Effects of Alfentanil on the Ventilatory Response to Sustained Hypoxia

1998 ◽  
Vol 89 (3) ◽  
pp. 612-619. ◽  
Author(s):  
Christopher R. Cartwright ◽  
Lindsey C. Henson ◽  
Denham Ward
Keyword(s):  
Ventilatory Response ◽  
Acute Hypoxia ◽  
Initial Increase ◽  
Absolute Value ◽  
Computer Controlled ◽  
The Absolute ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Hypoxia ◽  
Healthy Persons

Background The ventilatory response to acute hypoxia is biphasic, with an initial rapid increase followed by a slower decline. In humans, there is evidence that the magnitude of the decline in ventilation is proportional to the size of the initial increase. This study was done to define the role of exogenous opioids in the ventilatory decline seen with prolonged hypoxia. Methods Ten healthy persons were exposed to isocapnic hypoxia for 25 min, followed by 5 min of isocapnic normoxia and 5 min of isocapnic hypoxia. These conditions were repeated during a computer-controlled alfentanil infusion. Results Serum alfentanil levels were constant among the volunteers (38+/-12 ng/ml). Alfentanil decreased both the initial and second acute hypoxic responses (from 1.27+/-0.73 to 0.99+/-0.39 l x min(-1) x %(-1), P < 0.05; and from 0.99+/-0.70 to 0.41+/-0.29 l x min(-1) x %(-1), P < 0.05, respectively). The magnitude of the decrease in ventilation during the 25 min of hypoxia was not changed (10+/-3.3 l/min for control; 12.3+/-7.5 l/min for alfentanil). Conclusions Alfentanil reduced the acute ventilatory response to hypoxia. The absolute value of hypoxic ventilatory decline was not increased, but a measure of residual hypoxic ventilatory decline (the ratio of ventilation between the second and first steps into hypoxia) was decreased, which supports the hypothesis that opioids potentiate centrally mediated ventilatory decline.

Ventilatory response to sustained hypoxia in normal adults

1986 ◽  
Vol 61 (3) ◽  
pp. 906-911 ◽  
Author(s):  
P. A. Easton ◽  
L. J. Slykerman ◽  
N. R. Anthonisen
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Initial Increase ◽  
Fractional Concentration ◽  
Subsequent Decrease ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia ◽  
Normal Adults ◽  
Ventilatory Response To Hypoxia

We examined the ventilatory response to moderate (arterial O2 saturation 80%), sustained, isocapnic hypoxia in 20 young adults. During 25 min of hypoxia, inspiratory minute ventilation (VI) showed an initial brisk increase but then declined to a level intermediate between the initial increase and resting room air VI. The intermediate level of VI was a plateau that did not change significantly when hypoxia was extended up to 1 h. The relation between the amount of initial increase and subsequent decrease in ventilation during constant hypoxia was not random; the magnitude of the eventual decline correlated confidently with the degree of initial hyperventilation. Evaluation of breathing pattern revealed that during constant hypoxia there was little alteration in respiratory timing and that the changes in VI were related to significant alterations in tidal volume and mean inspiratory flow (VT/TI). None of the changes was reproduced during a sham control protocol, in which room air was substituted for the period of low fractional concentration of inspired O2. We conclude that ventilatory response to hypoxia in adults is not sustained; it exhibits some biphasic features similar to the neonatal hypoxic response.

Ventilatory responses to hypoxia in rats pretreated with nonpeptide NK1 receptor antagonist CP-96,345

1994 ◽  
Vol 76 (4) ◽  
pp. 1528-1532 ◽  
Author(s):  
G. T. De Sanctis ◽  
F. H. Green ◽  
X. Jiang ◽  
M. King ◽  
J. E. Remmers
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Frequency Component ◽  
Nk1 Receptor ◽  
Adult Rats ◽  
Nk1 Receptors ◽  
Before And After ◽  
Sites Of Action

This study reports experiments designed to evaluate the role of neurokinin-1 (NK1) receptors for substance P (SP) in the ventilatory response to acute hypoxia. Ventilation was measured by indirect plethysmography in eight unanesthetized unrestrained adult rats before and after bolus injection of 1, 5, or 10 mg/kg (ip) of CP-96,345 (Pfizer), a potent nonpeptide competitive antagonist of the SP NK1 receptor. Ventilation was measured while the rats breathed air or 8% O2–92% N2 with and without administration of SP antagonist. Pretreatment with CP-96,345 decreased the magnitude of the hypoxic response in a dose-dependent fashion. Minute ventilation in rats pretreated with CP-96,345 was reduced by 22.1% (P < 0.05) at the highest dose (10 mg/kg), largely because of an attenuation of the frequency component. Although both control and treated rats responded to hypoxia with a decrease in duration of inspiration and expiration rats pretreated with CP-96,345 displayed a smaller decrease in inspiration and expiration than control rats (P < 0.05). We have recently shown that neuropeptide-containing fibers are important for mediating the tachypnic response during acute isocapnic hypoxia in rats. The attenuation in minute ventilation at the highest dose (10 mg/kg) is comparable in magnitude to the attenuation observed with neonatal capsaicin treatment, which permanently ablates neuropeptide-containing unmyelinated fibers. Accordingly, this previously reported role of capsaicin-sensitive nerves in the hypoxic ventilatory response of rats is probably attributable to released SP acting at NK1 receptors. One of the likely sites of action of SP antagonists is the carotid body.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Role Of Glutamate On The Ventilatory Response To Hypoxia During Lactic Acid Infusion In Newborn Piglets. ♦ 1638

1998 ◽  
Vol 43 ◽  
pp. 280-280 ◽  
Author(s):  
Gianina Davila ◽  
Oscar Ovalle ◽  
Dorothy Hehre ◽  
Carlos Devia ◽  
Jian Huang ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Ventilatory Response ◽  
Acid Infusion ◽  
Newborn Piglets ◽  
Ventilatory Response To Hypoxia

scholarly journals Role of GABA on the Ventilatory Response to Hypoxia during Lactic Acid Infusion

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 300A-300A
Author(s):  
Gianina Davila ◽  
Carlos Devia ◽  
Dorothy Hehre ◽  
Jian Huang ◽  
Eduardo Bancalari ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Ventilatory Response ◽  
Acid Infusion ◽  
Ventilatory Response To Hypoxia

scholarly journals Evidence from high-altitude acclimatization for an integrated cerebrovascular and ventilatory hypercapnic response but different responses to hypoxia

2017 ◽  
Vol 123 (6) ◽  
pp. 1477-1486 ◽  
Author(s):  
Zachary M. Smith ◽  
Erin Krizay ◽  
Rui Carlos Sá ◽  
Ethan T. Li ◽  
Miriam Scadeng ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Control Mechanism ◽  
Integrated Control ◽  
Acute Hypoxia ◽  
Absolute Value ◽  
Ventilatory Responses ◽  
Two Systems ◽  
Hypercapnic Response ◽  
Sustained Hypoxia

Ventilation and cerebral blood flow (CBF) are both sensitive to hypoxia and hypercapnia. To compare chemosensitivity in these two systems, we made simultaneous measurements of ventilatory and cerebrovascular responses to hypoxia and hypercapnia in 35 normal human subjects before and after acclimatization to hypoxia. Ventilation and CBF were measured during stepwise changes in isocapnic hypoxia and iso-oxic hypercapnia. We used MRI to quantify actual cerebral perfusion. Measurements were repeated after 2 days of acclimatization to hypoxia at 3,800 m altitude (partial pressure of inspired O2 = 90 Torr) to compare plasticity in the chemosensitivity of these two systems. Potential effects of hypoxic and hypercapnic responses on acute mountain sickness (AMS) were assessed also. The pattern of CBF and ventilatory responses to hypercapnia were almost identical. CO2 responses were augmented to a similar degree in both systems by concomitant acute hypoxia or acclimatization to sustained hypoxia. Conversely, the pattern of CBF and ventilatory responses to hypoxia were markedly different. Ventilation showed the well-known increase with acute hypoxia and a progressive decline in absolute value over 25 min of sustained hypoxia. With acclimatization to hypoxia for 2 days, the absolute values of ventilation and O2 sensitivity increased. By contrast, O2 sensitivity of CBF or its absolute value did not change during sustained hypoxia for up to 2 days. The results suggest a common or integrated control mechanism for CBF and ventilation by CO2 but different mechanisms of O2 sensitivity and plasticity between the systems. Ventilatory and cerebrovascular responses were the same for all subjects irrespective of AMS symptoms. NEW & NOTEWORTHY Ventilatory and cerebrovascular hypercapnic response patterns show similar plasticity in CO2 sensitivity following hypoxic acclimatization, suggesting an integrated control mechanism. Conversely, ventilatory and cerebrovascular hypoxic responses differ. Ventilation initially increases but adapts with prolonged hypoxia (hypoxic ventilatory decline), and ventilatory sensitivity increases following acclimatization. In contrast, cerebral blood flow hypoxic sensitivity remains constant over a range of hypoxic stimuli, with no cerebrovascular acclimatization to sustained hypoxia, suggesting different mechanisms for O2 sensitivity in the two systems.

scholarly journals Ventilatory Response to Hypoxia during Endotoxemia in Young Rats: Role of Nitric Oxide

2007 ◽  
Vol 62 (2) ◽  
pp. 134-138 ◽  
Author(s):  
John Ladino ◽  
Eduardo Bancalari ◽  
Cleide Suguihara
Keyword(s):  
Nitric Oxide ◽  
Ventilatory Response ◽  
Young Rats ◽  
Ventilatory Response To Hypoxia

Role of nitric oxide in hypoxic hypometabolism in rats

1999 ◽  
Vol 87 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Henry Gautier ◽  
Cristina Murariu
Keyword(s):  
Nitric Oxide ◽  
Ventilatory Response ◽  
No Synthase ◽  
Adult Rats ◽  
Ambient Temperatures ◽  
Thermal Changes ◽  
Synthase Inhibitor ◽  
Colonic Temperature ◽  
Ventilatory Response To Hypoxia

Because it has been recently suggested that nitric oxide (NO) may mediate the effects of hypoxia on body temperature and ventilation, the present study was designed to assess more completely the effects of a neuronal NO synthase inhibitor (7-nitroindazole, 25 mg/kg ip), at ambient temperature of 26 and 15°C, on the ventilatory (V˙), metabolic (O2 consumption), and thermal changes (colonic and tail temperatures) induced by ambient hypoxia (fractional inspired O2 of 11%) or CO hypoxia (fractional inspired CO of 0.07%) in intact, unanesthetized adult rats. At both ambient temperatures, 7-nitroindazole decreased oxygen consumption, colonic temperature, andV˙ in normoxia. The drug reduced ambient or CO hypoxia-induced hypometabolism and ventilatory response, but the hypothermia persisted. It is concluded that NO arising from neural NO synthase plays an important role in the control of metabolism andV˙ in normoxia. As well, it mediates, in part, the hypometabolic and the ventilatory response to hypoxia. The results are consistent with the notion that central nervous system hypoxia resets the thermoregulatory set point by decreasing brain NO.

Respiration of conscious kittens in acute hypoxia and effect of almitrine bismesylate

1985 ◽  
Vol 59 (1) ◽  
pp. 18-23 ◽  
Author(s):  
H. B. McCooke ◽  
M. A. Hanson
Keyword(s):  
Ambient Temperature ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Second Phase ◽  
Biphasic Response ◽  
Almitrine Bismesylate ◽  
Peak Increase ◽  
Ventilatory Response To Hypoxia

Respiration was measured noninvasively in conscious kittens at an ambient temperature of 28–32 degrees C. Inspired O2 fraction (FIO2) was reduced abruptly from 0.21 to 0.12, 0.10, or 0.08 for 5 min on the day of birth and then on days 4, 7, 14, and 28. The ventilatory response to hypoxia was biphasic, as reported previously in anesthetized kittens, with minute ventilation (VE) increasing in the first minute and then falling towards control over the next 4 min. The fall in VE was due to a consistent fall in tidal volume, the changes in frequency during the second phase being more variable. The size of the first phase of the response increased up to 14 days, but the time at which the peak increase in VE occurred was not correlated with age. The degree of the secondary fall in VE was similar at each age and at each FIO2 studied. The degree of the biphasic response was significantly reduced after administration of almitrine (2 mg/kg ip) on days 1 and 4, but almitrine did not affect the response in older kittens.

Diphasic ventilatory response to hypoxia in newborn lambs

1984 ◽  
Vol 56 (1) ◽  
pp. 84-90 ◽  
Author(s):  
M. A. Bureau ◽  
R. Zinman ◽  
P. Foulon ◽  
R. Begin
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Major Determinant ◽  
Occlusion Pressure ◽  
Airway Occlusion ◽  
Age Related ◽  
Airway Occlusion Pressure ◽  
Respiratory Centers ◽  
Ventilatory Response To Hypoxia

The ventilatory response of newborn lambs to hypoxemia was evaluated in two groups of seven awake lambs studied at 2 and 7 days of life. Minute ventilation (VE) and airway occlusion pressure (P0.1) were monitored as the animals were exposed in sequence to room air, 12% O2 (15 min), 7% O2 (15 min), and room air. On 12 and 7% O2, 2-day-old lambs experienced a brisk hyperventilation followed by a VE depression, previously described in newborns of other species (diphasic response). The 7-day-old lambs had a clear diphasic VE response only on 7% O2 breathing. In the 2-day-old lambs, at the time of the relative VE depression to 12% O2, the respiratory centers showed a persisting responsiveness to further hypoxia; switching to 7% O2 caused a brisk increase in VE and P0.1 of 70 and 130%, respectively, which was followed again by a VE depression. The magnitude of the immediate VE response to hypoxia, taken as an index of the chemoreceptor strength, was inversely related to the magnitude of the VE depression (R = 0.81, P less than 0.001). It was concluded that 1) lambs as well as other neonates have an age-related diphasic VE response to hypoxia; 2) at the time of the VE depression, the respiratory centers maintain their responsiveness to further acute hypoxia; and 3) the weakness of the chemoreceptors in the newborn is a major determinant of the diphasic response.

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