Hypoxic ventilatory response in cats lightly anesthetized with ketamine: effects of halothane and sevoflurane in low concentrations

1991 ◽  
Vol 5 (3) ◽  
pp. 233-238 ◽  
Author(s):  
Chiharu Tamura ◽  
Matsuyuki Doi ◽  
Kazuyuki Ikeda
Keyword(s):  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Low Concentrations

scholarly journals Release of ATP by pre-Bötzinger complex astrocytes contributes to the hypoxic ventilatory response via a Ca2+ -dependent P2Y1 receptor mechanism

2017 ◽  
Vol 596 (15) ◽  
pp. 3245-3269 ◽  
Author(s):  
Vishaal Rajani ◽  
Yong Zhang ◽  
Venkatesh Jalubula ◽  
Vladimir Rancic ◽  
Shahriar SheikhBahaei ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
P2y1 Receptor ◽  
Hypoxic Ventilatory Response ◽  
Bötzinger Complex

Methysergide augments the acute, but not the sustained, hypoxic ventilatory response in goats

1999 ◽  
Vol 118 (1) ◽  
pp. 25-37 ◽  
Author(s):  
Jay K. Herman ◽  
Ken D. O’Halloran ◽  
Gordon S. Mitchell ◽  
Gerald E. Bisgard
Keyword(s):  
Ventilatory Response ◽  
Hypoxic Ventilatory Response

scholarly journals Chronic intermittent hyperoxia alters the development of the hypoxic ventilatory response in neonatal rats

2016 ◽  
Vol 220 ◽  
pp. 69-80 ◽  
Author(s):  
Sarah Logan ◽  
Kristina E. Tobin ◽  
Sarah C. Fallon ◽  
Kevin S. Deng ◽  
Amy B. McDonough ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Neonatal Rats ◽  
Hypoxic Ventilatory Response

Blunted hypoxic ventilatory drive in subjects susceptible to high-altitude pulmonary edema

1989 ◽  
Vol 66 (3) ◽  
pp. 1152-1157 ◽  
Author(s):  
Y. Matsuzawa ◽  
K. Fujimoto ◽  
T. Kobayashi ◽  
N. R. Namushi ◽  
K. Harada ◽  
...  
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Pulmonary Function Test ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
High Altitude Pulmonary Edema ◽  
Function Test ◽  
History Of ◽  
Low Altitude

It has been proposed that subjects susceptible to high-altitude pulmonary edema (HAPE) show exaggerated hypoxemia with relative hypoventilation during the early period of high-altitude exposure. Some previous studies suggest the relationship between the blunted hypoxic ventilatory response (HVR) and HAPE. To examine whether all the HAPE-susceptible subjects consistently show blunted HVR at low altitude, we evaluated the conventional pulmonary function test, hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) in ten lowlanders who had a previous history of HAPE and compared these results with those of eight control lowlanders who had no history of HAPE. HVR was measured by the progressive isocapnic hypoxic method and was evaluated by the slope relating minute ventilation to arterial O2 saturation (delta VE/delta SaO2). HCVR was measured by the rebreathing method of Read. All measurements were done at Matsumoto, Japan (610 m). All the HAPE-susceptible subjects showed normal values in the pulmonary function test. In HCVR, HAPE-susceptible subjects showed relatively lower S value, but there was no significant difference between the two groups (1.74 +/- 1.16 vs. 2.19 +/- 0.4, P = NS). On the other hand, HAPE-susceptible subjects showed significantly lower HVR than control subjects (-0.42 +/- 0.23 vs. -0.87 +/- 0.29, P less than 0.01). These results suggest that HAPE-susceptible subjects more frequently show low HVR at low altitude. However, values for HVR were within the normal range in 2 of 10 HAPE-susceptible subjects. It would seem therefore that low HVR alone need not be a critical factor for HAPE. This could be one of several contributing factors.

Living high-training low increases hypoxic ventilatory response of well-trained endurance athletes

2002 ◽  
Vol 93 (4) ◽  
pp. 1498-1505 ◽  
Author(s):  
Nathan E. Townsend ◽  
Christopher J. Gore ◽  
Allan G. Hahn ◽  
Michael J. McKenna ◽  
Robert J. Aughey ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Endurance Athletes ◽  
Hypoxic Exposure ◽  
Dependent Manner ◽  
Hypoxic Ventilatory Response ◽  
Ambient Conditions ◽  
Altitude Exposure ◽  
End Tidal

This study determined whether “living high-training low” (LHTL)-simulated altitude exposure increased the hypoxic ventilatory response (HVR) in well-trained endurance athletes. Thirty-three cyclists/triathletes were divided into three groups: 20 consecutive nights of hypoxic exposure (LHTLc, n = 12), 20 nights of intermittent hypoxic exposure (four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia, LHTLi, n = 10), or control (Con, n = 11). LHTLc and LHTLi slept 8–10 h/day overnight in normobaric hypoxia (∼2,650 m); Con slept under ambient conditions (600 m). Resting, isocapnic HVR (ΔV˙e/ΔSpO2 , whereV˙e is minute ventilation and SpO2 is blood O2 saturation) was measured in normoxia before hypoxia (Pre), after 1, 3, 10, and 15 nights of exposure (N1, N3, N10, and N15, respectively), and 2 nights after the exposure night 20 (Post). Before each HVR test, end-tidal Pco 2(Pet CO2 ) and V˙e were measured during room air breathing at rest. HVR (l · min−1 · %−1) was higher ( P < 0.05) in LHTLc than in Con at N1 (0.56 ± 0.32 vs. 0.28 ± 0.16), N3 (0.69 ± 0.30 vs. 0.36 ± 0.24), N10 (0.79 ± 0.36 vs. 0.34 ± 0.14), N15 (1.00 ± 0.38 vs. 0.36 ± 0.23), and Post (0.79 ± 0.37 vs. 0.36 ± 0.26). HVR at N15 was higher ( P < 0.05) in LHTLi (0.67 ± 0.33) than in Con and in LHTLc than in LHTLi. Pet CO2 was depressed in LHTLc and LHTLi compared with Con at all points after hypoxia ( P < 0.05). No significant differences were observed for V˙e at any point. We conclude that LHTL increases HVR in endurance athletes in a time-dependent manner and decreases Pet CO2 in normoxia, without change inV˙e. Thus endurance athletes sleeping in mild hypoxia may experience changes to the respiratory control system.

Acute hypoxic ventilatory response and exercise-induced arterial hypoxemia in men and women

2004 ◽  
Vol 143 (1) ◽  
pp. 37-48 ◽  
Author(s):  
Jordan A. Guenette ◽  
Tu T. Diep ◽  
Michael S. Koehle ◽  
Glen E. Foster ◽  
Jennifer C. Richards ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Men And Women ◽  
Arterial Hypoxemia ◽  
Exercise Induced

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.

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