Influence of ischemia and hypoxia on breathing in ducks

1983 ◽  
Vol 55 (2) ◽  
pp. 400-408 ◽  
Author(s):  
R. S. Lillo ◽  
D. R. Jones
Keyword(s):  
Carotid Body ◽  
Minute Ventilation ◽  
Severe Hypoxia ◽  
Lower Body ◽  
Ventilatory Responses ◽  
Pekin Ducks ◽  
Carotid Bodies ◽  
Thoracic Spinal ◽  
Spinal Section ◽  
The Brain

We examined the influence of whole and lower body hypoxia and lower body ischemia on breathing in White Pekin ducks, Anas platyrhynchos, excluding pathways involving the carotid bodies. Carotid body denervated birds breathing 10 or 5% O2 developed a tachypnea after a latency of 30-100 s. The tachypnea was more pronounced with the more severe hypoxia, resulting in almost a doubling of minute ventilation (VE). Occlusion of the abdominal aorta in unanesthetized ducks produced immediate development of hypertension. Ventilation was unaffected for the 1st min; a tachypnea then developed rapidly and persisted for the duration of the occlusion resulting in a 25% increase in VE. After thoracic spinal section, all ventilatory responses to occlusion were eliminated. Experimental perfusion of the brain and single intact carotid body in unanesthetized ducks with hyperoxic blood during low O2 breathing (6-9% O2) resulted in tachypnea, also after a considerable latency. These results suggest that severe hypoxia can affect breathing in birds via pathways other than those involving the carotid bodies.

Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

2004 ◽  
Vol 97 (4) ◽  
pp. 1401-1407 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Mieczyslaw Pokorski ◽  
Ikuo Homma
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Whole Body ◽  
Sudden Increase ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Before And After ◽  
Carotid Body Denervation

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O2 in N2 for 240 s), hypoxic hypoxia (10 and 15% O2 in N2 for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO2 in O2 for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O2 consumption or CO2 production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

Effects of hypoxia on thermal polypnea in intact and carotid body-denervated conscious cats

1989 ◽  
Vol 67 (2) ◽  
pp. 578-583 ◽  
Author(s):  
M. Bonora ◽  
H. Gautier
Keyword(s):  
Body Temperature ◽  
Carotid Body ◽  
Heat Load ◽  
Heat Exposure ◽  
Ambient Air ◽  
Severe Hypoxia ◽  
Central Action ◽  
Lower Body ◽  
Respiratory Response ◽  
Mild Hypoxia

The effects of the level of oxygenation on the respiratory response to heat exposure have been studied in conscious cats during normoxia, severe or mild hypocapnic hypoxia [inspired O2 fraction (FIO2) = 0.11 or 0.13], or hyperoxia. Several cats were also studied during severe normocapnic hypoxia. Experiments were repeated while the same animals were chronically carotid body denervated (CBD). The increase in respiratory frequency (f) leading to thermal tachypnea occurred at a lower body temperature (Tb) in severe hypocapnic hypoxia than in ambient air, but this effect was less pronounced when hypocapnia was corrected. No significant changes were observed during mild hypoxia or hyperoxia compared with normoxia in intact animals. After CBD, thermal tachypnea occurred at lower Tb in air than it did with intact animals in three of five cats, and it also occurred at lower Tb in mild hypocapnic hypoxia compared with air. It appears, therefore, that in conscious cats exposed to heat load 1) severe hypoxia enhances thermal tachypnea, 2) this effect persists after CBD, which suggests that it originates from a central action of hypoxia, and 3) the chemoreceptor afferents, to some degree, inhibit the onset of thermal tachypnea, as was previously observed for hypoxic tachypnea, which appears only in CBD cats (J. Appl. Physiol. 49: 769–777, 1980). Therefore, triggering of thermal and hypoxic tachypnea may involve common central mechanisms, probably located in the diencephalic structures under the control of afferents from arterial chemoreceptors.

The essential role of carotid body chemoreceptors in sleep apnea

2003 ◽  
Vol 81 (8) ◽  
pp. 774-779 ◽  
Author(s):  
Curtis A Smith ◽  
Hideaki Nakayama ◽  
Jerome A Dempsey
Keyword(s):  
Sleep Apnea ◽  
Carotid Body ◽  
Respiratory Acidosis ◽  
Periodic Breathing ◽  
Peripheral Chemoreceptors ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
The Difference ◽  
Carotid Body Chemoreceptors

Sleep apnea is attributable, in part, to an unstable ventilatory control system and specifically to a narrowed "CO2 reserve" (i.e., the difference in PaCO2 between eupnea and the apneic threshold). Findings from sleeping animal preparations with denervated carotid chemoreceptors or vascularly isolated, perfused carotid chemoreceptors demonstrate the critical importance of peripheral chemoreceptors to the ventilatory responses to dynamic changes in PaCO2. Specifically, (i) carotid body denervation prevented the apnea and periodic breathing that normally follow transient ventilatory overshoots; (ii) the CO2 reserve for peripheral chemoreceptors was about one half that for brain chemoreceptors; and (iii) hypocapnia isolated to the carotid chemoreceptors caused hypoventilation that persisted over time despite a concomitant, progressive brain respiratory acidosis. Observations in both humans and animals are cited to demonstrate the marked plasticity of the CO2 reserve and, therefore, the propensity for apneas and periodic breathing, in response to changing background ventilatory stimuli.Key words: sleep apnea, carotid bodies, hypocapnia, apneic threshold, periodic breathing.

Ventilatory response to drug-induced hypermetabolism

1975 ◽  
Vol 38 (5) ◽  
pp. 827-833 ◽  
Author(s):  
S. Levine ◽  
W. E. Huckabee
Keyword(s):  
Spinal Cord ◽  
Cervical Spinal Cord ◽  
Minute Ventilation ◽  
The Body ◽  
Low Oxygen ◽  
Drug Induced ◽  
Afferent Pathways ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Carotid Bodies

Previous workers have demonstrated that an increase in minute ventilation accompanies tissue hypermetabolism induced by uncouplers of oxidative phosphorylation. The mechanism of this increase in minute ventilation has not been established. Accordingly, 2.5 mg/kg of 2,4-dinitrophenol (DNP) or 8–15 mg/kg of ethyl methylene blue (EMB) were infused into chloralose-anesthetized mongrel dogs; Vo2 increased 105 plus or minus 3% and VE INCREASED 107 PLUS OR MINUS 14%. Heads of vagotomized dogs were then perfused entirely with normal unchanging blood. Spinal cord remained intact. (The carotid bodies lay within the region of the perfused head.) Ventilatory responses of these head-perfused animals to breathing low oxygen and to breathing high CO2 gas mixtures were greatly attenuated. However, when DNP or EMB was infused into the body, VO2 increased 114 plus or minus 23% and VE increased 123 plus or minus 22%. When similar doses of DNP or emb were selectively administered to the head, increases in VE were limited to 21 plus or minus 6%. It is concluded that a major portion of the stimulus to ventilation, which accompanies infusion of DNP or of EMB, arises in tissues other than arterial chemoreceptors and brain. Presumably, this ventilatory stimulus is transmitted to the respiratory center via afferent pathways of the cervical spinal cord.

Hypoxic arousal in intact and carotid chemodenervated sleeping cats

1981 ◽  
Vol 51 (5) ◽  
pp. 1294-1299 ◽  
Author(s):  
J. A. Neubauer ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Carotid Body ◽  
Rem Sleep ◽  
Severe Hypoxia ◽  
Rapid Eye Movement ◽  
Carotid Chemoreceptors ◽  
Carotid Bodies ◽  
Arterial O2 Saturation ◽  
Carotid Body Denervation

To determine whether the carotid chemoreceptors or hyperpnea are required for arousal from sleep by hypoxia, 14 sleep-deprived cats were studied during slow-wave (SWS) and rapid-eye-movement (REM) sleep. Rapid hypoxia was produced by inhalation of 5% O2 in N2 or 6% CO in 40% O2 by intact cats and 5% O2 in N2 after carotid body denervation. Preliminary studies identified a period of SWS unassociated with spontaneous arousals. In 69 studies during SWS unassociated with spontaneous arousals, arterial O2 saturation (SaO2) values at arousal were: 47.1 +/- 1.5% (mean +/- SE) (5% O2, intact); 48.9 +/- 1.4% (6% CO, intact); and 49.9 +/- 2.0% (5% O2, denervated). During SWS associated with spontaneous arousals, SaO2 values at arousal were 71.6 +/- 1.8% (5% O2, intact). Arousal from REM occurred at significantly lower values: 31.7 +/- 3.9% (6% CO, intact) and 43.5 +/- 2.3% (5% O2, intact). During both SWS and REM, inhalation of 5% O2 by intact animals caused a substantial increase in ventilation while 6% CO did not. We conclude that more severe hypoxia is required for arousal from SWS when studies are done in a period unassociated with spontaneous arousals than from SWS associated with spontaneous arousals. Hypoxic arousal does not appear to require activation of the carotid bodies or hyperpnea.

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.

Electrochemical detection of catecholamine release from rat carotid body in vitro

1993 ◽  
Vol 74 (5) ◽  
pp. 2330-2337 ◽  
Author(s):  
D. F. Donnelly
Keyword(s):  
Carbon Fiber ◽  
Carotid Body ◽  
Essential Element ◽  
Oxidation Potential ◽  
Catecholamine Release ◽  
Severe Hypoxia ◽  
Potential Range ◽  
Electrode Current ◽  
Carotid Bodies

Neurotransmitter secretion from carotid body glomus cells is hypothesized to be an essential element of chemotransduction. To address one aspect of this hypothesis, catecholamine release in response to hypoxic hypoxia and histotoxic hypoxia was examined using electrically treated carbon-fiber microelectrodes placed in rat carotid bodies in vitro. Carotid bodies of mature rats were removed, along with a portion of the sinus nerve, and suspended in oxygenated (95% O2–5% CO2) Ringer saline at 35 degrees C. The microelectrode differential current after a 50-mV step was recorded over the potential range of -300 to +500 mV. In some preparations, a suction electrode applied to the sinus nerve recorded single-fiber chemoreceptor afferent activity. Stimulation by severe hypoxia (Po2 approximately 0–10 Torr for 3 min, n = 10) and cyanide (2 mM for 2 min) caused an increase in sinus nerve activity and an increase in the carbon-fiber electrode current at a potential corresponding to the oxidation potential of dopamine. As measured in the amperometric mode (constant voltage), tissue catecholamine was 0.35 +/- 0.05 microM (n = 6) and increased to 1.64 +/- 0.43 microM by 1 min of severe hypoxia or to 1.06 +/- 0.17 microM at 2 min of moderate hypoxia (Po2 approximately 50 Torr). Exposure to calcium-free Ringer saline before hypoxia ablated the increase in electrode current, and the response was restored after reperfusion with calcium-containing saline. Repeated exposures to hypoxia (3-min duration) every 15 min resulted in significantly smaller nerve and catecholamine responses. By the third hypoxia exposure, nerve and catecholamine responses were diminished by 30–50%.

scholarly journals Ventilatory responses to specific CNS hypoxia in sleeping dogs

2000 ◽  
Vol 88 (5) ◽  
pp. 1840-1852 ◽  
Author(s):  
Aidan K. Curran ◽  
Joshua R. Rodman ◽  
Peter R. Eastwood ◽  
Kathleen S. Henderson ◽  
Jerome A. Dempsey ◽  
...  
Keyword(s):  
Eye Movement ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Whole Body ◽  
Hypoxic Exposure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Cardiorespiratory Control ◽  
Ventilatory Responses

Our study was concerned with the effect of brain hypoxia on cardiorespiratory control in the sleeping dog. Eleven unanesthetized dogs were studied; seven were prepared for vascular isolation and extracorporeal perfusion of the carotid body to assess the effects of systemic [and, therefore, central nervous system (CNS)] hypoxia (arterial [Formula: see text] = 52, 45, and 38 Torr) in the presence of a normocapnic, normoxic, and normohydric carotid body during non-rapid eye movement sleep. A lack of ventilatory response to systemic boluses of sodium cyanide during carotid body perfusion demonstrated isolation of the perfused carotid body and lack of other significant peripheral chemosensitivity. Four additional dogs were carotid body denervated and exposed to whole body hypoxia for comparison. In the sleeping dog with an intact and perfused carotid body exposed to specific CNS hypoxia, we found the following. 1) CNS hypoxia for 5–25 min resulted in modest but significant hyperventilation and hypocapnia (minute ventilation increased 29 ± 7% at arterial [Formula: see text] = 38 Torr); carotid body-denervated dogs showed no ventilatory response to hypoxia. 2) The hyperventilation was caused by increased breathing frequency. 3) The hyperventilatory response developed rapidly (<30 s). 4) Most dogs maintained hyperventilation for up to 25 min of hypoxic exposure. 5) There were no significant changes in blood pressure or heart rate. We conclude that specific CNS hypoxia, in the presence of an intact carotid body maintained normoxic and normocapnic, does not depress and usually stimulates breathing during non-rapid eye movement sleep. The rapidity of the response suggests a chemoreflex meditated by hypoxia-sensitive respiratory-related neurons in the CNS.

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.

Evidence for hypoxic depression of CO2-ventilation response in carotid body-resected humans

1991 ◽  
Vol 70 (2) ◽  
pp. 590-593 ◽  
Author(s):  
Y. Honda ◽  
I. Hashizume
Keyword(s):  
Carotid Body ◽  
Response Curve ◽  
Minute Ventilation ◽  
Neural Mechanisms ◽  
Control Groups ◽  
Response Curves ◽  
End Tidal ◽  
And Control ◽  
The Brain ◽  
Ventilation Response

Steady-state CO2-ventilation response curves with hyperoxia (end-tidal PO2 greater than 200 Torr) and mild hypoxia (end-tidal PO2 approximately equal to 60 Torr) were compared in five carotid body-resected (BR) patients and five control patients. The data were analyzed by fitting a linear equation, V = S(PETCO2-B), where V is minute ventilation S is the response curve slope. PETCO2 is end-tidal PCO2, and B is the response curve threshold. S slightly increased from hyperoxia to hypoxia in both BR and control groups. On the other hand, B moderately increased with hypoxia in BR patients, whereas it slightly decreased in controls. These changes were all not significant. However, in accordance with the change in B, the response curve to hypoxia at V of 10 1/min was significantly shifted in opposite directions in the two groups, i.e., rightward and leftward shift in BR and control groups, respectively. Thus the average magnitude of V calculated at PETCO2 of 40 Torr in hypoxia was significantly lower in BR patients than in controls (P less than 0.01). We conclude that this hypoxic depression of the CO2-ventilation response found in BR patients may have resulted, at least in part, from modulation of the brain stem neural mechanisms that were elicited by loss of afferent discharges from the carotid body.

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