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.

Effects of p-chlorophenylalanine on ventilatory control in goats

1983 ◽  
Vol 54 (1) ◽  
pp. 277-283 ◽  
Author(s):  
G. S. Mitchell ◽  
C. A. Smith ◽  
E. H. Vidruk ◽  
L. C. Jameson ◽  
J. A. Dempsey
Keyword(s):  
Tryptophan Hydroxylase ◽  
Ventilatory Response ◽  
Blood Gases ◽  
Co2 Production ◽  
Neural Pathways ◽  
Ventilatory Control ◽  
Arterial Pco2 ◽  
Carotid Bodies ◽  
Bilateral Carotid ◽  
O2 Concentration

The effects of tryptophan hydroxylase inhibition with p-chlorophenylalanine (PCPA; 100 mg/kg iv) on ventilatory control were studied in awake goats. Ventilation, CO2 production, and blood gases were measured 16–24 h after PCPA at rest and during mild exercise in normoxia and at rest in hypoxia and hypercapnia. PCPA increased ventilation 36% at rest, predominantly through an effect on respiratory frequency, and decreased arterial PCO2 (PaCO2) 6.5 Torr. Ventilatory gain in exercise (delta VI/deltaVCO2) was increased 20% by PCPA thereby maintaining PaCO2 at its new resting value. Hypoxia (fractional inspired O2 concentration = 0.12) had little effect on ventilation or PaCO2 at rest, either on control or on PCPA test days. Ventilatory sensitivity to CO2 at rest (delta VI/delta PaCO2) was unaffected by PCPA. Bilateral carotid body denervation (CBX) was performed in the animals, and experiments were repeated 3 mo after the first administration of PCPA. CBX alone decreased ventilation 29% and increased PaCO2 9.4 Torr. Administration of PCPA increased ventilation 35%, decreased PaCO2 by 10.2 Torr at rest, and increased ventilatory gain in exercise 26%. Thus carotid bodies are not necessary for the ventilatory response to PCPA. Furthermore, the primary neural pathways associated with exercise or hypercapnia are not specifically affected by inhibition of serotonin metabolism via PCPA.

Dopamine and ventilatory effects of hypoxia and almitrine in chronically hypoxic rats

1989 ◽  
Vol 67 (1) ◽  
pp. 186-192 ◽  
Author(s):  
R. A. Wach ◽  
D. Bee ◽  
G. R. Barer
Keyword(s):  
Carotid Body ◽  
Ventilatory Response ◽  
Response Curves ◽  
Enhancing Effect ◽  
Stimulus Response ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Ventilatory Effects ◽  
Ventilatory Response To Hypoxia

We hypothesized that the temporary blunted ventilatory response to hypoxia seen in chronically hypoxic rats could be related to the increased amount of dopamine found in their carotid bodies. Rats, kept 2–3 wk in 10% O2, showed reduced nonisocapnic ventilatory responses to 21–12% inspiratory O2 fraction compared with control rats. Stimulus-response curves to almitrine, which simulates the action of hypoxia on the carotid body, were also depressed in chronically hypoxic rats. Responses to hypoxia and almitrine were significantly correlated in the two groups of rats. Dopamine depressed ventilation during normoxia, hypoxia, and almitrine stimulation in both groups, an action abolished by the dopamine-2 antagonist domperidone. Domperidone slightly increased responses to hypoxia and almitrine in control rats but had a greater enhancing effect in chronically hypoxic rats, such that there was no longer a difference between the responses of the two groups.

scholarly journals Bilateral Carotid Endarterectomy with Attempted Preservation of Carotid Body Function

1972 ◽  
Vol 175 (2) ◽  
pp. 268-273 ◽  
Author(s):  
Robert F. Hickey ◽  
William K. Ehrenfeld ◽  
F. Norman Hamilton ◽  
C. Philip Labson
Keyword(s):  
Carotid Endarterectomy ◽  
Carotid Body ◽  
Body Function ◽  
Bilateral Carotid

Ventilatory response to medroxyprogesterone acetate in normal subjects: time course and mechanism

1978 ◽  
Vol 44 (6) ◽  
pp. 939-944 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey ◽  
D. G. Kaiser
Keyword(s):  
Medroxyprogesterone Acetate ◽  
Time Course ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Maximum Effect ◽  
Adult Males ◽  
Stimulant Effect ◽  
Unbound Fraction ◽  
Arterial Pco2 ◽  
Lumbar Cerebrospinal Fluid

The time course of ventilatory adaptation to medroxyprogesterone acetate (MPA) and potential mediators of this response in plasma and lumbar CSF were determined in five healthy adult males. A significant decrease in arterial PCO2 (PACO2) at rest and exercise was noted within 48 h of drug administration with the maximum effect reached within 7 days and amounting to a 5-Torr decrement in PACO2. Blood and lumbar cerebrospinal fluid pH because significantly alkaline to control as soon as the ventilatory resporse was noted and remained alkaline during the treatment period. The ventilatory and dP/dt max response to exogenous CO2 was unchanged but their response to moderate exercise was increased after MPA. MPA-rlated materials were detected in both the plasma and CSF as soon as the ventilatory response was noted. The increase in CSF MPA-related materials approximated the unbound fraction determined in plasma. We conclude that [H+] in plasma and CSF is a function rather than a cause of ventilator acclimatization to MPA. MPA-related materials are capable of crossing the blood-brain barrier and could potentially exert their ventilatory stimulant effect by some central mechanism.

Effect of prenatal nicotine exposure on biphasic hypoxic ventilatory response and protein kinase C expression in caudal brain stem of developing rats

2004 ◽  
Vol 96 (6) ◽  
pp. 2213-2219 ◽  
Author(s):  
Narong Simakajornboon ◽  
Vukmir Vlasic ◽  
Hong Li ◽  
Hemant Sawnani
Keyword(s):  
Brain Stem ◽  
Ventilatory Response ◽  
Whole Body ◽  
Current Evidence ◽  
Nicotine Exposure ◽  
Respiratory Drive ◽  
Hypoxic Ventilatory Response ◽  
Prenatal Nicotine Exposure ◽  
Pkc Β ◽  
Prenatal Nicotine

Current evidence suggests that maternal smoking is associated with decreased respiratory drive and blunted hypoxic ventilatory response (HVR) in the newborn. The effect of prenatal nicotine exposure on overall changes in HVR has been studied; however, there is limited data on the effect of nicotine exposure on each component of biphasic HVR. To examine this issue, 5-day timed-pregnant Sprague-Dawley rats underwent surgical implantation of an osmotic minipump containing either normal saline (Con) or a solution of nicotine tartrate (Nic) to continuously deliver free nicotine at 6 mg·kg of maternal weight-1·day-1. Rat pups at postnatal days 5, 10, 15, and 20 underwent hypoxic challenges with 10% O2 for 20 min using whole body plethysmography. At postnatal day 5, Nic was associated with attenuation of peak HVR; peak minute ventilaton increased 44.0 ± 6.8% (SE) from baseline in Nic pups, whereas that of Con pups increased 62.9 ± 5.1% ( P < 0.05). Nic pups also had a reduction in the magnitude of ventilatory roll-off; minute ventilation at 15 min decreased 7.3 ± 7.1% in Nic pups compared with 27.3 ± 4.0% in Con pups ( P < 0.05). No significant difference in HVR was noted at postnatal days 10, 15, and 20. Hypercapnic response was similar at all ages. We further investigated the effect of prenatal nicotine exposure on PKC expression in the caudal brain stem (CB) of developing rats. At postnatal day 5, Nic was associated with increased expression of PKC-β and PKC-δ in CB, whereas other PKC isoforms were not affected. It is concluded that prenatal nicotine exposure is associated with modulation of biphasic HVR and a selective increase in the expression of PKC-β and PKC-δ within the CB of developing rats.

Hypertensive Encephalopathy After Bilateral Carotid Endarterectomy

Stroke ◽  
1995 ◽  
Vol 26 (3) ◽  
pp. 488-491 ◽  
Author(s):  
O. Ille ◽  
F. Woimant ◽  
A. Pruna ◽  
O. Corabianu ◽  
J. M. Idatte ◽  
...  
Keyword(s):  
Carotid Endarterectomy ◽  
Hypertensive Encephalopathy ◽  
Bilateral Carotid

Hypoxic ventilatory response and arterial desaturation during heavy work

1989 ◽  
Vol 67 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
S. R. Hopkins ◽  
D. C. McKenzie
Keyword(s):  
Maximal Exercise ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Ideal Gas ◽  
Respiratory Drive ◽  
O2 Uptake ◽  
Arterial Blood ◽  
Arterial Desaturation ◽  
Exercise Ventilation ◽  
Arterial O2 Saturation

Arterial desaturation in athletes during intense exercise has been reported by several authors, yet the etiology of this phenomenon remains obscure. Inadequate pulmonary ventilation, due to a blunted respiratory drive, has been implicated as a factor. To investigate the relationship between the ventilatory response to hypoxia, exercise ventilation, and arterial desaturation, 12 healthy male subjects [age, 23.8 +/- 3.6 yr; height, 181.6 +/- 5.6 cm; weight, 73.7 +/- 6.2 kg; and maximal O2 uptake (VO2max), 63.0 +/- 2.2 ml.kg-1 min-1] performed a 5-min treadmill test at 100% of VO2max, during which arterial blood samples and ventilatory data were collected every 15 s. Alveolar PO2 (PAO2) was determined using the ideal gas equation. On a separate occasion the ventilatory response to isocapnic hypoxia was measured. Arterial PO2 decreased by an average of 29 Torr during the test, associated with arterial desaturation [arterial O2 saturation (SaO2) 92.0%]. PAO2 was maintained; however, alveolar-arterial gas pressure difference increased progressively to greater than 40 Torr. Minimal hypocapnia was observed, despite marked metabolic acidosis. There was no significant correlation observed between hypoxic drives and ventilation-to-O2 uptake ratio or SaO2 (r = 0.1 and 0.06, respectively, P = NS). These data support the conclusions that hypoxic drives are not related to maximal exercise ventilation or to the development of arterial desaturation during maximal exercise.

Ventilatory effects and interactions with change in PaO2 in awake goats

1991 ◽  
Vol 71 (4) ◽  
pp. 1254-1260 ◽  
Author(s):  
L. Daristotle ◽  
M. J. Engwall ◽  
W. Z. Niu ◽  
G. E. Bisgard
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Ventilatory Response ◽  
Respiratory Frequency ◽  
Systemic Hypoxia ◽  
Ventilatory Effects ◽  
Arterial Po2

We utilized selective carotid body (CB) perfusion while changing inspired O2 fraction in arterial isocapnia to characterize the non-CB chemoreceptor ventilatory response to changes in arterial PO2 (PaO2) in awake goats and to define the effect of varying levels of CB PO2 on this response. Systemic hyperoxia (PaO2 greater than 400 Torr) significantly increased inspired ventilation (VI) and tidal volume (VT) in goats during CB normoxia, and systemic hypoxia (PaO2 = 29 Torr) significantly increased VI and respiratory frequency in these goats. CB hypoxia (CB PO2 = 34 Torr) in systemic normoxia significantly increased VI, VT, and VT/TI; the ventilatory effects of CB hypoxia were not significantly altered by varying systemic PaO2. We conclude that ventilation is stimulated by systemic hypoxia and hyperoxia in CB normoxia and that this ventilatory response to changes in systemic O2 affects the CB O2 response in an additive manner.

The Durability of Bilateral Carotid Endarterectomy

1995 ◽  
Vol 9 (1) ◽  
pp. 16-20 ◽  
Author(s):  
Phillip J. Rossi ◽  
R. James Valentine ◽  
Stuart I. Myers ◽  
Patrick T. Brillant ◽  
Arun Chervu ◽  
...  
Keyword(s):  
Carotid Endarterectomy ◽  
Bilateral Carotid
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