Central Modulation of Arterial Chemoreceptor Control by Midazolam during Severe Arterial Hypoxia in the Rabbit

The nucleus tractus solitarius (NTS) is the primary site of termination of arterial baroreceptor and chemoreceptor afferent fibers. Excitatory amino acid (EAA) receptors within NTS have been shown to play an important role in the mediation of arterial baroreceptor reflexes; however, the importance of EAA receptors within NTS in the mediation of arterial chemoreceptor reflexes remains controversial. Therefore, in chloralose-urethan-anesthetized, mechanically ventilated, paralyzed rats, 4 nmol of the broad-spectrum EAA receptor antagonist kynurenic acid (Kyn) was injected into the NTS to observe the effects of EAA receptor blockade on the pressor responses evoked by either activation of ipsilateral carotid body chemoreceptors (by close arterial injection of CO2-saturated bicarbonate) or electrical stimulation of ipsilateral carotid sinus nerve (CSN). Under control conditions, activation of carotid body chemoreceptors and CSN stimulation evoked increases in arterial pressure of 27 +/- 2 (n = 24 sites) and 28 +/- 3% (n = 8), respectively. Kyn microinjection into NTS significantly reduced the pressor responses evoked by activation of carotid body chemoreceptors and electrical stimulation of the CSN for 20 and 25 min, respectively. Attenuation of pressor responses evoked by chemoreceptor activation were maximal at 20 min post-Kyn injection (13 +/- 2%), whereas CSN-evoked pressor responses were maximally attenuated at 15 min (6 +/- 4%). Microinjection into NTS of 4 nmol of xanthurenic acid, a structural analogue of Kyn with no EAA receptor antagonist properties, had no effect on chemoreceptor reflexes. We conclude that EAA receptors within NTS play an important role in the mediation of arterial chemoreceptor reflexes.

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Blood Pco2 and brain oxygenation at reduced ambient pressure

Journal of Applied Physiology ◽

10.1152/jappl.1962.17.6.899 ◽

1962 ◽

Vol 17 (6) ◽

pp. 899-908 ◽

Cited By ~ 7

Author(s):

E. C. Pierce ◽

C. J. Lambertsen ◽

M. J. Strong ◽

S. C. Alexander ◽

D. Steele

Keyword(s):

Ambient Pressure ◽

Minute Volume ◽

Pure Oxygen ◽

Chemical Stimulus ◽

Arterial Oxygenation ◽

Brain Oxygenation ◽

Respiratory Effect ◽

Cerebral Vasoconstriction ◽

Respiratory Stimulation ◽

Arterial Chemoreceptor

Hyperventilation during breathing of 100% oxygen elevates the Po2 of alveolar gas by the same amount that it lowers its Pco2. Since the development of arterial hypocapnia causes cerebral vasoconstriction, brain oxygenation is drastically decreased even while arterial oxygenation is improved by hyperventilation. Administration of 30% CO2 with oxygen at an ambient pressure equivalent to that at 39,000-ft altitude prevented alkalemia and, in spite of hyperventilation, restored cerebral venous oxygenation to a level at least equivalent to that found when pure oxygen was breathed at rest at the same altitude. The respiratory minute volume during administration of CO2 with O2 was greater than when O2 alone was breathed at reduced ambient pressure. Since neither arterial Po2 nor cerebral venous Pco2 values differed in these two experimental situations, the respiratory stimulation may represent the quantitative demonstration in man of a respiratory effect of CO2 mediated by arterial chemoreceptor activation and unrelated to change in the level of central chemical stimulus. Submitted on March 16, 1962

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Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension

Cardiovascular Research ◽

10.1093/cvr/16.3.163 ◽

1982 ◽

Vol 16 (3) ◽

pp. 163-172 ◽

Cited By ~ 128

Author(s):

A. TRZEBSKI ◽

M. TAFIL ◽

M. ZOLTOWSKI ◽

J. PRZYBYLSKI

Keyword(s):

Mild Hypertension ◽

Young Men ◽

Increased Sensitivity ◽

Arterial Chemoreceptor

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Influence of CO2 on cardiovascular response to hypoxia in conscious dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1980.239.4.h545 ◽

1980 ◽

Vol 239 (4) ◽

pp. H545-H545 ◽

Cited By ~ 13

Author(s):

Raymond C. Koehler ◽

Brian W. McDonald ◽

John A. Krasney

Keyword(s):

Cardiovascular Response ◽

Left Ventricular ◽

Vagal Afferents ◽

Conscious Dogs ◽

Coronary Vasodilation ◽

Circulatory Response ◽

Wide Range ◽

Before And After ◽

Tension Time ◽

Arterial Chemoreceptor

The modulating effect of CO2 on the circulatory response to hypoxia in chronically instrumented conscious dogs was examined over a wide range of arterial partial pressure of O2 [PaO2 (from 80 to 25 Torr)] during a 41-min rebreathing period at three CO2 levels: hypocapnia (from PaCO2 of 32 to 18 Torr), eucapnia (32 Torr), and mild hypercapnia (40 Torr). Eucapnic and hypercapnic hypoxic responses were also measured after sinoaortic denervation (SAD) to assess the arterial chemoreceptor and baroreceptor reflex contributions. Elevating PaCO2 attenuated the tachycardia during hypoxia and produced progressively greater systemic, renal, and splanchnic vasoconstriction before but not after SAD. Vagal block converted the rises in renal and splanchnic flows observed during hypocapnic hypoxia to declines. The increase in left ventricular dP/d tmax was not affected by varying PaCO2 either before or after SAD. Coronary flow increased an additional onefold during hypoxia when PaCO2 was elevated both before and after SAD, but the tension-time indices did not differ significantly. These results indicate that: a) cardiopulmonary vagal afferents effectively counteract chemoreflex-induced vasoconstriction during hypocapnic hypoxia; b) chemoreflex vasoconstriction predominates in the renal and splanchnic beds when PaCO2 is elevated; c) the sinoaortic reflexes restrain the heart rate, but not the contractility response to hypoxia when PaCO2 is increased; and d) the augmented coronary vasodilation produced by CO2 is probably mediated by local CO2-hypoxic interactions.

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Arterial chemoreceptor input to respiratory hypoglossal motoneurons

Journal of Applied Physiology ◽

10.1152/jappl.1990.69.2.700 ◽

1990 ◽

Vol 69 (2) ◽

pp. 700-709 ◽

Cited By ~ 7

Author(s):

S. W. Mifflin

Keyword(s):

Membrane Potential ◽

Upper Airway ◽

Excitatory Input ◽

Airway Patency ◽

Hypoglossal Motoneurons ◽

End Tidal ◽

Carotid Body Chemoreceptors ◽

Excitatory Drive ◽

Arterial Chemoreceptor

To better understand the role of the arterial chemoreceptors in the regulation of upper airway patency at the level of the oropharynx, intracellular recordings were obtained from inspiratory hypoglossal motoneurons (IHMs), and the responses to selective activation of the carotid body chemoreceptors were examined. In pentobarbital-anesthetized, vagotomized, paralyzed, and artificially ventilated cats, chemoreceptor activation enhanced the inspiratory depolarization of membrane potential in 32 of 36 IHMs. This was manifested as an increase in either the amplitude (n = 13) or duration (n = 3) or an increase in both amplitude and duration (n = 16) of the inspiratory membrane potential depolarization. The amplitude and duration of the inspiratory membrane potential depolarization increased 98 +/- 15% (n = 29) and 78 +/- 13% (n = 19), respectively. Similar patterns of enhanced activity (increased duration and/or amplitude of membrane depolarization) were observed in five expiratory hypoglossal motoneurons (EHMs) after chemoreceptor activation. In 16 of the 32 IHMs, chemoreceptor activation also evoked changes in IHM membrane potential during expiration: enhanced post-inspiratory discharge (n = 6), expiratory depolarization/discharge (n = 6), and tonic depolarization/discharge, which persisted for several respiratory cycles (n = 4). The arterial chemoreceptors provide a powerful excitatory input to IHMs during both inspiration and expiration. This excitatory drive to IHMs and EHMs will aid in the maintenance of upper airway patency throughout the respiratory cycle during increases in end-tidal CO2.

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