Ventilatory reflexes originated from carotid and extracarotid chemoreceptors in rats

1983 ◽  
Vol 244 (1) ◽  
pp. R119-R125 ◽  
Author(s):  
H. Cardenas ◽  
P. Zapata
Keyword(s):  
Tidal Volume ◽  
Respiratory Frequency ◽  
Intravenous Injections ◽  
Ventilatory Responses ◽  
Laryngeal Nerves ◽  
Carotid Bodies ◽  
Nodose Ganglia ◽  
Bilateral Carotid ◽  
Ventilatory Depression ◽  
Thoracic And Abdominal

Ventilatory responses to transient stimulation and inhibition of arterial chemoreceptors--by hypoxia and hyperoxia, respectively--were studied in 10 pentobarbitone-anesthetized rats. N2 tests and intravenous injections of NaCN provoked transient increases in tidal volume and respiratory frequency, while O2 tests elicited decreases of these parameters. After bilateral carotid neurotomy, ventilatory responses to N2 and NaCN were still present although reduced in all rats, while ventilatory depression in response to O2 tests was observed in 60% of these rats. Further bilateral sectioning of main vagus, aortic, and superior laryngeal nerves immediately below the nodose ganglia abolished the ventilatory responses to NaCN in only one of the five rats subjected to this procedure, the remaining animals showing moderate hyperventilation in response to large doses of this drug. Mild ventilatory depression in response to hyperoxia, indicative of a persistent peripheral chemosensory drive, was still present in two of these rats. It is concluded that, although the carotid bodies constitute the main source of ventilatory chemoreflexes in rats, other vagally and nonvagally innervated chemoreceptors (presumably thoracic and abdominal) may elicit ventilatory reflexes in this species.

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.

Effect of verapamil on ventilation and chemical control of breathing in anesthetized rats

1985 ◽  
Vol 63 (12) ◽  
pp. 1608-1611 ◽  
Author(s):  
Richard W. Chapman
Keyword(s):  
Tidal Volume ◽  
Respiration Rate ◽  
Channel Blocker ◽  
Minute Volume ◽  
Respiratory Frequency ◽  
Deep Breathing ◽  
Ventilatory Responses ◽  
Anesthetized Rats ◽  
Dose Dependent Increase ◽  
Dose Dependent

The calcium channel blocker, verapamil (0.1–1.0 mg/kg, i.v.) was administered to anesthetized rats to determine its effects on ventilation and on ventilatory responses to hypoxia and CO2. Verapamil produced a dose-dependent increase in tidal volume (VT) and a decrease in respiration rate (f). The bradypnea due to verapamil was characterized by an increase in expiratory duration (TE) and no change of inspiratory duration (TI). Verapamil produced similar changes in VT and f in vagotomized rats. The increase in respiration rate and minute volume due to hypoxia were inhibited by verapamil (0.5 and 1.0 mg/kg) but the increase in tidal volume due to hypoxia was depressed only with the 1.0 mg/kg dose. On the other hand, the increase in VT due to breathing CO2 was not changed by verapamil (0.1–1.0 mg/kg), but depression of the respiratory frequency response to CO2 occurred with 1.0 mg/kg of verapamil. These results indicate that verapamil produced slow, deep breathing and these responses were not mediated by vagal mechanisms. Ventilatory responses to hypoxia were depressed by verapamil. However, since the calcium blocker demonstrated no effect on the VT-CO2 relationship, verapamil did not change ventilatory chemosensitivity to CO2. The data also suggest that mechanisms governing the control of respiratory frequency are more sensitive to verapamil than tidal volume responses.

Diaphragmatic and ventilatory responses to alveolar hypoxia and hypercapnia in conscious kittens

1992 ◽  
Vol 72 (1) ◽  
pp. 203-210 ◽  
Author(s):  
M. Bonora ◽  
M. Boule ◽  
H. Gautier
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Central Mechanism ◽  
Respiratory Frequency ◽  
Emg Activity ◽  
Phasic Change ◽  
Ventilatory Responses ◽  
Alveolar Hypoxia ◽  
The Difference

Ventilation and electromyographic (EMG) activity of the diaphragm were recorded in unanesthetized kittens 2 and 10 wk of age during normoxia, hypercapnia (2 and 4% CO2), and hypoxia (12 and 10% O2). We measured integrated diaphragmatic EMG activity at end inspiration (DIAI) and end expiration (DIAE); the difference (DIAI-E), which represents the phasic change of the diaphragmatic activity, was considered responsible for a given tidal volume (VT). During hypercapnia, the 2-wk-old kittens increased minute ventilation (V) by increases in both VT and respiratory frequency (f), whereas the 10-wk-old kittens increased V primarily by an increase in VT. At both ages, DIAI and DIAI-E increased during hypercapnia, whereas DIAE did not change significantly. During hypoxia, in the young kittens, V and VT decreased while f increased markedly; in the older kittens, V, VT, and f did not change significantly. In kittens of both ages, DIAI increased during hypoxia; because diaphragmatic activity persisted into expiration, DIAE also increased. DIAI-E, as well as VT, was decreased in the young kittens, whereas in the older ones DIAI-E was slightly increased despite an unchanged VT. Finally, the ventilatory and diaphragmatic response to hypoxia changes with maturation in contrast to the response to hypercapnia. It is concluded that 1) the hypoxia-induced reduction of VT may result from prolongation of diaphragmatic activity into expiration, inasmuch as it induces a reduction of the phasic change of the diaphragmatic activity, and 2) because DIAI-E indirectly reflects central inspiratory output, a central mechanism should be involved in the reduced VT and V in response to hypoxia in newborns.

scholarly journals Carotid body denervation in dogs: eupnea and the ventilatory response to hyperoxic hypercapnia

2001 ◽  
Vol 91 (1) ◽  
pp. 328-335 ◽  
Author(s):  
J. R. Rodman ◽  
A. K. Curran ◽  
K. S. Henderson ◽  
J. A. Dempsey ◽  
C. A. Smith
Keyword(s):  
Data Collection ◽  
Tidal Volume ◽  
Volume Change ◽  
Time Course ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Intravenous Injections ◽  
Carotid Bodies ◽  
Volume Response ◽  
End Tidal

We assessed the time course of changes in eupneic arterial Pco 2(PaCO2 ) and the ventilatory response to hyperoxic rebreathing after removal of the carotid bodies (CBX) in awake female dogs. Elimination of the ventilatory response to bolus intravenous injections of NaCN was used to confirm CBX status on each day of data collection. Relative to eupneic control (PaCO2 = 40 ± 3 Torr), all seven dogs hypoventilated after CBX, reaching a maximum PaCO2 of 53 ± 6 Torr by day 3post-CBX. There was no significant recovery of eupneic PaCO2 over the ensuing 18 days. Relative to control, the hyperoxic CO2 ventilatory (change in inspired minute ventilation/change in end-tidal Pco 2) and tidal volume (change in tidal volume/ change in end-tidal Pco 2) response slopes were decreased 40 ± 15 and 35 ± 20% by day 2 post-CBX. There was no recovery in the ventilatory or tidal volume response slopes to hyperoxic hypercapnia over the ensuing 19 days. We conclude that 1) the carotid bodies contribute ∼40% of the eupneic drive to breathe and the ventilatory response to hyperoxic hypercapnia and 2) there is no recovery in the eupneic drive to breathe or the ventilatory response to hyperoxic hypercapnia after removal of the carotid chemoreceptors, indicating a lack of central or aortic chemoreceptor plasticity in the adult dog after CBX.

Ventilatory effects of hypoxia and adenosine infusion in patients after bilateral carotid endarterectomy

1990 ◽  
Vol 78 (1) ◽  
pp. 25-31 ◽  
Author(s):  
T. L. Griffiths ◽  
S. J. Warren ◽  
A. D. B. Chant ◽  
S. T. Holgate
Keyword(s):  
Carotid Endarterectomy ◽  
Ventilatory Response ◽  
Adenosine Infusion ◽  
Respiratory Drive ◽  
Stimulant Effect ◽  
Carotid Bodies ◽  
Ventilatory Drive ◽  
Bilateral Carotid ◽  
Respiratory Stimulant ◽  
Ventilatory Effects

1. We have studied the carotid body contribution to hypoxic respiratory drive, using a hypoxic/hyperoxic switching technique, and the ventilatory response to intravenous infusion of adenosine, a recently described respiratory stimulant, in five patients with bilateral carotid endarterectomy. 2. The contribution made by the carotid bodies to total ventilatory drive during hypoxia varied from 2.5% to 45.9%. 3. The ventilatory response to adenosine infusion varied from a 7% decrease to a 25% increase in ventilation. 4. Those patients with intact hypoxic ventilatory drive showed respiratory stimulation, whereas of the two patients with attenuated chemoreflexes, one showed no stimulation and the other depression of ventilation in response to adenosine infusion. 5. We conclude that adenosine exerts its respiratory stimulant effect via an action on the peripheral chemoreceptors. This may coexist with a centrally mediated respiratory depression that is masked when the carotid bodies are intact.

Ventilatory response to hypoxia in unanesthetized newborn kittens

1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Sleep ◽  
Newborn Kitten ◽  
Peripheral Mechanism ◽  
Flow Through ◽  
Ventilatory Response To Hypoxia

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.

Effect of a synthetic progestin on ventilatory response to hypoxia in anesthetized rats

1989 ◽  
Vol 67 (5) ◽  
pp. 1754-1758 ◽  
Author(s):  
H. Kimura ◽  
M. Mikami ◽  
T. Kuriyama ◽  
Y. Fukuda
Keyword(s):  
Regulatory Mechanism ◽  
Carotid Sinus ◽  
Ventilatory Response ◽  
Break Point ◽  
Male Rat ◽  
Carotid Sinus Nerve ◽  
Ventilatory Responses ◽  
Chlormadinone Acetate ◽  
Ventilatory Depression ◽  
Ventilatory Response To Hypoxia

Effects on ventilatory responses to progressive isocapnic hypoxia of a synthetic potent progestin, chlormadinone acetate (CMA), were determined in the halothane-anesthetized male rat. Ventilation during the breathing of hyperoxic gas was largely unaffected by treatment with CMA when carotid chemoreceptor afferents were kept intact. The sensitivity to hypoxia evaluated by hyperbolic regression analysis of the response curve did not differ between the control and CMA groups. The reduction of ventilation after bilateral section of the carotid sinus nerve (CSN) in hyperoxia was less severe in CMA-treated than in untreated animals. Furthermore, the CMA-treated rats showed a larger increase in ventilation during the hypoxia test and a lower PO2 break point for ventilatory depression. Inhibition of hypoxic ventilatory depression by CMA persisted even after the denervation of CSN. We conclude that exogenous progestin likely protects regulatory mechanism(s) for respiration against hypoxic depression through a stimulating action independent of carotid chemoreceptor afferents and without a change in the sensitivity of the ventilatory response to hypoxia.

scholarly journals Impact of cervical spinal cord contusion on the breathing pattern across the sleep-wake cycle in the rat

2019 ◽  
Vol 126 (1) ◽  
pp. 111-123 ◽  
Author(s):  
Kun-Ze Lee
Keyword(s):  
Spinal Cord ◽  
Tidal Volume ◽  
Spinal Injury ◽  
Cervical Spinal Cord ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Breathing Patterns ◽  
Cord Injury ◽  
Spinal Contusion ◽  
Cervical Spinal Injury

The present study was designed to investigate breathing patterns across the sleep-wake state following a high cervical spinal injury in rats. The breathing patterns (e.g., respiratory frequency, tidal volume, and minute ventilation), neck electromyogram, and electroencephalography of unanesthetized adult male rats were measured at the acute (i.e., 1 day), subchronic (i.e., 2 wk), and/or chronic (i.e., 6 wk) injured stages after unilateral contusion of the second cervical spinal cord. Cervical spinal cord injury caused a long-term reduction in the tidal volume but did not influence the sleep-wake cycle duration. The minute ventilation during sleep was usually lower than that during the wake period in uninjured animals due to a decrease in respiratory frequency. However, this sleep-induced reduction in respiratory frequency was not observed in contused animals at the acute injured stage. By contrast, the tidal volume was significantly lower during sleep in contused animals but not uninjured animals from the acute to the chronic injured stage. Moreover, the frequency of sigh and postsigh apnea was elevated in acutely contused animals. These results indicated that high cervical spinal contusion is associated with exacerbated sleep-induced attenuation of the tidal volume and higher occurrence of sleep apnea, which may be detrimental to respiratory functional recovery after cervical spinal cord injury. NEW & NOTEWORTHY Cervical spinal injury is usually associated with sleep-disordered breathing. The present study investigated breathing patterns across sleep-wake state following cervical spinal injury in the rat. Unilateral cervical spinal contusion significantly impacted sleep-induced alteration of breathing patterns, showing a blunted frequency response and exacerbated attenuated tidal volume and occurrence of sleep apnea. The result enables us to investigate effects of cervical spinal injury on the pathogenesis of sleep-disordered breathing and evaluate potential therapies to improve respiration.

Maturation of baseline breathing and of hypercapnic and hypoxic ventilatory responses in newborn mice

2001 ◽  
Vol 281 (5) ◽  
pp. R1746-R1753 ◽  
Author(s):  
Sylvain Renolleau ◽  
Stéphane Dauger ◽  
Fanny Autret ◽  
Guy Vardon ◽  
Claude Gaultier ◽  
...  
Keyword(s):  
Cesarean Section ◽  
Tidal Volume ◽  
Mammalian Species ◽  
Whole Body ◽  
Body Plethysmography ◽  
Genetic Studies ◽  
Newborn Mice ◽  
Ventilatory Responses ◽  
Neuronal Mechanisms ◽  
Whole Body Plethysmography

Breathing during the first postnatal hours has not been examined in mice, the preferred mammalian species for genetic studies. We used whole body plethysmography to measure ventilation (V˙e), breath duration (TTOT), and tidal volume (Vt) in mice delivered vaginally (VD) or by cesarean section (CS). In experiment 1, 101 VD and 100 CS pups aged 1, 6, 12, 24, or 48 h were exposed to 8% CO2 or 10% O2for 90 s. In experiment 2, 31 VD pups aged 1, 12, or 24 h were exposed to 10% O2 for 5 min. Baseline breathing maturation was delayed in CS pups, but V˙eresponses to hypercapnia and hypoxia were not significantly different between VD and CS pups [at postnatal age of 1 h (H1): 48 ± 44 and 18 ± 32%, respectively, in VD and CS pups combined]. TheV˙e increase induced by hypoxia was greater at H12 (46 ± 27%) because of TTOT response maturation. At all ages, hypoxic decline was ascribable mainly to a Vtdecrease, and posthypoxic decline was ascribable to a TTOTincrease with apneas, suggesting different underlying neuronal mechanisms.

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