Hyperoxia diminished the response of both aortic and carotid chemoreceptors to HbCO, indicating a lowered tissue PO2 as the stimulus source. We hypothesize that the aortic bodies have a much lower perfusion relative to their O2 utilization compared to the carotid bodies. As a consequence, the aortic chemoreceptors are able to act as a sensitive monitor of O2 delivery and to generate a circulatory chemoreflex for O2 homeostasis. carotid chemoreceptors monitor O2 tension and initiate strong reflex effects on the level of ventilation.

Blood flow and relative tissue PO2 of brain and muscle: role of carotid chemoreceptors

1978 ◽  
Vol 45 (3) ◽  
pp. 419-424 ◽  
Author(s):  
J. A. Neubauer ◽  
R. S. Feldman ◽  
J. T. Huang ◽  
J. Vinten-Johansen ◽  
H. R. Weiss
Keyword(s):  
Blood Flow ◽  
Biceps Brachii ◽  
Gas Mixtures ◽  
Cerebral White Matter ◽  
Adrenergic Blockade ◽  
Carotid Bodies ◽  
Tissue Po2 ◽  
Intact Condition ◽  
The Brain ◽  
Intact Rats

The effects of inspiration of low O2 and/or high CO2 gas mixtures on relative tissue PO2 and perfusion of brain and muscle were studied in 60 pentobarbital-anesthetized spontaneously respiring rats. These animals were studied in intact condition, after administration of phenoxybenzamine hydrochloride, 2 mg/kg, or after bilateral denervation of their carotid bodies. In the intact rats, the relative tissue PO2 ratio of biceps brachii to cerebral white matter always decreased after exposure to the above gas mixtures. This indicated a better maintenance of O2 supply to demand in the brain than in muscle. After either carotid denervation or alpha adrenergic blockade, this change in the ratio was no longer significant. Further, cerebral blood flow responses to these gas mixtures were attenuated (avg + 5.3%) compared to previous work in intact rats. It is concluded that the brain is best protected against hypoxia and/or hypercapnia when the carotid chemoreflex is intact.

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