No effect of brain blood flow on ventilatory depression during sustained hypoxia

Suzuki, Akihiko; Nishimura, Masaharu; Yamamoto, Hiroshi; Miyamoto, Kenji; Kishi, Fujiya; Kawakami, Yoshikazu

doi:10.1152/jappl.1989.66.4.1674

Cited by 33 publications

(30 citation statements)

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“…Extending these findings, Brown and Lawson (22) demonstrated an acidotic shift in brain stem extracellular fluid during the late ventilatory depression in neonatal piglets. Also, Suzuki et al (23) recently showed no differences in jugular venous Pco, (which was used as an index of brain tissue Pco2) between human adults with sustained and unsustained ventilatory response to hypoxia.…”

Section: Resultsmentioning

confidence: 99%

Brain Blood Flow and Ventilatory Response to Hypoxia in Sedated Newborn Piglets

1990

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ABSTRACT. To evaluate the relationship between brain blood flow and ventilatory response to hypoxia, seventeen sedated, spontaneously breathing newborn piglets were studied. Minute ventilation (VE) was measured by pneumotachograph, cardiac output by thermodilution and total brain and brain stem blood flows with radiolabeled microspheres. Measurements were performed while the animals were breathing room air and after 10 min of hypoxia induced by breathing 10% Oz. Two patterns of ventilatory response to hypoxia were observed in the study animals. All animals increased VE during the 1st min of hypoxia, but nine (mean 2 SD; age 5 2 1.3 d; wt 1828 2 437 g) sustained increased VE after 10 min of hypoxia (T VE group). The remaining eight animals (age 5 f 1.2 d; wt 1751 k 168 g) had decreased VE at 10 rnin of hypoxia to values less than their room air baseline (J VE group). The decrease in Paoz during hypoxia was similar in both groups, however the Pacoz decreased significantly only in the TVE group. Although cardiac output increased significantly during hypoxia in both groups, the,values during normoxia and hypoxia were lower in the JVE group (p < 0.001). Arterial blood pressure increased significantly during hypoxia only in the TVE group. The increase in total brain and brain stem blood flows with hypoxia was similar in both groups, despite the two different patterns of ventilatory response to hypoxia. These data suggest that in this animal model the distinct patterns of ventilatory response to hypoxia are not related to the changes in total brain or brain stem blood flows that occur during hypoxia. (Pediatr Res 27: 327-331,1990) Abbreviations vE, minute ventilation CO, cardiac output BBF, total brain blood flow BSBF, brain stem blood flow RA, room air ABP, arterial blood pressure V,, tidal volume Cdyn, dynamic lung compliance Rb pulmonary resistanceThe ventilatory response to hypoxia during the first days after birth is characterized in humans and several animal species by a transient initial increase in ventilation (1-2 min), followed by a marked decline in vE to values slightly above or below prehypoxia basal values (1-6). The mechanism responsible for this biphasic response to hypoxia has not been completely elucidated. Various neurotransmitters or modulators released during hypoxia such as endorphins, y-aminobutyric acid, prostaglandins, and adenosine have been suggested as possible mediators of the late decrease in ventilation (2,7-10). Other possible explanations have included changes in lung mechanics, a decrease in the metabolic rate, respiratory muscle fatigue, and inhibition of peripheral chemoreceptors (3, 1 1 -14). The increase in cerebral blood flow that occurs in response to hypoxia can induce a decrease in P C O~ and Hf in the CNS extracellular fluid and this may also account for the decrease in respiratory drive (15). Conversely, the absence of a normal cardiovascular response and the increase in cerebral blood flow that normally occurs during hypoxemia can aggravate CNS hypoxia and lead to CNS de...

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Section: Resultsmentioning

confidence: 99%

Brain Blood Flow and Ventilatory Response to Hypoxia in Sedated Newborn Piglets

1990

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“…Qb(i)/Qb(2) was obtained from the Doppler data, and an assumed value of 8-7 mmHg for (Pb,co2 (1) -Pa,co2(1)) was used (Suzuki et al 1989) (see Discussion).…”

Section: Estimation Of Ventilation During Eucapnia and Hypercapniamentioning

confidence: 99%

“…(Pb,C02(2) -Pb,CO2 (01)) where, VE(1) and VE (2) are the values for expiratory ventilation during eucapnia and hypercapnia, respectively, and (Pb,co2(2) -Pb,c02 (1) Vb,CO2() (16) Equation (16) gives the change in Pb,co with hypoxia as a function of the ratio of blood flow in the euoxic and hypoxic conditions (obtained from the Doppler data) and the difference in PCO2 between brain tissue and arterial blood in euoxic eucapnia for which a value of 8-7 is assumed (Suzuki et al 1989) (again, see Discussion).…”

Section: Estimation Of Ventilation During Eucapnia and Hypercapniamentioning

confidence: 99%

“…These data were used to calculate the ventilatory sensitivity to changes in brain tissue Pco, Definition of' terms: gh1 the ratio of the sensitivity decrease to the decrease in the arterial fractional oxygen saturation; g,oo, the steady-state chemoreflex sensitivity to hypoxia when oxygen saturation has been sustained at 100 %; kp, offset so that peripheral ventilatioti can take a non-zero value when saturation is 100%; Trp, the time constant for the rapid peripheral chemoreflex response for the on-transient; TP21 the time constant for the rapid peripheral chemoreflex response for the off-transient; Th, the time constant associated with the development of hypoxic ventilatory decline: V,, the central chemoreflex contribution to ventilation; dp, the peripheral time delay. APbCo2 for a given change in cerebral blood flow is calculated from eqn 16; dVEpred is calculated from eqn (17); HVD is obtained from the data in Table 1. (AVE/APb ,C2) Also presented in Table 3 are the data showing the calculated change in brain tissue PC02 with hypoxia, related to the change in MCAF, also assuming a difference of 8-7 mmHg in PCO2 between brain tissue and arterial blood in euoxic eucapnia (Suzuki et al 1989). Table 3 also shows the predicted fall in VE through changes in cerebral blood flow and the actual measured values for HVD.…”

Section: Cerebral Blood Flow Responses To Hypoxia and Hypercapniamentioning

confidence: 99%

“…In humans, Suzuki, Nishimura, Yamamoto, Miyamoto, Kishi & Kawakami (1989) examined the time course of the response of jugular venous PC02 to a step into isocapnic hypoxia. While they observed a reduction in jugular venous PCO2 with hypoxia, they concluded that this reduction was too rapid to underlie HVD, which had a slower onset.…”

Section: Introductionmentioning

confidence: 99%

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Influence of cerebral blood flow on the ventilatory response to hypoxia in humans

Poulin¹,

Robbins²

1998

Experimental Physiology

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SUMMARYThe purpose of this study was to quantify the possible reduction in ventilation that could be attributed to changes in cerebral blood flow (CBF) with hypoxia to determine whether it could be of sufficient magnitude to underlie hypoxic ventilatory decline (HVD). Six subjects underwent 20 min of isocapnic hypoxia (end-tidal Po2, 50 mmHg). An index of CBF was obtained using transcranial Doppler ultrasound of the middle cerebral artery. The CBF sensitivities to hypoxia and hypercapnia were obtained from the percentage changes in CBF between the last 3 min of the hypoxic or hypercapnic exposure and the 3 min period prior to the exposure. The magnitude of HVD during hypoxia was estimated by fitting a simple model of the ventilatory response to the hypoxic stimulus. The predicted fall in expiratory ventilation (VE) due to a reduction in brain PCO, generated by the increase in CBF with hypoxia in all subjects was less than the measured magnitude of HVD (33 %). Thus, the results from this study suggest that, in awake humans, changes in CBF during acute isocapnic hypoxia are quantitatively insufficient to underlie HVD in humans.

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Ventilation and hypoxic ventilatory response of Tibetan and Aymara high altitude natives

Beall

Strohl

Blangero

et al. 1997

Am. J. Phys. Anthropol.

198

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Newcomers acclimatizing to high altitude and adult male Tibetan high altitude natives have increased ventilation relative to sea level natives at sea level. However, Andean and Rocky Mountain high altitude natives have an intermediate level of ventilation lower than that of newcomers and Tibetan high altitude natives although generally higher than that of sea level natives at sea level. Because the reason for the relative hypoventilation of some high altitude native populations was unknown, a study was designed to describe ventilation from adolescence through old age in samples of Tibetan and Andean high altitude natives and to estimate the relative genetic and environmental influences. This paper compares resting ventilation and hypoxic ventilatory response (HVR) of 320 Tibetans 9-82 years of age and 542 Bolivian Aymara 13-94 years of age, native residents at 3,800-4,065 m. Tibetan resting ventilation was roughly 1.5 times higher and Tibetan HVR was roughly double that of Aymara. Greater duration of hypoxia (older age) was not an important source of variation in resting ventilation or HVR in either sample. That is, contrary to previous studies, neither sample acquired hypoventilation in the age ranges under study. Within populations, greater severity of hypoxia (lower percent of oxygen saturation of arterial hemoglobin) was associated with slightly higher resting ventilation among Tibetans and lower resting ventilation and HVR among Aymara women, although the associations accounted for just 2-7% of the variation. Between populations, the Tibetan sample was more hypoxic and had higher resting ventilation and HVR. Other systematic environmental contrasts did not appear to elevate Tibetan or depress Aymara ventilation. There was more intrapopulation genetic variation in these traits in the Tibetan than the Aymara sample. Thirty-five percent of the Tibetan, but none of the Aymara, resting ventilation variance was due to genetic differences among individuals. Thirty-one percent of the Tibetan HVR, but just 21% of the Aymara, HVR variance was due to genetic differences among individuals. Thus there is greater potential for evolutionary change in these traits in the Tibetans. Presently, there are two different ventilation phenotypes among high altitude natives as compared with sea level populations at sea level: lifelong sustained high resting ventilation and a moderate HVR among Tibetans in contrast with a slightly elevated resting ventilation and a low HVR among Aymara.

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No effect of brain blood flow on ventilatory depression during sustained hypoxia

Cited by 33 publications

References 0 publications

Brain Blood Flow and Ventilatory Response to Hypoxia in Sedated Newborn Piglets

Brain Blood Flow and Ventilatory Response to Hypoxia in Sedated Newborn Piglets

Influence of cerebral blood flow on the ventilatory response to hypoxia in humans

Ventilation and hypoxic ventilatory response of Tibetan and Aymara high altitude natives

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