Adult carotid chemoafferent responses to hypoxia after 1, 2, and 4 wk of postnatal hyperoxia

2003 ◽  
Vol 95 (3) ◽  
pp. 946-952 ◽  
Author(s):  
G. E. Bisgard ◽  
E. B. Olson ◽  
Z.-Y. Wang ◽  
R. W. Bavis ◽  
D. D. Fuller ◽  
...  
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Carotid Sinus Nerve ◽  
Newborn Rats ◽  
Adult Rats ◽  
Neural Input ◽  
Hyperoxic Exposure ◽  
Depressed Response

Exposing newborn rats to postnatal hyperoxia (60% O2) for 1-4 wk attenuates the ventilatory and phrenic nerve responses to acute hypoxia in adult rats. The goal of this research was to increase our understanding of the carotid chemoreceptor afferent neural input in this depressed response with different durations of postnatal hyperoxic exposure. Rats were exposed from a few days before birth to 1, 2, or 4 wk of 60% O2 and studied after 3-5 mo in normoxia. The rats were anesthetized with urethane. Whole carotid sinus nerve (CSN) responses to NaCN (40 μg/kg iv), 10 s of asphyxia and acute isocapnic hypoxia (arterial Po2 45 Torr) were determined. Mean CSN responses to stimuli after postnatal hyperoxia were reduced compared with controls. Responses in rats exposed to 1 wk of postnatal hyperoxia were less affected than those exposed to 2 and 4 wk of hyperoxia, which were equivalent to each other. These studies illustrate the importance of normoxia during the first 2 wk of life in development of carotid chemoreceptor afferent function.

Time-dependent phrenic nerve responses to carotid afferent activation: intact vs. decerebellate rats

1993 ◽  
Vol 265 (4) ◽  
pp. R811-R819 ◽  
Author(s):  
F. Hayashi ◽  
S. K. Coles ◽  
K. B. Bach ◽  
G. S. Mitchell ◽  
D. R. McCrimmon
Keyword(s):  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Short Term ◽  
Nerve Activity ◽  
A Value ◽  
Afferent Activation ◽  
Term Potentiation ◽  
Long Term Facilitation

The objectives were to determine 1) respiratory responses to carotid chemoreceptor inputs in anesthetized rats and 2) whether the cerebellar vermis plays a role in these responses. A carotid sinus nerve was stimulated (20 Hz) with five 2-min trains, each separated by approximately 3 min. During stimulation, respiratory frequency (f), peak amplitude of integrated phrenic nerve activity (integral of Phr), and their product (f x integral of Phr) immediately increased. As stimulation continued, integral of Phr progressively increased to a plateau [short-term potentiation (STP)], but f and f x integral of Phr decreased [short-term depression (STD)] to a value still above control. Upon stimulus termination, integral of Phr progressively decreased but remained above control; f and f x integral of Phr transiently decreased below baseline. After the final stimulation, integral of Phr remained above control for at least 30 min [long-term facilitation (LTF)]. Repeated 5-min episodes of isocapnic hypoxia also elicited STP, STD, and LTF. Vermalectomy lowered the CO2-apneic threshold and eliminated LTF. In conclusion, carotid chemoreceptor activation in rats elicits STP and LTF similar to that in cats; the vermis may play a role in LTF. A new response, STD, was observed.

Dose-dependent Effects of Halothane on the Phrenic Nerve Responses to Acute Hypoxia in Vagotomized Dogs 

1997 ◽  
Vol 87 (6) ◽  
pp. 1428-1439 ◽  
Author(s):  
Eckehard A. E. Stuth ◽  
Zoran Dogas ◽  
Mirko Krolo ◽  
John P. Kampine ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Carotid Body ◽  
Phrenic Nerve ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Hypoxic Response ◽  
Nerve Response ◽  
Bilateral Carotid ◽  
Dose Dependent

Background Previous studies in dogs and humans suggest that the carotid body chemoreceptor response to hypoxia is selectively impaired by halothane. The present studies in an open-loop canine preparation were performed to better delineate the effects of anesthetic concentrations of halothane on the carotid body chemoreceptor-mediated phrenic nerve response to an acute hypoxic stimulus. Methods Three protocols were performed to study the effects of halothane anesthesia on the phrenic nerve response to 1 min of isocapnic hypoxia (partial pressure of oxygen [PaO2] at peak hypoxia, 35-38 mmHg) in unpremedicated, anesthetized, paralyzed, vagotomized dogs during constant mechanical ventilation. In protocol 1, the dose-dependent effects of halothane from 0.5-2.0 minimum alveolar concentration (MAC) on the hypoxic response during moderate hypercapnia (partial pressure of carbon dioxide [PaCO2], 60-65 mmHg) were studied in 10 animals. In protocol 2, the hypoxic responses at 1 MAC halothane near normocapnia (PaCO2, 40-45 mmHg) and during moderate hypercapnia were compared in an additional four animals. In protocol 3, the hypoxic response of 4 of 10 dogs from protocol 1 was also studied under sodium thiopental (STP) anesthesia after they completed protocol 1. Results Protocol 1: Peak phrenic nerve activity (PPA) increased significantly during the hypoxic runs compared with the isocapnic hyperoxic controls at all halothane doses. The phrenic nerve response to the hypoxic stimulus was present even at the 2 MAC dose. Protocol 2: The net hypoxic responses for the two carbon dioxide background levels at 1 MAC were not significantly different. Protocol 3: The net hypoxic response of PPA for the STP anesthetic was not significantly different from the 1 MAC halothane dose. Bilateral carotid sinus denervation abolished the PPA response to hypoxia. Conclusions The phrenic nerve response to an acute, moderately severe isocapnic hypoxic stimulus is dose-dependently depressed but not abolished by surgical doses of halothane. This analysis does not suggest a selective depression of the carotid body chemoreceptor response by halothane. The observed hypoxic phrenic response was mediated by the carotid body chemoreceptors in vagotomized dogs because bilateral carotid sinus denervation abolished all increases in PPA.

scholarly journals Essential role of hemoglobin beta-93-cysteine in posthypoxia facilitation of breathing in conscious mice

2014 ◽  
Vol 116 (10) ◽  
pp. 1290-1299 ◽  
Author(s):  
Benjamin Gaston ◽  
Walter J. May ◽  
Spencer Sullivan ◽  
Sean Yemen ◽  
Nadzeya V. Marozkina ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Essential Role ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Carotid Sinus Nerve ◽  
Short Term ◽  
Ventilatory Responses ◽  
Term Potentiation ◽  
Β Chain

When erythrocyte hemoglobin (Hb) is fully saturated with O2, nitric oxide (NO) covalently binds to the cysteine 93 residue of the Hb β-chain (B93-CYS), forming S-nitrosohemoglobin. Binding of NO is allosterically coupled to the O2 saturation of Hb. As saturation falls, the NO group on B93-CYS is transferred to thiols in the erythrocyte, and in the plasma, forming circulating S-nitrosothiols. Here, we studied whether the changes in ventilation during and following exposure to a hypoxic challenge were dependent on erythrocytic B93-CYS. Studies were performed in conscious mice in which native murine Hb was replaced with human Hb (hB93-CYS mice) and in mice in which murine Hb was replaced with human Hb containing an alanine rather than cysteine at position 93 on the Bchain (hB93-ALA). Both strains expressed human γ-chain Hb, likely allowing a residual element of S-nitrosothiol-dependent signaling. While resting parameters and initial hypoxic (10% O2, 90% N2) ventilatory responses were similar in hB93-CYS mice and hB93-ALA mice, the excitatory ventilatory responses (short-term potentiation) that occurred once the mice were returned to room air were markedly diminished in hB93-ALA mice. Further, short-term potentiation responses were virtually absent in mice with bilateral transection of the carotid sinus nerves. These data demonstrate that hB93-CYS plays an essential role in mediating carotid sinus nerve-dependent short-term potentiation, an important mechanism for recovery from acute hypoxia.

Chronic hypoxia enhances the phrenic nerve response to arterial chemoreceptor stimulation in anesthetized rats

1999 ◽  
Vol 87 (2) ◽  
pp. 817-823 ◽  
Author(s):  
M. R. Dwinell ◽  
F. L. Powell
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Phrenic Nerve ◽  
Chronic Hypoxia ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Phrenic Nerve Activity ◽  
Hypoxic Group ◽  
Arterial Chemoreceptor

Chronic exposure to hypoxia results in a time-dependent increase in ventilation called ventilatory acclimatization to hypoxia. Increased O2 sensitivity of arterial chemoreceptors contributes to ventilatory acclimatization to hypoxia, but other mechanisms have also been hypothesized. We designed this experiment to determine whether central nervous system processing of peripheral chemoreceptor input is affected by chronic hypoxic exposure. The carotid sinus nerve was stimulated supramaximally at different frequencies (0.5–20 Hz, 0.2-ms duration) during recording of phrenic nerve activity in two groups of anesthetized, ventilated, vagotomized rats. In the chronically hypoxic group (7 days at 80 Torr inspired [Formula: see text]), phrenic burst frequency (fR, bursts/min) was significantly higher than in the normoxic control group with carotid sinus nerve stimulation frequencies >5 Hz. In the chronically hypoxic group, peak amplitude of integrated phrenic nerve activity ( ∫ Phr, percent baseline) or change in ∫ Phr was significantly greater at stimulation frequencies between 5 and 17 Hz, and minute phrenic activity ( ∫ Phr × fR) was significantly greater at stimulation frequencies >5 Hz. These experiments show that chronic hypoxia facilitates the translation of arterial chemoreceptor afferent input to ventilatory efferent output through a mechanism in the central nervous system.

scholarly journals Carotid sinus nerve section and the increase in plasma cortisol during acute hypoxia in fetal sheep.

1994 ◽  
Vol 477 (1) ◽  
pp. 75-80 ◽  
Author(s):  
D A Giussani ◽  
H H McGarrigle ◽  
P J Moore ◽  
L Bennet ◽  
J A Spencer ◽  
...  
Keyword(s):  
Plasma Cortisol ◽  
Carotid Sinus ◽  
Acute Hypoxia ◽  
Carotid Sinus Nerve ◽  
Nerve Section ◽  
Fetal Sheep

Hypoglossal and phrenic nerve responses to carotid baroreceptor stimulation

1993 ◽  
Vol 75 (3) ◽  
pp. 1395-1403 ◽  
Author(s):  
M. J. Wasicko ◽  
R. W. Giering ◽  
S. L. Knuth ◽  
J. C. Leiter
Keyword(s):  
Phrenic Nerve ◽  
Hypoglossal Nerve ◽  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Carotid Baroreceptor ◽  
Baroreceptor Stimulation ◽  
Sinus Pressure ◽  
Carotid Baroreceptor Stimulation

We examined the relationship between hypoglossal and phrenic nerve activities and carotid sinus pressure. In 12 adult cats that were decerebrate, vagotomized, paralyzed, and mechanically ventilated, we isolated the left carotid sinus for perfusion and denervated the right carotid sinus. Mean arterial blood pressure was maintained at 90–100 mmHg using a low resistance-reservoir containing saline and connected to the abdominal aorta. Constant pressure was applied to the carotid sinus region. We found that increased carotid sinus pressure immediately inhibited inspiratory-synchronous (phasic) hypoglossal nerve activity and that there was a direct inverse relationship between phasic hypoglossal activity and carotid sinus pressure up to a carotid pressure of 285 mmHg. Increased carotid sinus pressure had no effect on tonic hypoglossal nerve activity and only slightly inhibited phrenic nerve activity. Cutting the left carotid sinus nerve abolished this response. We also applied pressure pulses to the carotid sinus at discrete times during the phrenic cycle. We found that baroreceptor inhibition of phasic hypoglossal nerve activity was gated during the phrenic cycle: maximum inhibition occurred when the pulse was applied in late expiration. We conclude that carotid baroreceptor stimulation preferentially inhibits inspiratory synchronous hypoglossal nerve activity and that this afferent information traveling in the carotid sinus nerve is gated by the respiratory control center.

Carotid sinus nerve responses and ventilatory acclimatization to hypoxia in adult rats following 2 weeks of postnatal hyperoxia

2006 ◽  
Vol 150 (2-3) ◽  
pp. 155-164 ◽  
Author(s):  
Julie M. Wenninger ◽  
E. Burt Olson ◽  
Zunyi Wang ◽  
Ingegerd M. Keith ◽  
Gordon S. Mitchell ◽  
...  
Keyword(s):  
Carotid Sinus ◽  
Carotid Sinus Nerve ◽  
Adult Rats
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